Medline 1 - 100

Base de datos: Buscar en Ovid Medline
Estrategia de búsqueda:
--------------------------------------------------------------------------------
1 Kidney transplantation.mp. or exp Kidney Transplantation/ (98250)
2 exp Metabolic Syndrome/ (29903)
3 insulin resistance.mp. or Insulin Resistance/ (91564)
4 2 or 3 (112904)
5 1 and 4 (383)
***************************
<1>
Unique Identifier
30852120
Title
Successful Kidney Transplantation Is Associated With Weight Gain From Truncal Obesity and Insulin
Resistance.
Source
Journal of Renal Nutrition. 2019 Mar 06.
VI 1
Record Owner
From MEDLINE, a database of the U.S. National Library of Medicine.
Status
Publisher
Authors
Workeneh B; Moore LW; Nolte Fong JV; Shypailo R; Gaber AO; Mitch WE.
Authors Full Name
Workeneh, Biruh; Moore, Linda W; Nolte Fong, Joy V; Shypailo, Roman; Gaber, A Osama; Mitch,
William E.
Institution
Workeneh, Biruh. Department of Medicine, MD Anderson Cancer Center, Houston, Texas; Division of
Nephrology, Baylor College of Medicine, Houston, Texas. Electronic address:
BTWorkeneh@mdanderson.org.
Moore, Linda W. Department of Surgery, Houston Methodist Hospital, Houston, Texas.
Nolte Fong, Joy V. Department of Surgery, Houston Methodist Hospital, Houston, Texas.
Shypailo, Roman. Division of Pediatrics, Baylor College of Medicine, Houston, Texas.
Gaber, A Osama. Department of Surgery, Houston Methodist Hospital, Houston, Texas; Weill Cornell
Medical College, Houston, Texas.
Mitch, William E. Division of Nephrology, Baylor College of Medicine, Houston, Texas.
Abstract
OBJECTIVE: The objective of this study is to compare changes in body composition, lifestyle factors,
and metabolic responses occurring in living kidney transplant recipient patients after transplantation.
DESIGN AND METHODS: The study was a single-site, prospective, observational study. To identify
metabolic responses during the initial years after transplantation, we obtained state-of-the-art, high-
resolution measurements of body composition from a 4-compartment model using dual-energy X-ray
absorptiometry, air displacement plethysmography, and total body potassium and nitrogen counters. We
also assessed dietary recalls and actigraphy before transplantation and 3- and 12-month after
transplantation. The study was conducted at a quaternary care hospital outpatient transplant center and a
United States Department of Agriculture Agricultural Research Service center. Thirty-one adults receiving
a living donor kidney allograft were studied. The main outcome measures were change in body
composition at 3 months and 1 year after transplantation, and this was correlated with the occurrence of
insulin resistance.
RESULTS: In patients receiving a successful kidney transplant from living donors treated with standard
immunosuppression, significant increases in body weight were detected at 3 and 12 months after
transplantation (2.2 kg, P = .03 and 6.6 kg, P < .0001, respectively). Weight gain was principally due to
adipose tissue accumulation in the truncal region. There was no increase in muscle mass or fluid
accumulation. Weight gain was not associated with changes in resting energy expenditure or physical
activity. Notably, increases in visceral and subcutaneous adipose tissue were positively correlated with
insulin resistance.
CONCLUSION: Successful transplantation was associated with increased insulin resistance and weight
gain without increases in muscle or fluid. This metabolic pattern suggests potential interventions that could
prevent or mitigate the consequences of adipose tissue accumulation in transplant recipients. Copyright ©
2019 National Kidney Foundation, Inc. Published by Elsevier Inc. All rights reserved.
Publication Type
Journal Article.
Year of Publication
2019
Link to the Ovid Full Text or citation:

Click here for full text options
<2>
Unique Identifier
31450550
Title
Association of Low Serum l-Carnitine Levels with Peripheral Arterial Stiffness in Patients Who Undergo
Kidney Transplantation.
Source
Nutrients. 11(9), 2019 Aug 24.
VI 1
Record Owner
Status
In-Process
Authors
Lai YH; Lee MC; Ho GJ; Liu CH; Hsu BG.
Author NameID
Lee, Ming-Che; ORCID: https://orcid.org/0000-0002-0321-910X
Hsu, Bang-Gee; ORCID: https://orcid.org/0000-0001-9364-4558
Authors Full Name
Lai, Yu-Hsien; Lee, Ming-Che; Ho, Guan-Jin; Liu, Chin-Hung; Hsu, Bang-Gee.
Institution
Lai, Yu-Hsien. Division of Nephrology, Hualien Tzu Chi Hospital, Buddhist Tzu Chi Medical
Foundation, Hualien 97004, Taiwan.
Lai, Yu-Hsien. Program in Pharmacology and Toxicology, Tzu Chi University, Hualien 97004, Taiwan.
Lee, Ming-Che. Department of Surgery, Hualien Tzu Chi Hospital, Buddhist Tzu Chi Medical
Foundation, Hualien 97004, Taiwan.
Lee, Ming-Che. School of Medicine, Tzu Chi University, Hualien 97004, Taiwan.
Ho, Guan-Jin. Department of Surgery, Hualien Tzu Chi Hospital, Buddhist Tzu Chi Medical Foundation,
Hualien 97004, Taiwan.
Ho, Guan-Jin. School of Medicine, Tzu Chi University, Hualien 97004, Taiwan.
Page 2
Liu, Chin-Hung. Program in Pharmacology and Toxicology, Tzu Chi University, Hualien 97004, Taiwan.
chinhung@mail.tcu.edu.tw.
Liu, Chin-Hung. Department of Pharmacology, Tzu Chi University, Hualien 97004, Taiwan.
chinhung@mail.tcu.edu.tw.
Hsu, Bang-Gee. Division of Nephrology, Hualien Tzu Chi Hospital, Buddhist Tzu Chi Medical
Foundation, Hualien 97004, Taiwan. gee.lily@msa.hinet.net.
Hsu, Bang-Gee. School of Medicine, Tzu Chi University, Hualien 97004, Taiwan.
gee.lily@msa.hinet.net.
Keyword Heading
brachial-ankle pulse wave velocity
kidney transplantation
l-carnitine
peripheral arterial stiffness
Abstract
l-carnitine is an important co-factor in fatty-acid metabolism, and its deficiency is associated with insulin
resistance, which is independently associated with arterial stiffness. This study evaluated the relationship
between serum l-carnitine level and peripheral arterial stiffness (PAS) in kidney transplantation (KT).
Fasting blood samples were collected from 65 patients who underwent KT. We measured the brachial-
ankle pulse wave velocity, and 36 patients (55.4%) had PAS. Patients with PAS had a significantly higher
percentage of diabetes (p = 0.001), hypertension (p = 0.033), and metabolic syndrome (p = 0.044); higher
waist circumference (p = 0.010), systolic blood pressure (p = 0.002), serum triglyceride level (p = 0.040),
insulin level (p = 0.002), and homeostasis model assessment of insulin resistance (p = 0.002); lower high-
density lipoprotein cholesterol (p = 0.036) and serum l-carnitine levels (p < 0.001); older age (p = 0.041);
and a longer KT duration (p = 0.025) than those without PAS. Statistical analysis revealed an independent
association between PAS in KT and KT duration (95% confidence interval (CI): 1.003-1.054, p = 0.029)
and serum l-carnitine levels (95% CI: 0.842-0.998, p = 0.044). The area under the receiver operating
characteristic curve indicated that the diagnostic power of l-carnitine to predict PAS was 0.789 (95% CI:
0.670-0.881, p < 0.001). Serum-free l-carnitine level is negatively associated with PAS in patients who
undergo KT.
Publication Type
Journal Article.
Year of Publication
2019

<3>
Unique Identifier
31252561
Title
Comparison of Glucose Tolerance between Kidney Transplant Recipients and Healthy Controls.
Source
Journal of Clinical Medicine. 8(7), 2019 Jun 27.
VI 1
Record Owner
Status
PubMed-not-MEDLINE
Authors
Shimada H; Uchida J; Nishide S; Kabei K; Kosoku A; Maeda K; Iwai T; Naganuma T; Takemoto Y;
Nakatani T.
Author NameID
Page 3
Uchida, Junji; ORCID: https://orcid.org/0000-0002-0113-8058
Iwai, Tomoaki; ORCID: https://orcid.org/0000-0003-2021-0673
Authors Full Name
Shimada, Hisao; Uchida, Junji; Nishide, Shunji; Kabei, Kazuya; Kosoku, Akihiro; Maeda, Keiko; Iwai,
Tomoaki; Naganuma, Toshihide; Takemoto, Yoshiaki; Nakatani, Tatsuya.
Institution
Shimada, Hisao. Department of Urology, Osaka City University Graduate School of Medicine, Osaka
545-8585, Japan.
Uchida, Junji. Department of Urology, Osaka City University Graduate School of Medicine, Osaka 545-
8585, Japan. uchida@msic.med.osaka-cu.ac.jp.
Nishide, Shunji. Department of Urology, Osaka City University Graduate School of Medicine, Osaka
545-8585, Japan.
Kabei, Kazuya. Department of Urology, Osaka City University Graduate School of Medicine, Osaka 545-
8585, Japan.
Kosoku, Akihiro. Department of Urology, Osaka City University Graduate School of Medicine, Osaka
545-8585, Japan.
Maeda, Keiko. Department of Nursing, Osaka City University Hospital, Osaka 545-8585, Japan.
Iwai, Tomoaki. Department of Urology, Osaka City University Graduate School of Medicine, Osaka 545-
8585, Japan.
Naganuma, Toshihide. Department of Urology, Osaka City University Graduate School of Medicine,
Osaka 545-8585, Japan.
Takemoto, Yoshiaki. Department of Urology, Osaka City University Graduate School of Medicine,
Osaka 545-8585, Japan.
Nakatani, Tatsuya. Department of Urology, Osaka City University Graduate School of Medicine, Osaka
545-8585, Japan.
Keyword Heading
glucose intolerance
healthy subject
insulin resistance
insulin secretion
oral glucose tolerance test
Abstract
Post-transplant hyperglycemia and new-onset diabetes mellitus after transplantation (NODAT) are
common and important metabolic complications. Decreased insulin secretion and increased insulin
resistance are important to the pathophysiologic mechanism behind NODAT. However, the progression of
glucose intolerance diagnosed late after kidney transplantation remains clearly unknown. Enrolled in this
study were 94 kidney transplant recipients and 134 kidney transplant donors, as the healthy controls, who
were treated at our institution. The 75 g-oral glucose tolerance test (OGTT) was performed in the
recipients, and the healthy controls received an OGTT before donor nephrectomy. We assessed the
prevalence of glucose intolerance including impaired fasting glucose and/or impaired glucose tolerance, as
well as insulin secretion and insulin resistance using the homeostasis model assessment, and compared the
results between the two groups. Multivariate analysis after adjustment for age, gender, body mass index,
estimated glomerular filtration rate, and systolic blood pressure showed that the prevalence of glucose
intolerance, insulin resistance, insulin secretion, and 2 h plasma glucose levels were significantly higher in
the kidney transplant recipients compared to the healthy controls. Elevation of insulin secretion in kidney
transplant recipients may be compensatory for increase of insulin resistance. Impaired compensatory
pancreas beta cell function may lead to glucose intolerance and NODAT in the future.
Publication Type
Journal Article.
Year of Publication
2019

Page 4
<4>
Unique Identifier
30526503
Title
Early onset of graft glomerulopathy in a patient with post-transplant diabetes mellitus after renal
transplantation: a case report.
Source
BMC Nephrology. 19(1):348, 2018 12 07.
VI 1
Record Owner
Status
In-Process
Authors
Gregorini M; Sepe V; Pattonieri FE; Allesina A; Rampino T.
Author NameID
Gregorini, Marilena; ORCID: https://orcid.org/0000-0003-1440-6872
Authors Full Name
Gregorini, Marilena; Sepe, Vincenzo; Pattonieri, Francesca Eleonora; Allesina, Anna; Rampino, Teresa.
Institution
Gregorini, Marilena. Nephrology, Dialysis and Renal Transplant Unit, IRCCS Policlinico San Matteo
Foundation, P.le Golgi 19, 27100, Pavia, Italy. marilena.gregorini@unipv.it.
Gregorini, Marilena. Department of Internal Medicine and Therapeutics, University of Pavia, Via Aselli
43/45, 27100, Pavia, Italy. marilena.gregorini@unipv.it.
Sepe, Vincenzo. Nephrology, Dialysis and Renal Transplant Unit, IRCCS Policlinico San Matteo
Foundation, P.le Golgi 19, 27100, Pavia, Italy.
Pattonieri, Francesca Eleonora. Nephrology, Dialysis and Renal Transplant Unit, IRCCS Policlinico San
Matteo Foundation, P.le Golgi 19, 27100, Pavia, Italy.
Pattonieri, Francesca Eleonora. PhD in Experimental Medicine, University of Pavia, Via Forlanini 6,
27100, Pavia, Italy.
Allesina, Anna. Nephrology, Dialysis and Renal Transplant Unit, IRCCS Policlinico San Matteo
Rampino, Teresa. Nephrology, Dialysis and Renal Transplant Unit, IRCCS Policlinico San Matteo
Keyword Heading
*CNI
*HbA1c
*Kidney transplantation; diabetic nephropathy
*Mesangiolysis
*Microalbuminuria
*PTDM
*mTOR inhibitors
Abstract
BACKGROUND: Post-transplant diabetes mellitus (PTDM) is an emerging problem in kidney
transplantation, representing an important risk factor for kidney function loss. Diabetic nephropathy (DN)
occurrence in transplanted kidneys is poorly investigated. Current knowledge describes DN recurrence in
graft 5.9 years from kidney transplantation however there is little data about PTDM and DN. Here, we
report a clinical case peculiar for an early appearance of advanced glomerular diabetic lesions, after kidney
transplantation.
CASE PRESENTATION: A 45-year-old Caucasian male affected by autosomal polycystic kidney

disease was transplanted with a cadaveric-kidney-donor from 58-year-old male. Induction
immunosuppressive therapy included basiliximab and steroids while the maintenance treatment included,
Page 5
tacrolimus, mofetil micophenolate and methylprednisolone. One month after transplantation the patient
developed diabetes requiring treatment with repaglinide quickly replaced with insulin to obtain an
acceptable glycemic control (HbA1c 52 mmol/mol). Glycosuria was detected persistently during the first
six months after transplantation. To achieve further improvement in glycemic control, a shift from
tacrolimus to cyclosporine (CyA) was made and steroids were rapidly tapered and stopped. To minimize
calcineurin inhibitors toxicity, which was revealed in the 1-year-protocol-biopsy, everolimus was
introduced thereby lowering CyA through levels. Moderate hypertension was well controlled with
doxazosin. Thirty months after transplantation a second graft biopsy was performed owing to renal function
decline and microalbuminuria appearance. Histological analysis surprisingly showed mesangiolysis and
microaneurysms; glomerular sclero-hyalinosis and basal membrane thickness and typical nodular
glomerulosclerosis. C4d staining was negative and no evidence of immune deposits were detected. Donor
Specific Antibodies, serum C3 and C4 levels and autoimmunity tests were negative. Retrospective analysis
on donor history didn't show diabetes or insulin resistance and no diabetic lesions were found in kidney
pre-implant biopsy.
CONCLUSIONS: In our knowledge, this is the first report describing a very early onset of advanced
diabetic glomerular lesions in a graft biopsy after PTDM. We hypothesize that additional factors such as
everolimus and hypertension, may have contribute to kidney damage.
Publication Type
Journal Article.
Year of Publication
2018

<5>
Unique Identifier
30049444
Title
Leptin - A new marker for development of post-transplant diabetes mellitus?.
Source
Journal of Diabetes & its Complications. 32(9):863-869, 2018 09.
VI 1
Record Owner
Status
In-Process
Authors
Dedinska I; Mackova N; Kantarova D; Kovacikova L; Granak K; Laca L; Miklusica J; Skalova P; Galajda
P; Mokan M.
Authors Full Name
Dedinska, Ivana; Mackova, Nadezda; Kantarova, Daniela; Kovacikova, Lea; Granak, Karol; Laca,
Ludovit; Miklusica, Juraj; Skalova, Petra; Galajda, Peter; Mokan, Marian.
Institution
Dedinska, Ivana. Department of Surgery and Transplantation Center, University Hospital Martin and
Jessenius Medical Faculty of Comenius University, Slovak Republic. Electronic address:
dedinska@unm.sk.
Mackova, Nadezda. Immunological Center, Martin, Slovak Republic.
Kantarova, Daniela. Immunological Center, Martin, Slovak Republic. Electronic address:
kantarova@unm.sk.
Kovacikova, Lea. Department of Surgery and Transplantation Center, University Hospital Martin and
Jessenius Medical Faculty of Comenius University, Slovak Republic.
Page 6
Granak, Karol. Department of Surgery and Transplantation Center, University Hospital Martin and
Laca, Ludovit. Department of Surgery and Transplantation Center, University Hospital Martin and
Miklusica, Juraj. Department of Surgery and Transplantation Center, University Hospital Martin and
Skalova, Petra. Department of Surgery and Transplantation Center, University Hospital Martin and
Galajda, Peter. Ist Department of Internal Diseases, University Hospital Martin and Jessenius Medical
Faculty of Comenius University, Slovak Republic.
Mokan, Marian. Ist Department of Internal Diseases, University Hospital Martin and Jessenius Medical
Keyword Heading
*Adiponectin
*Kidney transplantation
*Leptin
*Post-transplant diabetes mellitus
*acute rejection
Abstract
INTRODUCTION: Obese patients have increased leptin production and selective resistance to its central
anti-adipogenic effects, yet its pro-inflammatory immunostimulating effects persist.
MATERIAL AND METHODS: In a group of 70 patients who underwent primary kidney transplantation
(KT) we examined adiponectin and leptin levels at the time of KT and 6months post-transplantation.
Patients with diabetes mellitus type 1 or type 2 at the time of KT were excluded from the study.
RESULTS: We found that leptin levels significantly increased during the post-transplant period
(P=0.0065). Overall, leptin levels were positively correlated with the level of triacylglycerols, post-
transplant diabetes mellitus (PTDM) development and acute rejection (AR). We discovered that, in
particular, high leptin levels were associated with AR [OR 2.1273; 95% CI 1.0130-4.4671 (P=0.0461)] and
PTDM development [OR 7.200; 95% CI 1.0310-50.2836 (P=0.0465)], whereas, low adiponectin levels
represent a risk factor for the development of insulin resistance [HR 38.6135; 95% CI 13.3844-67.7699
(P<0.0001)] and obesity [HR 3.0821; 95% CI 0.8700-10.9192 (P=0.0053)].
CONCLUSION: We found that a high serum concentration of leptin before KT is associated with both
PTDM development and AR and merits further investigation in relation to KT. Copyright © 2018 Elsevier
Inc. All rights reserved.
Publication Type
Journal Article.
Year of Publication
2018

<6>
Unique Identifier
30755355
Title
Role of sex in post-transplant diabetes mellitus development: Are men and women equal?.
Source
Journal of Diabetes & its Complications. 33(4):315-322, 2019 Apr.
VI 1
Page 7
Record Owner
Status
In-Data-Review
Authors
Dedinska I; Granak K; Vnucak M; Skalova P; Kovacikova L; Laca L; Miklusica J; Pridavkova D; Galajda
P; Mokan M.
Authors Full Name
Dedinska, Ivana; Granak, Karol; Vnucak, Matej; Skalova, Petra; Kovacikova, Lea; Laca, Ludovit;
Miklusica, Juraj; Pridavkova, Dana; Galajda, Peter; Mokan, Marian.
Institution
Dedinska, Ivana. Department of Surgery and Transplantation Centre, University Hospital Martin and
Jessenius Medical Faculty of Comenius University, Slovak Republic. Electronic address:
dedinska@unm.sk.
Granak, Karol. Department of Surgery and Transplantation Centre, University Hospital Martin and
Vnucak, Matej. Department of Surgery and Transplantation Centre, University Hospital Martin and
Skalova, Petra. Department of Surgery and Transplantation Centre, University Hospital Martin and
Kovacikova, Lea. Department of Surgery and Transplantation Centre, University Hospital Martin and
Laca, Ludovit. Department of Surgery and Transplantation Centre, University Hospital Martin and
Miklusica, Juraj. Department of Surgery and Transplantation Centre, University Hospital Martin and
Pridavkova, Dana. Ist Department of Internal Diseases, University Hospital Martin and Jessenius Medical
Galajda, Peter. Ist Department of Internal Diseases, University Hospital Martin and Jessenius Medical
Mokan, Marian. Ist Department of Internal Diseases, University Hospital Martin and Jessenius Medical
Keyword Heading
C-peptide
Insuline resistance
Kidney transplantation
Post-transplant diabetes mellitus
Sex differences
Abstract
INTRODUCTION: Sex differences are defined as biology-linked differences between women and men
that occur through the sex chromosomes and their effects on organ systems.
MATERIAL AND METHODS: The objective of this prospective study was to determine risk factors for
post-transplant diabetes mellitus (PTDM) in men and women.
RESULTS: A total of 417 patients (271 men and 146 women) were included in the monitored group. Age
at the time of kidney transplantation (KT) >60years and hypovitaminosis D at the time of KT (<20mug/l)
were identified as independent risk factors for PTDM in both men and women. It was further confirmed as
an independent risk factor for men a waist circumference at the time of KT >94cm, C-peptide at the time of
KT >5ng/ml, HOMA-IR >2 and triacylglycerols at the time of KT >1.7mmol/l. In case of women, the
dominant factor was BMI at the time of KT >30kg/m2 and menopause at the time of KT. A significant
decrease in C-peptide was recorded in women with PTDM.
CONCLUSION: It was confirmed that there are gender differences with regard to the development of
PTDM after KT. Women show pancreas beta cell dysfunction, whereas insulin resistance and metabolic
syndrome are dominant in men. Copyright © 2018 Elsevier Inc. All rights reserved.
Page 8
Publication Type
Journal Article.
Year of Publication
2019

<7>
Unique Identifier
30793446
Title
Post-transplant metabolic syndrome in children: Know better to cure better.
Source
Pediatric Transplantation. 23(3):e13367, 2019 05.
VI 1
Record Owner
Status
MEDLINE
Authors
Nobili V; Pietrobattista A; Valenti L; Spada M.
Author NameID
Nobili, Valerio; ORCID: https://orcid.org/0000-0002-4570-3979
Authors Full Name
Nobili, Valerio; Pietrobattista, Andrea; Valenti, Luca; Spada, Marco.
Institution
Nobili, Valerio. Hepatology, Gastroenterology and Nutrition Unit, IRCCS "Bambino Gesu" Children's
Hospital, Rome, Italy.
Nobili, Valerio. Department of Pediatric, University "La Sapienza", Rome, Italy.
Pietrobattista, Andrea. Hepatology, Gastroenterology and Nutrition Unit, IRCCS "Bambino Gesu"
Children's Hospital, Rome, Italy.
Valenti, Luca. Department of Pathophysiology and Transplantation, University of Milan, Milan, Italy.
Valenti, Luca. Internal Medicine and Metabolic Diseases, Fondazione IRCCS Ca' Granda Ospedale
Maggiore Policlinico Milano, Milan, Italy.
Spada, Marco. Division of Abdominal Transplantation and Hepatobiliopancreatic Surgery, Bambino
Gesu Children's Research Hospital IRCCS, Rome, Italy.
Comments
Comment on (CON)
MeSH Subject Headings
Child
Humans
*Kidney Transplantation
*Liver Transplantation
*Metabolic Syndrome
Risk Factors
Surveys and Questionnaires
Publication Type
Editorial. Comment.
Year of Publication
2019
Page 9
<8>
Unique Identifier
29079835
Title
Circulating Haptoglobin and Metabolic Syndrome in Renal Transplant Recipients.
Source
Scientific Reports. 7(1):14264, 2017 10 27.
VI 1
Record Owner
Status
MEDLINE
Authors
Minovic I; Eisenga MF; Riphagen IJ; van den Berg E; Kootstra-Ros J; Frenay AS; van Goor H; Rimbach
G; Esatbeyoglu T; Levy AP; Gaillard CAJM; Geleijnse JM; Eggersdorfer ML; Navis GJ; Kema IP; Bakker
SJL.
Authors Full Name
Minovic, Isidor; Eisenga, Michele F; Riphagen, Ineke J; van den Berg, Else; Kootstra-Ros, Jenny; Frenay,
Anne-Roos S; van Goor, Harry; Rimbach, Gerald; Esatbeyoglu, Tuba; Levy, Andy P; Gaillard, Carlo A J
M; Geleijnse, Johanna M; Eggersdorfer, Manfred L; Navis, Gerjan J; Kema, Ido P; Bakker, Stephan J L.
Institution
Minovic, Isidor. Department of Internal Medicine, Division of Nephrology, University of Groningen,
University Medical Center Groningen, Hanzeplein 1, 9700 RB, Groningen, The Netherlands.
i.minovic@umcg.nl.
Minovic, Isidor. Top Institute Food and Nutrition, Nieuwe Kanaal 9-A, 6709 PA, Wageningen, The
Netherlands. i.minovic@umcg.nl.
Minovic, Isidor. Department of Laboratory Medicine, University of Groningen, University Medical
Center Groningen, Hanzeplein 1, 9700 RB, Groningen, The Netherlands. i.minovic@umcg.nl.
Eisenga, Michele F. Department of Internal Medicine, Division of Nephrology, University of Groningen,
Riphagen, Ineke J. Department of Internal Medicine, Division of Nephrology, University of Groningen,
van den Berg, Else. Department of Internal Medicine, Division of Nephrology, University of Groningen,
Kootstra-Ros, Jenny. Department of Laboratory Medicine, University of Groningen, University Medical
Center Groningen, Hanzeplein 1, 9700 RB, Groningen, The Netherlands.
Frenay, Anne-Roos S. Department of Pathology, University of Groningen, University Medical Center
Groningen, Hanzeplein 1, 9700 RB, Groningen, The Netherlands.
van Goor, Harry. Department of Pathology, University of Groningen, University Medical Center
Rimbach, Gerald. Institute of Human Nutrition and Food Science, Christian-Albrechts-University of Kiel,
Kiel, Germany.
Esatbeyoglu, Tuba. Institute of Human Nutrition and Food Science, Christian-Albrechts-University of
Kiel, Kiel, Germany.
Levy, Andy P. Faculty of Medicine, Technion Institute of Technology, Efron Street 1, Haifa, Israel.
Gaillard, Carlo A J M. Department of Internal Medicine, Division of Nephrology, University of
Groningen, University Medical Center Groningen, Hanzeplein 1, 9700 RB, Groningen, The Netherlands.
Geleijnse, Johanna M. Division of Human Nutrition, Wageningen University, Droevendaalsesteeg 4,
6708 PB, Wageningen, The Netherlands.
Eggersdorfer, Manfred L. DSM Nutritional Products, Wurmisweg 576, 4303, Kaiseraugst, Switzerland.
Page 10
Navis, Gerjan J. Department of Internal Medicine, Division of Nephrology, University of Groningen,
Kema, Ido P. Department of Laboratory Medicine, University of Groningen, University Medical Center
Bakker, Stephan J L. Department of Internal Medicine, Division of Nephrology, University of Groningen,
Bakker, Stephan J L. Top Institute Food and Nutrition, Nieuwe Kanaal 9-A, 6709 PA, Wageningen, The
Netherlands.
Comments
Erratum in (EIN)
Biomarkers/bl [Blood]
Female
*Haptoglobins/me [Metabolism]
Humans
Male
*Metabolic Syndrome/bl [Blood]
*Metabolic Syndrome/th [Therapy]
Middle Aged
Treatment Outcome
Abstract
Haptoglobin (Hp) is an acute phase protein that has recently been linked to components of the metabolic
syndrome (MetS). We aimed to evaluate Hp as marker of MetS, and to assess its association with long-term
outcome in renal transplant recipients (RTR). We measured plasma Hp in a prospective cohort of 699
stable RTR and 149 healthy controls. Median plasma Hp concentration in RTR was 1.4 [interquartile range
(IQR), 1.0-1.8] g/L, which was higher compared to 1.1 [0.9-1.4] g/L in controls (P < 0.001). Hp was
independently associated with the MetS (beta = 0.10) (P = 0.005). During follow-up of 5.4 [4.8-6.1] years,
150 (21%) recipients died, of whom 60 (9%) due to cardiovascular causes, and 83 (12%) RTR developed
graft failure. High (>=2.0 g/L) and low (<=0.9 g/L) plasma Hp were associated with increased risk of
mortality (HR's 2.3 [1.3-4.1] and 1.9 [1.0-3.5], resp.), predominantly cardiovascular. The association of
high Hp lost significance upon adjustment for inflammation markers (HR 1.5 [0.8-2.7]), while low Hp was
independently associated with mortality (HR 2.2 [1.2-4.0]). Hp was not associated with graft failure (P =
0.49). In conclusion, plasma Hp is independently associated with MetS in RTR. Importantly, high and low
Hp are associated with increased mortality risk, independent of MetS.
Registry Number/Name of Substance
0 (Biomarkers). 0 (Haptoglobins).
Publication Type
Journal Article.
Year of Publication
2017

<9>
Unique Identifier
31076145
Title
Homeostatic Model Assessment in Kidney Transplantation.
Source
Transplantation Proceedings. 51(5):1357-1361, 2019 Jun.
VI 1
Page 11
Record Owner
Status
MEDLINE
Authors
Wang HH; Lin KJ; Liu KL; Huang CW; Lin CT; Chu SH; Chiang YJ.
Authors Full Name
Wang, Hsu-Han; Lin, Kuo-Jen; Liu, Kuan-Lin; Huang, Ching-Wei; Lin, Chih-Te; Chu, Sheng-Hsien;
Chiang, Yang-Jen.
Institution
Wang, Hsu-Han. Department of Urology, Chang Gung Memorial Hospital at Linkou, Chang Gung
University College of Medicine, Taoyuan, Taiwan.
Lin, Kuo-Jen. Department of Urology, Chang Gung Memorial Hospital at Linkou, Chang Gung
Liu, Kuan-Lin. Department of Urology, Chang Gung Memorial Hospital at Linkou, Chang Gung
Huang, Ching-Wei. Department of Urology, Chang Gung Memorial Hospital at Linkou, Chang Gung
Lin, Chih-Te. Department of Urology, Chang Gung Memorial Hospital at Linkou, Chang Gung
Chu, Sheng-Hsien. Department of Urology, Chang Gung Memorial Hospital at Linkou, Chang Gung
Chiang, Yang-Jen. Department of Urology, Chang Gung Memorial Hospital at Linkou, Chang Gung
University College of Medicine, Taoyuan, Taiwan. Electronic address: zorro@cgmh.org.tw.
Adult
Female
*Glomerular Filtration Rate/ph [Physiology]
Humans
*Insulin Resistance/ph [Physiology]
Male
Middle Aged
Retrospective Studies
Abstract
INTRODUCTION: Long-term kidney transplantation survival has been limited to cardiovascular-disease-
associated death, which may be related to insulin resistance. The aim of this study is to evaluate the
association between homeostatic model assessment (HOMA) and renal graft function.
MATERIALS AND METHODS: From January 2013 to March 2015, 55 nondiabetic kidney recipients
were reviewed retrospectively with their baseline fasting serum insulin and glucose levels as the basis the
following indexes: 1. HOMA insulin resistance (HOMA-IR), 2. HOMA-beta, and 3. insulin-glucose ratio
(IGR). These patients were divided into 2 groups according to their HOMA indexes, and the serum
creatinine (Cr) and estimated glomerular filtration rate (eGFR) were analyzed on the basis of every 6
months up to 3 years after kidney transplantation. Finally, we evaluate whether these HOMA indexes are a
determinant factor of eGFR at post-transplant 1 year, 2 year, and 3 year.
RESULTS: There was no persisting difference in Cr and eGFR between high- and low-HOMA indexes
except that the Cr and eGFR difference by HOMA-beta stratification increased with time and became
nearly significant at 3 years after transplantation. Further univariate and multivariate linear regression
models showed no factor affected the 1-year eGFR independently, while weight affected the 2-year eGFR
and only HOMA-beta affected the 3-year eGFR independently.
CONCLUSION: In non-diabetic kidney recipients, the eGFR difference between high- and low-HOMA-
beta patients increases over time. In multivariate linear regression, HOMA-beta, but not HOMA-IR nor
Page 12
IGR, has independent significant association with eGFR at 3 years after transplantation. Copyright © 2019
Elsevier Inc. All rights reserved.
Publication Type
Journal Article.
Year of Publication
2019

<10>
Unique Identifier
30418189
Title
Pre, peri and posttransplant diabetes mellitus. [Review]
Source
Current Opinion in Nephrology & Hypertension. 28(1):47-57, 2019 01.
VI 1
Record Owner
Status
MEDLINE
Authors
El Essawy B; Kandeel F.
Authors Full Name
El Essawy, Basset; Kandeel, Fouad.
Institution
El Essawy, Basset. Renal Division, Transplantation Research Center, Brigham and Women's
Hospital/Harvard Medical School, Boston, Massachusetts, USA.
El Essawy, Basset. Al-Azhar University, Cairo, Egypt.
El Essawy, Basset. RAK College of Medical Sciences, Medical and Health Sciences University, Ras-al-
Khaimah, UAE.
Kandeel, Fouad. Department of Diabetes, Endocrinology and Metabolism, City of Hope National
Medical Center, Duarte, California, USA.
*Diabetes Mellitus/et [Etiology]
Humans
Immunosuppressive Agents/tu [Therapeutic Use]
Insulin Resistance
*Kidney Transplantation/ae [Adverse Effects]
Renal Insufficiency, Chronic/co [Complications]
Abstract
PURPOSE OF REVIEW: The leading cause of death in both chronic kidney disease (CKD) and renal
transplant patients is cardiovascular events. Post-transplant diabetes mellitus (PTx-DM), which is a major
cardiovascular risk factor, is a metabolic disorder that affects 5.5-60.2% of renal allograft recipients by 1-
year posttransplant (PTx). PTx-DM has been associated with a negative impact on patient and graft
outcomes and survival.
RECENT FINDINGS: Individuals who develop PTx-DM are usually prone to this condition prior to
and/or after developing CKD. Genetic factors, obesity, inflammation, medications and CKD all are risk
factors for PTx-diabetes mellitus. The path to development of disease continues PTx frequently augmented
by the use of diabetogenic maintenance immunosuppressive and some nonimmunosuppressive medications.
Page 13
These risk factors are usually associated with an increase in insulin resistance, a decrease in insulin gene
expression and/or beta-cell dysfunction and apoptosis.
SUMMARY: Some new anti-diabetes mellitus medications may help to improve the overall outcome;
however, there is a real need for developing a preventive strategy. Identifying and targeting PTx-DM risk
factors may help to guide the development of an effective programme. This could include the adoption of
nondiabetogenic immunosuppressive protocols for high-risk patients.
0 (Immunosuppressive Agents).
Publication Type
Journal Article. Review.
Year of Publication
2019

<11>
Unique Identifier
28352021
Title
Prevalence of the metabolic syndrome in kidney transplant recipients: A single-center study.
Source
Saudi Journal of Kidney Diseases & Transplantation. 28(2):362-367, 2017 Mar-Apr.
VI 1
Record Owner
Status
MEDLINE
Authors
Hami M; Sabbagh MG; Sefidgaran A; Mojahedi MJ.
Authors Full Name
Hami, Maryam; Sabbagh, M Ghorban; Sefidgaran, A; Mojahedi, M J.
Institution
Hami, Maryam. Kidney Transplantation Complications Research Center, Ghaem Hospital, Faculty of
Medicine, Mashhad University of Medical Sciences, Mashhad, Iran.
Sabbagh, M Ghorban. Kidney Transplantation Complications Research Center, Ghaem Hospital, Faculty
of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran.
Sefidgaran, A. Kidney Transplantation Complications Research Center, Ghaem Hospital, Faculty of
Mojahedi, M J. Kidney Transplantation Complications Research Center, Ghaem Hospital, Faculty of
Adult
Body Mass Index
Body Weight
Cross-Sectional Studies
Female
Glomerular Filtration Rate
Graft Survival
Humans
Iran/ep [Epidemiology]
Kidney/pp [Physiopathology]
Page 14
*Kidney/su [Surgery]
Kidney Transplantation/ae [Adverse Effects]
Male
Metabolic Syndrome/di [Diagnosis]
*Metabolic Syndrome/ep [Epidemiology]
Metabolic Syndrome/pc [Prevention & Control]
Middle Aged
Prevalence
Risk Assessment
Risk Factors
*Transplant Recipients
Treatment Outcome
Young Adult
Abstract
Metabolic syndrome (MS) is characterized by a combination of cardiovascular (CV) risk factors
(hypertension, dyslipidemia, obesity, and alterations in glucose homeostasis). Insulin resistance is
suggested to be the common pathogenic background. This syndrome is also a risk factor for diabetes and
chronic kidney disease. In renal transplant recipients, MS has been shown to be an independent risk factor
for chronic allograft dysfunction, graft failure, new-onset diabetes, and CV disease. We performed a cross-
sectional study on 106 stable renal transplant recipients to detect MS between January 2013 and August
2013. This syndrome was diagnosed according to the National Cholesterol Education Program-Adult
Treatment Panel III criteria. Patients with history of diabetes mellitus were excluded from the study. In this
group of patients, 56 (52.8%) had MS. There were 32 males (57.1%) and 24 females (42.9%). The mean
age of the MS group was significantly higher than the non-MS group. The mean serum creatinine was
higher in the MS group than the non-MS group, but there was no significant difference between them (P
>0.05). The calculated glomerular filtration rate was also similar in the two groups (P >0.05). The patients
with MS had higher body weight (64.61 +/- 14.17 kg vs. 58.76 +/- 11.70 kg, P <0.05) and also higher body
mass index (BMI) (P <0.05). The prevalence of BMI >25 kg/m2 in the MS group was 75% versus 25% in
the non-MS group (P <0.05). Since MS is an important and common risk factor in renal transplant
recipients, we have to try to prevent it by educating the patients to control it by modifying their lifestyle.
Efforts toward promoting healthy diets, physical activity, and blood pressure control must be undertaken.
Publication Type
Journal Article.
Year of Publication
2017

<12>
Unique Identifier
30701912
Title
Nephrological aspects of surgical weight correction in morbid obesity. [Review]
Source
Terapevticheskii Arkhiv. 90(6):98-104, 2018 Jun 20.
VI 1
Record Owner
Status
MEDLINE
Authors
Page 15
Bobkova IN; Gussaova SS; Stavrovskaya EV; Struve AV.
Authors Full Name
Bobkova, I N; Gussaova, S S; Stavrovskaya, E V; Struve, A V.
Institution
Bobkova, I N. I.M. Sechenov First Moscow State Medical University, Ministry of Health of Russia
(Sechenov University), Moscow, Russia.
Gussaova, S S. I.M. Sechenov First Moscow State Medical University, Ministry of Health of Russia
Stavrovskaya, E V. I.M. Sechenov First Moscow State Medical University, Ministry of Health of Russia
Struve, A V. I.M. Sechenov First Moscow State Medical University, Ministry of Health of Russia
Bariatric Surgery/ae [Adverse Effects]
*Bariatric Surgery
Humans
*Kidney Diseases/et [Etiology]
Obesity
Obesity, Morbid/su [Surgery]
*Obesity, Morbid
Observational Studies as Topic
Prospective Studies
Weight Loss
Keyword Heading
albuminuria
bariatric surgery
chronic kidney disease
glomerular filtration rate
hyperfiltration
morbid obesity
proteinuria.
Abstract
Obesity, including morbid obesity, is a growing worldwide problem. The adverse effect of obesity on the
kidneys is associated with the development of comorbid conditions, such as insulin resistance (IR),
metabolic syndrome (MS), diabetes mellitus (DM), arterial hypertension (AH), which are the recognized
risk factors of chronic kidney disease (SKD). Obesity also causes direct kidney damage with the
development of non-immune focal segmental glomerulosclerosis. The leading pathophysiological
mechanisms of kidney damage in obesity are intrarenal hemodynamic disorders with the formation of
hyperfiltration and damaging effects of adipokines produced by adipose tissue. Bariatric surgery (BS) has
taken a leading position in the treatment of morbid obesity, demonstrating its effectiveness not only in
long-term weight loss, but also in the correction of IR, MS, DM, AH. Nephroprotective effect of significant
and persistent weight loss is caused by the elimination of hyperfiltration and damaging effect of adipokines.
Results of the observational studies of the immediate and long-term effects of BS have demonstrated
positive renal outcomes, in particular, the decrease in albuminuria/proteinuria, the improvement or
stabilization of glomerular filtration rate, the delay of end-stage renal failure development; surgical
correction of body weight in dialysis patients with morbid obesity lets them realize subsequent kidney
transplantation. Large, randomized prospective studies with a longer follow-up are needed; analysis of the
long-term renal consequences of BS in obesity patients with pre-existing renal impairment, including
dialysis patients, is required; stratification of the BS risk of renal complications (acute kidney damage,
nephrolithiasis, nephrocalcinosis) and effective strategy for managing these risks need to be developed.
Publication Type
Year of Publication
2018
Page 16
<13>
Unique Identifier
30979462
Title
Pretransplant Homeostasis Model Assessment of Insulin Resistance and Fasting Plasma Glucose Predict
New-Onset Diabetes After Renal Transplant in Chinese Patients.
Source
Transplantation Proceedings. 51(3):768-773, 2019 Apr.
VI 1
Record Owner
Status
MEDLINE
Authors
Cai R; Wu M; Lin M; Guo X; Xing Y.
Authors Full Name
Cai, R; Wu, M; Lin, M; Guo, X; Xing, Y.
Institution
Cai, R. Department of Organ Transplantation, The Third Affiliated Hospital of Guangzhou Medical
University, Guangzhou, Guangdong, China.
Wu, M. Department of Nephrology, Longyan First Hospital, Longyan, Fujian, China.
Lin, M. Department of Organ Transplantation, The Third Affiliated Hospital of Guangzhou Medical
Guo, X. Department of Organ Transplantation, The Third Affiliated Hospital of Guangzhou Medical
Xing, Y. Department of Nephrology, The Third Affiliated Hospital of Guangzhou Medical University,
Guangzhou, Guangdong, China. Electronic address: 2574410512@qq.com.
Adult
Asian Continental Ancestry Group
*Blood Glucose/an [Analysis]
Fasting/bl [Blood]
Female
Homeostasis
Humans
Male
Middle Aged
Proportional Hazards Models
Risk Factors
Abstract
BACKGROUND AND AIM: The present study aims to determine if homeostasis model assessment of
insulin resistance (HOMA-IR) index, fasting plasma glucose (FPG), and plasma insulin (Ins) are able to
predict development of new onset diabetes after transplant (NODAT) for kidney recipients.
METHODS: We performed a single-center retrospective study of 123 nondiabetic patients receiving a

first renal transplant. The NODAT was diagnosed between 1 month and 1 year post transplant. Both
Page 17
univariate and multivariable analyses, including logistic regression analysis and Cox proportional hazards
model, were applied to dissect potential pretransplant risk factors of NODAT.
RESULTS: A total of 26.8% (33/123) of recipients developed NODAT in the first year post transplant.
The NODAT patients showed higher HOMA-IR index and increased levels of FPG and Ins than non-
NODAT. Interestingly, we consistently revealed that both FPG (logistic: odds ratio [OR], 3.17 [1.41-6.45];
P = .01; Cox: OR, 2.75 [1.26-4.56]; P = .02) and HOMA-IR index (logistic: OR, 1.73 [1.21-2.87]; P = .02;
Cox: OR, 1.72 [1.21-2.46]; P = .002) robustly predicted the development of NODAT. However, these
analyses showed that neither plasma Ins nor hemoglobin A1c was associated with NODAT.
CONCLUSION: Our findings suggest that pretransplant HOMA-IR and FPG are independent predictors
for the development of NODAT in Chinese nondiabetic patients receiving a first renal transplant. Copyright
© 2019 Elsevier Inc. All rights reserved.
0 (Blood Glucose).
Publication Type
Journal Article.
Year of Publication
2019

<14>
Unique Identifier
30130326
Title
Obesity and Metabolic Syndrome in Kidney Transplantation: The Role of Dietary Fructose and Systemic
Endotoxemia.
Source
Transplantation. 103(1):191-201, 2019 01.
VI 1
Record Owner
Status
MEDLINE
Authors
Chan W; Smith B; Stegall M; Borrows R.
Authors Full Name
Chan, Winnie; Smith, Byron; Stegall, Mark; Borrows, Richard.
Institution
Chan, Winnie. Department of Nephrology and Kidney Transplantation, Queen Elizabeth Hospital
Birmingham, Mindelsohn Way, Edgbaston, Birmingham, United Kingdom.
Chan, Winnie. Department of Nutrition and Dietetics, Queen Elizabeth Hospital Birmingham, Edgbaston,
Birmingham, United Kingdom.
Smith, Byron. Division of Biomedical Statistics & Informatics, Department of Health Sciences Research,
Mayo Clinic, Rochester, MN.
Stegall, Mark. Division of Transplantation Surgery, Department of Medicine, Mayo Clinic, Rochester,
MN.
Stegall, Mark. The William J. von Liebig Center for Transplantation and Clinical Regeneration, Mayo
Clinic, Rochester, MN.
Borrows, Richard. Department of Nephrology and Kidney Transplantation, Queen Elizabeth Hospital
Birmingham, Mindelsohn Way, Edgbaston, Birmingham, United Kingdom.
Page 18
Borrows, Richard. School of Infection and Immunity. University of Birmingham, Edgbaston,
Birmingham, United Kingdom.
Adult
Blood Glucose/me [Metabolism]
Body Mass Index
*Dietary Sugars/ae [Adverse Effects]
Endotoxemia/bl [Blood]
Endotoxemia/di [Diagnosis]
*Endotoxemia/ep [Epidemiology]
Endotoxins/bl [Blood]
England/ep [Epidemiology]
Female
*Fructose/ae [Adverse Effects]
Humans
Lipids/bl [Blood]
Male
Metabolic Syndrome/bl [Blood]
Metabolic Syndrome/di [Diagnosis]
Middle Aged
Obesity/bl [Blood]
Obesity/di [Diagnosis]
*Obesity/ep [Epidemiology]
Prevalence
Risk Assessment
Risk Factors
Time Factors
Treatment Outcome
Abstract
BACKGROUND: The concepts that obesity is merely a consequence of overeating, and that metabolic
health then reflects obesity, may be insufficient and potentially flawed. The role of fructose intake and
metabolic endotoxemia has gained attention recently, but data in kidney transplantation are lacking. This
study evaluated the risk factors for metabolic syndrome (MS), its components, and other associated
markers in kidney transplant recipients (KTRs), focusing particularly on fructose intake and systemic
endotoxemia.
METHODS: This cross-sectional observational study enrolled 128 KTRs longer than 1 year
posttransplantation. Clinical, biochemical, anthropometric, and questionnaire assessments were undertaken.
RESULTS: Obesity (body mass index, >=30 kg/m) and MS (International Diabetes Federation
Definition) were found in 36.7% and 50% of KTRs, respectively. Both increased fructose intake (P = 0.01)
and endotoxin level (P = 0.02) were independently associated with MS; and higher fructose intake was
independently associated with obesity (P < 0.001). Specifically, increased fructose intake was associated
with the central obesity (P = 0.01) and hyperglycemia (P < 0.001) criteria of MS, whereas higher endotoxin
level was associated with the hypertriglyceridemia (P = 0.003) and low HDL cholesterol concentration (P =
0.002) criteria of MS. Neither saturated fat nor total caloric intakes were independently associated with
obesity and MS; and neither obesity nor central obesity were independently associated with the
dyslipidemia and hyperglycemia criteria of MS. Principal component analysis demonstrated relationships
between higher levels of endotoxin, soluble endothelial selectin, triglycerides, and insulin resistance (r >
0.6), as well as relationships between increased fructose intake, inflammation, and blood glucose (r > 0.6).
Page 19
CONCLUSIONS: Dietary modifications through decreasing fructose intake and addressing systemic
endotoxemia are plausible targets for improving metabolic health of KTRs.
0 (Biomarkers). 0 (Blood Glucose). 0 (Dietary Sugars). 0 (Endotoxins). 0 (Lipids). 30237-26-4 (Fructose).
Publication Type
Journal Article. Observational Study. Research Support, Non-U.S. Gov't.
Year of Publication
2019

<15>
Unique Identifier
29393089
Title
Renal Effects of Hyperuricemia.
Source
Contributions to Nephrology. 192:8-16, 2018.
VI 1
Record Owner
Status
MEDLINE
Authors
Mendez Landa CE.
Authors Full Name
Mendez Landa, Carlos Enrique.
Institution
Mendez Landa, Carlos Enrique. Department of Nephrology, General Hospital and Medical Unit
Ambulatory Care, Mexican Institute of Social Security, Mexico City, Mexico.
*Acute Kidney Injury/et [Etiology]
Animals
Disease Models, Animal
Humans
Hypertension/co [Complications]
*Hyperuricemia/co [Complications]
Hyperuricemia/ep [Epidemiology]
Kidney Transplantation
*Kidney Tubules, Collecting/pa [Pathology]
*Kidney Tubules, Proximal/pa [Pathology]
Metabolic Syndrome/ep [Epidemiology]
*Renal Insufficiency, Chronic/et [Etiology]
Renal Insufficiency, Chronic/pa [Pathology]
*Uric Acid/me [Metabolism]
Abstract
BACKGROUND: From a clinical point of view, uric acid has been dismissed as a cause of injury and
renal progression, and the mechanisms by which uric acid directly causes renal injury have not been fully
understood. Hyperuricemia is associated with metabolic syndrome, diabetes, hypertension, and kidney and
cardiovascular diseases. Although it remains controversial whether hyperuricemia is a causal factor for
kidney disease, kidneys play a major role in the regulation of serum uric acid levels.
Page 20
SUMMARY: Similar to the management of other substances, renal uric acid management occurs mainly
in the proximal tubule. The elevation of uric acid in blood is mainly due to an increase in its intake or a
defect in its secretion. The mechanisms of renal damage go beyond the deposition of crystals at the tubular
level; in this sense, renal damage also contributes to the production of chemotactic cytokines, cell
proliferation, and inflammation, with the development of afferent arteriolopathy, glomerular hypertrophy
and tubulointersticial fibrosis. Nevertheless, whether or not hyperuricemia plays a causal role or simply is a
marker arising in the course of each related disorder remains unresolved. Although a strong relationship
between hyperuricemia and metabolic syndrome has been established through animal and epidemiological
studies, the potential pathophysiological mechanisms by which uric acid contributes to this disease state are
just beginning to be explained and clarified. Key Messages: Experimental studies performed in animals
have limitations due to the differences that exist between humans and other mammals in purine metabolism
and in renal uric acid handling. Additional experimental studies aimed at evaluating the effects of lowering
urate levels on the courses of these disorders are warranted in the future. Copyright © 2018 S. Karger AG,
Basel.
268B43MJ25 (Uric Acid).
Publication Type
Journal Article.
Year of Publication
2018

<16>
Unique Identifier
30307290
Title
[Causes and components of the metabolic syndrome in renal transplant recipients from a gender
perspective]. [Spanish]
Original Title
Causas y componentes del sindrome metabolico en receptores de trasplante renal desde una perspectiva de
genero.
Source
Nutricion Hospitalaria. 35(5):1079-1084, 2018 Oct 05.
VI 1
Record Owner
Status
MEDLINE
Authors
Martin Salvador A; Fernandez Castillo R; Garcia Garcia I; Aguilar Cordero MJ; Bravo Soto J.
Authors Full Name
Martin Salvador, Adelina; Fernandez Castillo, Rafael; Garcia Garcia, Inmaculada; Aguilar Cordero, Maria
Jose; Bravo Soto, Juan.
Institution
Martin Salvador, Adelina. ademartin@ugr.es.
Adult
Aged
Female
Graft Rejection
Page 21
Humans
Kidney Function Tests
Male
Metabolic Syndrome/pp [Physiopathology]
Middle Aged
*Postoperative Complications/ep [Epidemiology]
Postoperative Complications/pp [Physiopathology]
Prevalence
Risk Factors
Sex Characteristics
Abstract
INTRODUCTION: the appearance of metabolic syndrome (MS) among renal recipients is one of the
greatest post-transplant complications and is associated with an increased risk of graft failure and high rates
of obesity and new onset diabetes.
OBJECTIVE: the objective of this work is to identify the relationship between the glomerular filtration
rate measured by two different methods and the components of the metabolic syndrome and their
combinations in kidney transplant patients according to gender.
MATERIAL AND METHOD: the samples consisted of 500 kidney transplant recipients, of whom 190
had MS, 121 men and 69 women. All subjects underwent clinical evaluation and blood sampling for
laboratory measurements. The MS was determined according to the criteria of the National Cholesterol
Education Program Adult Treatment Panel III (NCEP-ATP-III). Renal function was estimated using
AMDRD equations and CrS determinations.
RESULTS: the average age was 55.5 years. The prevalence of MS was significantly higher in men
(23.1% < vs 9.8%). High blood pressure (HBP) was the most observed component of MS. Significant
correlations (Pearson, p < 0.05) between TFG-AMDRD and TFG CrS and metabolic markers were
observed more in men than in women. The body mass index (BMI) was significantly higher in women than
in men. CONCLUSIONES: the decrease in renal function associated with the components of MS, HBP and
obesity represent a high risk of adverse cardiovascular events and graft rejections.
Other Abstract
Publisher: INTRODUCCION: la aparicion del sindrome metabolico (SM) entre los receptores renales es
una de las mayores complicaciones postrasplante y se asocia con un mayor riesgo de fracaso del injerto y
altas tasas de obesidad y diabetes de nueva aparicion. OBJETIVO: el objetivo de este trabajo es identificar
la relacion entre la tasa de filtracion glomerular medida por dos metodos distintos y los componentes del
sindrome metabolico y sus combinaciones en pacientes trasplantados renales segun genero. MATERIAL Y
METODO: la muestra estuvo formada por 500 pacientes trasplantados renales, de los cuales 190 padecian
SM, 121 hombres y 69 mujeres. Todos los sujetos se sometieron a evaluacion clinica y toma de muestras de
sangre para mediciones de laboratorio. El SM se determino segun los criterios del National Cholesterol
Education Program Adult Treatment Panel III (NCEP-ATP-III). La funcion renal se estimo usando
ecuaciones AMDRD y determinaciones de creatinina serica (CrS). RESULTADOS: la media de edad fue
de 55,5 anos. La prevalencia del SM fue significativamente mayor en hombres (23,1% < vs. 9,8%). La
hipertension arterial (HTA) fue el componente del SM mas observado. Se observaron correlaciones
significativas (Pearson; p < 0,05) entre TFG-AMDRD y TFG CrS y marcadores metabolicos mas en
hombres que en mujeres. El indice de masa corporal (IMC) fue significativamente mayor en mujeres que en
hombres. CONCLUSIONES: la disminucion de la funcion renal asociada con los componentes del SM, la
HTA y la obesidad representan un riesgo elevado de eventos cardiovasculares adversos y rechazos del
injerto.; Language: Spanish
Publication Type
Journal Article.
Year of Publication
2018
Page 22
<17>
Unique Identifier
30316385
Title
Inverse Association of N-terminal Pro-B-type Natriuretic Peptide Level With Metabolic Syndrome in
Kidney Transplant Patients.
Source
Transplantation Proceedings. 50(8):2496-2501, 2018 Oct.
VI 1
Record Owner
Status
MEDLINE
Authors
Lee KM; Lee MC; Lee CJ; Chen YC; Hsu BG.
Authors Full Name
Lee, K-M; Lee, M-C; Lee, C-J; Chen, Y-C; Hsu, B-G.
Institution
Lee, K-M. School of Medicine, Tzu Chi University, Hualien, Taiwan.
Lee, M-C. School of Medicine, Tzu Chi University, Hualien, Taiwan; Department of Surgery, Buddhist
Tzu Chi General Hospital, Hualien, Taiwan.
Lee, C-J. Department of Nursing, Tzu Chi University of Science and Technology, Hualien, Taiwan.
Chen, Y-C. School of Medicine, Tzu Chi University, Hualien, Taiwan; Department of Surgery, Buddhist
Tzu Chi General Hospital, Hualien, Taiwan.
Hsu, B-G. School of Medicine, Tzu Chi University, Hualien, Taiwan; Division of Nephrology, Buddhist
Tzu Chi General Hospital, Hualien, Taiwan. Electronic address: gee.lily@msa.hinet.net.
Adult
Aged
Body Mass Index
Creatinine/bl [Blood]
Female
Humans
Male
*Metabolic Syndrome/bl [Blood]
Middle Aged
*Natriuretic Peptide, Brain/bl [Blood]
*Peptide Fragments/bl [Blood]
Prevalence
Waist Circumference
Abstract
BACKGROUND: Low levels of natriuretic peptide may activate the renin-angiotensin-aldosterone
system, which may contribute to the development of obesity. Therefore, in study we aim to evaluate the
relationship between metabolic syndrome (MetS) and serum N-terminal pro-B-type natriuretic peptide
(NT-proBNP) concentration in kidney transplant recipients.
METHODS: Fasting blood samples were obtained from 66 kidney transplant recipients. MetS and its
components were defined using the diagnostic criteria of the International Diabetes Federation.
Page 23
RESULTS: A total of 20 patients (30.3%) had MetS. Hypertension, prevalence of diabetes, use of statin
or fibrate, body weight, body mass index, waist circumference, body fat mass, and levels of systolic blood
pressure, total cholesterol, triglyceride, blood urea nitrogen, insulin, and HOMA-IR were higher, whereas
the levels of high-density lipoprotein cholesterol and NT-proBNP were lower in patients with MetS.
Logarithmically transformed creatinine and log-HOMA-IR were associated with NT-proBNP levels in a
multivariable linear regression analysis. Multivariate logistic regression analysis revealed that NT-proBNP
was an independent predictor of MetS in kidney transplant recipients.
CONCLUSION: Our study has revealed that fasting level of NT-proBNP was negatively associated with
MetS and that serum creatinine and HOMA-IR were independent predictors of serum NT-proBNP level in
kidney transplant recipients. Copyright © 2018 Elsevier Inc. All rights reserved.
0 (Peptide Fragments). 0 (pro-brain natriuretic peptide (1-76)). 114471-18-0 (Natriuretic Peptide, Brain).
AYI8EX34EU (Creatinine).
Publication Type
Journal Article.
Year of Publication
2018

<18>
Unique Identifier
30316388
Title
Geriatric Nutritional Risk Index, a Simplified Nutritional Screening Index, Is a Strong Predictor of
Handgrip Strength in Renal Transplant Recipients.
Source
Transplantation Proceedings. 50(8):2509-2514, 2018 Oct.
VI 1
Record Owner
Status
MEDLINE
Authors
Lin IH; Wong TC; Nien SW; Wang HH; Chiang YJ; Yang SH.
Authors Full Name
Lin, I-H; Wong, T-C; Nien, S-W; Wang, H-H; Chiang, Y-J; Yang, S-H.
Institution
Lin, I-H. Department of Medical Nutrition Therapy, Linkou Chang Gung Memorial Hospital, Taoyuan,
Taiwan; School of Nutrition and Health Sciences, College of Nutrition, Taipei Medical University, Taipei,
Taiwan.
Wong, T-C. Department of Nutrition and Health Sciences, Chinese Culture University, Taipei, Taiwan.
Nien, S-W. Department of Medical Nutrition Therapy, Linkou Chang Gung Memorial Hospital, Taoyuan,
Taiwan.
Wang, H-H. Department of Urology, Linkou Chang Gung Memorial Hospital, Taoyuan, Taiwan.
Chiang, Y-J. Department of Urology, Linkou Chang Gung Memorial Hospital, Taoyuan, Taiwan.
Yang, S-H. School of Nutrition and Health Sciences, College of Nutrition, Taipei Medical University,
Taipei, Taiwan; Nutrition Research Center, Taipei Medical University Hospital, Taipei, Taiwan. Electronic
address: sherry@tmu.edu.tw.
Page 24
Adult
Aged
Aged, 80 and over
Female
*Geriatric Assessment/mt [Methods]
*Hand Strength
Humans
Male
Middle Aged
*Nutrition Assessment
Nutritional Status
Predictive Value of Tests
Abstract
BACKGROUND: The Geriatric Nutritional Risk Index (GNRI) is a useful predictor of prognosis in older
patients and those receiving hemodialysis. However, the predictive value of the GNRI in renal transplant
recipients (RTRs) is unclear. In this study we investigated the correlation between the GNRI and muscle
function, as indicated by handgrip strength (HGS).
METHODS: A cross-sectional study was performed on 42 RTRs (50% women), with a mean age of 49.0
+/- 10.8 years. The GNRI was derived from patients' body weight and serum albumin level by using the
following equation: GNRI = [14.89 x albumin (g/dL)] + [41.7 x (body weight/ideal body weight)]. HGS
was evaluated in dominant arms; HGS measurement was repeated 3 times, and the highest value was used.
Multivariable stepwise regression analyses were performed to obtain adjusted correlates, and the
significance levels for entry and remaining were set at 0.1.
RESULTS: The mean values of the GNRI and HGS were 105.0 +/- 5.4 and 29.0 +/- 9.4, respectively.
The GNRI was positively correlated with HGS (r = 0.36, P = .02). Linear and stepwise multivariable
adjustment analyses revealed that the homeostatic model assessment of insulin resistance (HOMA-IR) and
GNRI were independent determinants of HGS (betaHOMA-IR = 0.53 and betaGNRI = 0.43, adjusted R2 =
0.45) after adjustment for age, sex, total muscle mass, and C-reactive protein level as covariates.
CONCLUSION: This study has shown that the GNRI is a favorable predictor of muscle function in
RTRs. Copyright © 2018 Elsevier Inc. All rights reserved.
Publication Type
Journal Article.
Year of Publication
2018

<19>
Unique Identifier
1861463
Title
Hyperglycaemia associated with lactic acidaemia in a renal allograft recipient with type I glycogen
storage disease.
Source
Journal of Inherited Metabolic Disease. 14(1):80-6, 1991.
VI 1
Record Owner
Page 25
Status
MEDLINE
Authors
Chen YT; Scheinman JI.
Authors Full Name
Chen, Y T; Scheinman, J I.
Institution
Chen, Y T. Department of Pediatrics, Duke University Medical Center, Durham, North Carolina 27710.
*Acidosis, Lactic/co [Complications]
Adolescent
C-Peptide/bl [Blood]
Female
Glucocorticoids/ae [Adverse Effects]
Glucocorticoids/tu [Therapeutic Use]
Glycogen Storage Disease Type I/bl [Blood]
*Glycogen Storage Disease Type I/co [Complications]
Humans
*Hyperglycemia/et [Etiology]
Insulin/bl [Blood]
*Kidney Transplantation/ph [Physiology]
Abstract
Renal disease is a frequent and serious complication of type I glycogen storage disease. A type I glycogen
storage disease patient with focal segmental glomerulosclerosis and progressive renal insufficiency
underwent a renal allograft transplantation. Despite the same cornstarch therapy, the post-transplantation
course was complicated by worsening of the metabolic control manifested by exacerbated lactic acidaemia
and hyperlipidaemia. This lactic acidaemia was remarkable for its association with hyperglycaemia.
Hyperglycaemia accompanied by lactic acidaemia is strikingly unusual in type I glycogen storage disease,
since this is a disease characterized by hypoglycaemia and an inverse relationship between blood glucose
concentration and lactate levels. Both fasting insulin and C-peptide levels in the patient were greater than
similar age-matched type I glycogen storage disease controls, indicating hyperinsulinaemia. The most
likely mechanism responsible for the combined hyperglycaemia and lactic acidaemia was insulin resistance
due to glucocorticoid treatment, instituted for immunosuppression. The hyperglycaemia associated with the
lactic acidaemia was transient and resolved with steroid tapering. The exacerbated hyperlipidaemia,
however, persisted after renal transplantation. Type I glycogen storage disease patients may be prone to
glucocorticoid-induced insulin resistance, since the cellular metabolism in these patients may already be
compromised with ineffective insulin action and/or reduced insulin output.
0 (Blood Glucose). 0 (C-Peptide). 0 (Glucocorticoids). 0 (Insulin). AYI8EX34EU (Creatinine).
Publication Type
Case Reports. Journal Article. Research Support, Non-U.S. Gov't. Research Support, U.S. Gov't, P.H.S..
Year of Publication
1991

<20>
Unique Identifier
2253832
Page 26
Title
Reduction of insulin resistance by combined kidney-pancreas transplantation in type 1 (insulin-dependent)
diabetic patients.
Source
Diabetologia. 33(9):549-56, 1990 Sep.
VI 1
Record Owner
Status
MEDLINE
Authors
Luzi L; Secchi A; Facchini F; Battezzati A; Staudacher C; Spotti D; Castoldi R; Ferrari G; Di Carlo V;
Pozza G.
Authors Full Name
Luzi, L; Secchi, A; Facchini, F; Battezzati, A; Staudacher, C; Spotti, D; Castoldi, R; Ferrari, G; Di Carlo,
V; Pozza, G.
Institution
Luzi, L. Department of Internal Medicine, Istituto Scientifico San Raffaele, University of Milan, Italy.
Adult
Blood Pressure
Diabetes Mellitus, Type 1/dt [Drug Therapy]
Diabetes Mellitus, Type 1/pp [Physiopathology]
*Diabetes Mellitus, Type 1/su [Surgery]
Fatty Acids, Nonesterified/bl [Blood]
Female
Glucagon/bl [Blood]
Glucose/me [Metabolism]
Glycated Hemoglobin A/an [Analysis]
Humans
Insulin/bl [Blood]
Insulin Infusion Systems
*Insulin Resistance
Kidney Failure, Chronic/su [Surgery]
Kidney Transplantation/ph [Physiology]
Male
Pancreas Transplantation/ph [Physiology]
*Pancreas Transplantation
Reference Values
Abstract
To evaluate the effect of combined kidney and pancreas transplantation on insulin action and glucose
metabolism, 15 Type 1 (insulin-dependent) diabetic patients who were undergoing combined kidney-
pancreas transplantation were studied before transplantation by means of the euglycaemic
hyperinsulinaemic clamp technique combined with 3-3H-glucose infusion and indirect calorimetry. Nine of
the original 15 patients were studied again after four months and six after 12 months, successful combined
kidney-pancreas transplantation with the same experimental protocol. Nine volunteers formed the group of
normal subjects. Combined kidney-pancreas transplantation normalised hepatic glucose production and
reduced peripheral insulin resistance in Type 1 diabetic uraemic patients, despite chronic
immunosuppressive therapy. To further evaluate the hypothesis that residual insulin resistance was due to
chronic steroid therapy. 11 additional subjects with chronic uveitis (six of whom were treated with only
prednisone, and five treated only with cyclosporin) underwent the same protocol demonstrating a normal
hepatic glucose production. The insulin-stimulated peripheral glucose uptake was reduced in the
prednisone-treated group, but normal in cyclosporin-treated subjects. Four additional diabetic patients with
a kidney transplant were also studied. They showed a peripheral insulin sensitivity intermediate between
Page 27
diabetic uraemic patients and patients after combined transplant. We conclude that short-term (one year)
combined kidney-pancreas transplantation improves glucose metabolism by restoring normal rates of
hepatic glucose production and reducing peripheral insulin resistance; chronic steroid therapy is the major
determinant of residual reduced insulin action. Both kidney and pancreas substitution play a role in
reducing peripheral insulin resistance.
0 (Blood Glucose). 0 (Fatty Acids, Nonesterified). 0 (Glycated Hemoglobin A). 0 (Insulin). 9007-92-5
(Glucagon). IY9XDZ35W2 (Glucose).
Publication Type
Clinical Trial. Comparative Study. Journal Article. Research Support, Non-U.S. Gov't.
Year of Publication
1990

<21>
Unique Identifier
1936700
Title
Insulin action and insulin binding following pancreas transplantation.
Source
Diabetologia. 34 Suppl 1:S71-5, 1991 Aug.
VI 1
Record Owner
Status
MEDLINE
Authors
Saudek F; Pelikanova T; Bartos V; Reneltova I; Kazdova L; Kovar J; Karasova L.
Authors Full Name
Saudek, F; Pelikanova, T; Bartos, V; Reneltova, I; Kazdova, L; Kovar, J; Karasova, L.
Institution
Saudek, F. Institute for Clinical and Experimental Medicine, Prague, Czechoslovakia.
Adult
*Blood Glucose/me [Metabolism]
Diabetes Mellitus, Type 1/bl [Blood]
Diabetic Nephropathies/bl [Blood]
*Diabetic Nephropathies/su [Surgery]
*Erythrocytes/me [Metabolism]
Female
Humans
*Insulin/bl [Blood]
Kinetics
Male
*Pancreas Transplantation/ph [Physiology]
*Receptor, Insulin/me [Metabolism]
Reference Values
Abstract
Page 28
Insulin action and insulin specific binding to erythrocytes were examined in ten recipients of a pancreatic
segment and renal graft (Group 1), in nine non-diabetic kidney recipients (Group 2) and in ten age- and
weight-matched healthy control subjects (Group 3). All transplant recipients were normoglycaemic without
need of insulin, received the same immunosuppression and had good renal graft function at 11-18 months
post-transplantation, when the investigation was performed. Using the insulin clamp technique, insulin
action was expressed as the metabolic clearance rate of glucose at insulin infusion rates of 1.0
(MCRsubmax) and 10.0 (MCRmax) mU.kg-1.min-1. In comparison with the healthy control subjects,
fasting free insulin and C-peptide levels were significantly higher in Groups 1 and 2, but no differences
between Groups 1 and 2 were found (p greater than 0.05). Mean values +/- SEM of MCRsubmax in Groups
1, 2 and 3 were 6.30 +/- 0.55, 6.09 +/- 0.69 and 10.52 +/- 1.10 ml.kg-1.min-1 respectively, and of MCRmax
12.65 +/- 0.78, 13.14 +/- 0.92 and 19.28 +/- 1.42 ml.kg-1.min-1 respectively. Insulin action was
significantly decreased in Groups 1 and 2 at the low as well as the high insulin infusion rates but there was
no difference between the two groups of recipients (p greater than 0.05). No differences in binding data
(specific binding, number of binding sites per cell) were found. It is concluded that insulin resistance is
common to all immunosuppressed organ recipient and is not related to the pancreas graft. The decrease
maximal response to insulin and normal insulin binding to erythrocytes tend to suggest a post-receptor
defect in insulin action.
0 (Blood Glucose). 0 (C-Peptide). 0 (Insulin). EC 2-7-10-1 (Receptor, Insulin).
Publication Type
Journal Article.
Year of Publication
1991

<22>
Unique Identifier
1936698
Title
Metabolic and hormonal studies of type 1 (insulin-dependent) diabetic patients after successful pancreas
and kidney transplantation.
Source
VI 1
Record Owner
Status
MEDLINE
Authors
Landgraf R; Nusser J; Riepl RL; Fiedler F; Illner WD; Abendroth D; Land W.
Authors Full Name
Landgraf, R; Nusser, J; Riepl, R L; Fiedler, F; Illner, W D; Abendroth, D; Land, W.
Institution
Landgraf, R. Department of Internal Medicine, Klinikum Innenstadt, FRG.
Adult
Arginine
Epinephrine/bl [Blood]
Page 29
Female
Glucagon/bl [Blood]
Glucose Tolerance Test
Growth Hormone/bl [Blood]
*Hormones/bl [Blood]
Humans
*Insulin/bl [Blood]
Kidney Transplantation/mt [Methods]
Male
Norepinephrine/bl [Blood]
Pancreas Transplantation/mt [Methods]
Prolactin/bl [Blood]
Prospective Studies
Reference Values
Abstract
Long-term normalization of glucose metabolism is necessary to prevent or ameliorate diabetic
complications. Although pancreatic grafting is able to restore normal blood glucose and glycated
haemoglobin, the degree of normalization of the deranged diabetic metabolism after pancreas
transplantation is still questionable. Consequently glucose, insulin, C-peptide, glucagon, and pancreatic
polypeptide responses to oral glucose and i.v. arginine were measured in 36 Type 1 (insulin-dependent)
diabetic recipients of pancreas and kidney allografts and compared to ten healthy control subjects. Despite
normal HbA1 (7.2 +/- 0.2%; normal less than 8%) glucose disposal was normal only in 44% and impaired
in 56% of the graft recipients. Normalization of glucose tolerance was achieved at the expense of
hyperinsulinaemia in 52% of the subjects. C-peptide and glucagon were normal, while pancreatic
polypeptide was significantly higher in the graft recipients. Intravenous glucose tolerance (n = 21) was
normal in 67% and borderline in 23%. Biphasic insulin release was seen in patients with normal glucose
tolerance. Glucose tolerance did not deteriorate up to 7 years post-transplant. In addition, stress hormone
release (cortisol, growth hormone, prolactin, glucagon, catecholamines) to insulin-induced hypoglycaemia
was examined in 20 graft recipients and compared to eight healthy subjects. Reduced blood glucose decline
indicates insulin resistance, but glucose recovery was normal, despite markedly reduced catecholamine and
glucagon release. These data demonstrate the effectiveness of pancreatic grafting in normalizing glucose
metabolism, although hyperinsulinaemia and deranged counterregulatory hormone response are observed
frequently.
0 (Blood Glucose). 0 (Hormones). 0 (Insulin). 9002-62-4 (Prolactin). 9002-72-6 (Growth Hormone).
9007-92-5 (Glucagon). 94ZLA3W45F (Arginine). X4W3ENH1CV (Norepinephrine). YKH834O4BH
(Epinephrine).
Publication Type
Clinical Trial. Comparative Study. Journal Article. Research Support, Non-U.S. Gov't.
Year of Publication
1991

<23>
Unique Identifier
1936693
Title
Metabolic risk factors for cardiovascular disease in pancreas and kidney transplant recipients.
Source
Page 30
VI 1
Record Owner
Status
MEDLINE
Authors
Nyberg G; Fager G; Mjornstedt L; Olausson M.
Authors Full Name
Nyberg, G; Fager, G; Mjornstedt, L; Olausson, M.
Institution
Nyberg, G. Transplant Unit, Sahlgrenska Hospital, Goteborg, Sweden.
Adult
*Cardiovascular Diseases/et [Etiology]
*Cholesterol/bl [Blood]
Cholesterol, HDL/bl [Blood]
Diabetes Mellitus, Type 1/pp [Physiopathology]
Female
Humans
Male
Risk Factors
*Triglycerides/bl [Blood]
*Uremia/su [Surgery]
Abstract
Hyperinsulinaemia when combined with insulin resistance and hypertriglyceridaemia is a risk factor for
cardiovascular disease. We have studied the serum lipid profile and glycaemic control in 27 uraemic
diabetic patients, 23 Type 1 (insulin-dependent) diabetic kidney recipients, 18 non-diabetic kidney
recipients, and 30 recipients of kidney and pancreas transplants at 6 months post-transplantation. Fasting
serum triglycerides were increased in the uraemic diabetic patients and nondiabetic kidney transplanted
patients but not in diabetic kidney transplanted patients whether or not they had received a pancreas. Total
cholesterol was increased only in the uraemic diabetic patients while HDL cholesterol was normal in all
groups. Within the pancreas and kidney transplanted group triglyceride values correlated with glomerular
filtration rate (r = -0.55) but not with plasma insulin, glycated haemoglobin or kG-value following an
intravenous glucose load. Plasma insulin was increased. Whether such isolated hyperinsulinaemia confers
an increased risk of cardiovascular disease is not known. There may be adaptive feed-back mechanisms to
protect target cells. Increasing the surgical risk in attempts to secure insulin delivery to the portal
circulation does not seem warranted.
0 (Cholesterol, HDL). 0 (Triglycerides). 97C5T2UQ7J (Cholesterol).
Publication Type
Journal Article.
Year of Publication
1991

<24>
Page 31
Unique Identifier
1936692
Title
Metabolic characteristics in patients with long-term pancreas graft with systemic or portal venous
drainage.
Source
VI 1
Record Owner
Status
MEDLINE
Authors
Esmatjes E; Fernandez-Cruz L; Ricart MJ; Casamitjana R; Lopez-Boado MA; Astudillo E.
Authors Full Name
Esmatjes, E; Fernandez-Cruz, L; Ricart, M J; Casamitjana, R; Lopez-Boado, M A; Astudillo, E.
Institution
Esmatjes, E. Endocrinology and Diabetes Unit, University of Barcelona, Spain.
Adult
Female
Follow-Up Studies
Humans
Insulin/bl [Blood]
Insulin/me [Metabolism]
Insulin Secretion
Male
Pancreas Transplantation/mt [Methods]
Portal Vein/su [Surgery]
Reference Values
Abstract
Between January 1983 and June 1990, 32 simultaneous pancreas and kidney transplantations were
performed at the University of Barcelona. Insulin-secretion was assessed by intravenous glucose tolerance
test performed 24h after transplantation and oral glucose tolerance test during the follow-up. Insulin
secretion was also studied in seven non-diabetic patients with kidney transplants. Insulin levels in patients
with pancreas and kidney transplantations both at the basal level and after glucose stimulation were higher
than normal but not different than those observed in patients with kidney transplantation only. Patients with
both pancreas and kidney transplantations and kidney transplantation only presented a mild insulin
resistance, measured by the glucose/insulin ratio. Insulin levels during the follow-up of a patient with portal
venous drainage were similar to those observed in patients with systemic venous drainage. In conclusion,
pancreas transplantation allows a long-term maintenance of glucose homeostasis, although coexisting with
an insulin resistance, probably related of the immunosuppressive therapy.
0 (Blood Glucose). 0 (C-Peptide). 0 (Insulin).
Publication Type
Comparative Study. Journal Article.
Year of Publication
1991
Page 32
<25>
Unique Identifier
1644247
Title
Minimal model analysis of insulin sensitivity and glucose-mediated glucose disposal in type 1 (insulin-
dependent) diabetic pancreas allograft recipients.
Source
Diabetologia. 35(7):676-80, 1992 Jul.
VI 1
Record Owner
Status
MEDLINE
Authors
Osei K; Cottrell DA; Henry ML; Tesi RJ; Ferguson RM; O'Dorisio TM.
Authors Full Name
Osei, K; Cottrell, D A; Henry, M L; Tesi, R J; Ferguson, R M; O'Dorisio, T M.
Institution
Osei, K. Department of Internal Medicine and Surgery, Ohio State University Hospitals, Columbus.
Adult
Body Mass Index
Body Weight
*Diabetes Mellitus, Type 1/pp [Physiopathology]
Female
Humans
*Insulin/bl [Blood]
Male
Tolbutamide/pd [Pharmacology]
Transplantation, Homologous
Abstract
Decreased insulin sensitivity and glucose-dependent glucose disposal (glucose effectiveness) have been
demonstrated in poorly-controlled Type 1 (insulin-dependent) diabetic patients. We have therefore
examined the effects of successful pancreas transplantation that results in long-term physiologic
normoglycaemia as measured by insulin sensitivity index and glucose effectiveness in 14 Type 1 diabetic
recipients (Group 1) using the Bergman minimal model method. Their results were compared with those of
five non-diabetic patients with kidney transplant alone (Group 2) and 10 healthy control subjects (Group 3).
Mean plasma glucose levels were indistinguishable in Group 1 when compared to Groups 2 and 3.
However, mean basal plasma insulin levels were two- and eight-fold greater in Group 1 (36 +/- 6
microU/ml) than in Group 2 (17 +/- 7 microU/ml) and Group 3 (4.5 +/- 0.6 microU/ml), respectively.
Following intravenous glucose (t = 0 min) and tolbutamide (t = 20), peak incremental insulin levels were
significantly (p less than 0.001) greater in Group 1 vs Groups 2 and 3. Mean insulin sensitivity index was
65% and 50% lower in Group 1 (2.89 +/- 0.45) and Group 2 (4.11 +/- 1.30), respectively, when compared
to Group 3 (8.40 +/- 1.24 x 10(-1) min-1 (microU/ml)-1. In contrast, glucose effectiveness was similar in
the three groups (Group 1, 2.48 +/- 0.26; Group 2, 2.05 +/- 0.21; and Group 3, 2.10 +/- 0.17 x 10(-2).min-
Page 33
1). We conclude that, despite prednisone-induced insulin resistance, normal glucose tolerance is achieved
by hyperinsulinaemia and normalisation of glucose-dependent glucose disposal following pancreas-kidney
transplantation in Type 1 diabetic patients.
0 (Blood Glucose). 0 (Insulin). 982XCM1FOI (Tolbutamide).
Publication Type
Journal Article. Research Support, Non-U.S. Gov't. Research Support, U.S. Gov't, P.H.S..
Year of Publication
1992

<26>
Unique Identifier
12666073
Title
Insulin resistance as putative cause of chronic renal transplant dysfunction. [Review] [99 refs]
Source
American Journal of Kidney Diseases. 41(4):859-67, 2003 Apr.
VI 1
Record Owner
Status
MEDLINE
Authors
de Vries AP; Bakker SJ; van Son WJ; Homan van der Heide JJ; The TH; de Jong PE; Gans RO.
Authors Full Name
de Vries, Aiko P J; Bakker, Stephan J L; van Son, Willem J; Homan van der Heide, Jaap J; The, T Hauw;
de Jong, Paul E; Gans, Reinold O b.
Institution
de Vries, Aiko P J. Division of Nephrology Department of Medicine, Groningen University Medical
Center, Groningen, The Netherlands. a.p.j.de.vries@int.azg.nl
Arteriosclerosis/ep [Epidemiology]
Diabetes Mellitus/ep [Epidemiology]
Diet/ae [Adverse Effects]
Forecasting
*Graft Survival/ph [Physiology]
Humans
Hyperlipidemias/ep [Epidemiology]
Hypertension/ep [Epidemiology]
*Insulin Resistance
*Kidney/pp [Physiopathology]
Kidney Failure, Chronic/dh [Diet Therapy]
Kidney Failure, Chronic/ep [Epidemiology]
Kidney Failure, Chronic/th [Therapy]
*Metabolic Syndrome/co [Complications]
Obesity/ep [Epidemiology]
Postoperative Complications/ep [Epidemiology]
Page 34
*Postoperative Complications/et [Etiology]
Proteinuria/ep [Epidemiology]
Renal Dialysis
Risk Factors
Abstract
Transplantation is the preferred organ replacement therapy for most patients with end-stage renal disease.
Despite impressive improvements over recent years in the treatment of acute rejection, approximately half
of all grafts will loose function within 10 years after transplantation. Chronic renal transplant dysfunction,
also known as transplant atherosclerosis, is a leading cause of late allograft loss. To date, no specific
treatment for chronic renal transplant dysfunction is available. Although its precise pathophysiology
remains unknown, it is believed that it involves a multifactorial process of alloantigen-dependent and
alloantigen-independent risk factors. Obesity, posttransplant diabetes mellitus, dyslipidemia, hypertension,
and proteinuria have all been identified as alloantigen-independent risk factors. Notably, these recipient-
related risk factors are well-known risk factors for cardiovascular disease, which cluster within the insulin
resistance syndrome in the general population. Insulin resistance is considered the central pathophysiologic
feature of this syndrome. It is therefore tempting to speculate that it is insulin resistance that underlies the
recipient-related risk factors for chronic renal transplant dysfunction. Recognition of insulin resistance as a
central feature underlying many, if not all, recipient-related risk factors would not only improve our
understanding of the pathophysiology of chronic renal transplant dysfunction, but also stimulate
development of new treatment and prevention strategies. [References: 99]
Publication Type
Journal Article. Research Support, Non-U.S. Gov't. Review.
Year of Publication
2003

<27>
Unique Identifier
178180
Title
Effects of glucocorticoids on carbohydrate metabolism.
Source
American Journal of the Medical Sciences. 271(2):202-10, 1976 Mar-Apr.
VI 1
Record Owner
Status
MEDLINE
Authors
Olefsky JM; Kimmerling G.
Authors Full Name
Olefsky, J M; Kimmerling, G.
Animals
Diabetes Complications
*Glucocorticoids/pd [Pharmacology]
*Glucose/me [Metabolism]
Graft Rejection
Humans
*Hyperglycemia/ci [Chemically Induced]
Page 35
Insulin Resistance
Kidney Failure, Chronic/co [Complications]
Male
Middle Aged
Prednisolone/ae [Adverse Effects]
Prednisolone/tu [Therapeutic Use]
Rats
Receptors, Cell Surface/de [Drug Effects]
Abstract
A patient with pre-existing diabetes mellitus who was receiving corticosteroids in an effort to prevent
transplant rejection was presented. The patient's hyperglycemia was exacerbated by the corticosteroids, and
the discussion centered around this aspect of the case. The clinical effects of glucocorticoids on
carbohydrate metabolism were reviewed, and four general points were made: (1) the chronic effects of
corticoids on glucose tolerance are much less pronounced than the acute effects; (2) the degree of
impariment is proportional to the pre-existing status of glucose tolerance; (3) development of frank diabetes
mellitus in a previously normal patient is unusual; and (4) the abnormalities of carbohydrate metabolism
induced by glucocorticoids fit the pattern of an insulin resistant state. The subject was reviewed and
relevant in vivo and in vitro observations were presented in support of the above concepts, and to help
identify the pathophysiologic mechanisms involved. It was postulated that glucocorticoids affect glucose
metabolism by decreasing glucose utilization and by increasing hepatic glucose production. The possible
mechanisms underlying these effects were discussed.
0 (Glucocorticoids). 0 (Insulin). 0 (Receptors, Cell Surface). 9PHQ9Y1OLM (Prednisolone).
IY9XDZ35W2 (Glucose).
Publication Type
Case Reports. Journal Article.
Year of Publication
1976

<28>
Unique Identifier
16340782
Title
Rosiglitazone therapy of posttransplant diabetes mellitus.
Source
Transplantation. 80(10):1402-5, 2005 Nov 27.
VI 1
Record Owner
Status
MEDLINE
Authors
Villanueva G; Baldwin D.
Authors Full Name
Villanueva, Griselda; Baldwin, David.
Institution
Villanueva, Griselda. Section of Endocrinology, Rush University Medical Center, Chicago, IL 60612,
USA.
Page 36
Adult
Aged
Cyclosporine/ad [Administration & Dosage]
*Diabetes Mellitus, Type 2/ci [Chemically Induced]
*Diabetes Mellitus, Type 2/dt [Drug Therapy]
Female
Humans
Insulin/tu [Therapeutic Use]
Liver Transplantation/ae [Adverse Effects]
Male
Middle Aged
*Organ Transplantation/ae [Adverse Effects]
PPAR gamma/ag [Agonists]
Prospective Studies
Rosiglitazone
Tacrolimus/ad [Administration & Dosage]
*Thiazolidinediones/tu [Therapeutic Use]
Abstract
BACKGROUND: The new onset of posttransplant diabetes mellitus (PTDM) is a common problem after
solid organ transplantation. Because insulin resistance plays a significant role in the development of
PTDM, we treated 40 consecutive patients with PTDM after liver and kidney transplantation with the
insulin sensitizer rosiglitazone (ROSI).
METHODS: Thirty-three of 40 patients with PTDM were initially stabilized with twice-daily NPH and
regular insulin. All patients subsequently began ROSI 4 mg per day. Patients were followed for a mean of
26 weeks and insulin was adjusted using home blood glucose data and hemoglobin A1C (HBA1C).
RESULTS: During 12 months of study, 32/107 liver transplant patients (30%) and 8/205 kidney
transplant patients (4%) patients developed PTDM. After 3-4 months of insulin and ROSI therapy, insulin
was able to be discontinued in 30/33 (91%) patients with PTDM. In all, 12/40 (30%) patients maintained
normal HBA1C levels (5.6+/-0.8%) with ROSI monotherapy, whereas 25/40 (63%) required ROSI and a
sulfonylurea to meet this goal. Three of 40 (7.5%) had persistent insulin dependence. 25/40 (63%)
continued on 4 mg/day of ROSI, and 15/40 (37%) required an increase to 8 mg/day. Mild edema developed
in 13% of patients; significant weight gain did not occur.
CONCLUSIONS: Rosiglitazone is the first highly effective oral agent for PTDM. The majority of
patients with PTDM may be safely treated with ROSI +/- a sulfonylurea. After the expected 3-6 week delay
in the onset of ROSI action, most patients with PTDM will no longer require long-term insulin therapy.
0 (Glycated Hemoglobin A). 0 (Insulin). 0 (PPAR gamma). 0 (Thiazolidinediones). 05V02F2KDG
(Rosiglitazone). 83HN0GTJ6D (Cyclosporine). WM0HAQ4WNM (Tacrolimus).
Publication Type
Journal Article. Research Support, Non-U.S. Gov't.
Year of Publication
2005

<29>
Unique Identifier
Page 37
16249742
Title
Free fatty acids are associated with obesity, insulin resistance, and atherosclerosis in renal transplant
recipients.
Source
Transplantation. 80(7):937-44, 2005 Oct 15.
VI 1
Record Owner
Status
MEDLINE
Authors
Armstrong KA; Hiremagalur B; Haluska BA; Campbell SB; Hawley CM; Marks L; Prins J; Johnson DW;
Isbel NM.
Authors Full Name
Armstrong, Kirsten A; Hiremagalur, Balaji; Haluska, Brian A; Campbell, Scott B; Hawley, Carmel M;
Marks, Lisa; Prins, Johannes; Johnson, David W; Isbel, Nicole M.
Institution
Armstrong, Kirsten A. Department of Renal Medicine, University of Queensland at Princess Alexandra
Hospital, Brisbane, Queensland, Australia. kirsty@ascom.net
Atherosclerosis/di [Diagnosis]
*Atherosclerosis/ep [Epidemiology]
Cohort Studies
*Fatty Acids, Nonesterified/bl [Blood]
Female
Humans
*Insulin Resistance
Male
Middle Aged
Obesity/di [Diagnosis]
*Obesity/ep [Epidemiology]
Prevalence
Sex Factors
Tunica Intima/pa [Pathology]
Abstract
BACKGROUND: Insulin resistance (IR) may be implicated in the pathogenesis of atherosclerosis in renal
transplant recipients (RTRs) and be contributed to, in part, by free fatty acids (FFAs), produced in excess in
centrally obese individuals. The aim of this study was to determine the prevalence of IR and the
relationships between FFAs, central obesity, and atherosclerosis in a cohort of prevalent RTRs.
METHODS: Observational data were collected on 85 RTRs (mean age 54 years; 49% male, 87%
Caucasian). Fasting serum was analyzed for FFAs, glucose, and insulin; IR was calculated using the
homeostasis model assessment (HOMA-IR) score. Vascular structure was assessed by carotid intima-media
thickness (IMT) measurement. Linear regression analyses were performed to determine the factors
associated with IR and atherosclerosis.
RESULTS: IR occurred in 75% of RTRs, and FFA levels were independently associated with its
occurrence (beta: -0.55, 95% CI: -1.02 to -0.07, P = 0.02). Other variables independently associated with IR
were male sex, body mass index, central obesity, diabetes, systolic blood pressure and corticosteroid use.
There was a significant correlation between FFA levels and IMT (r = 0.3, P=0.01). On multivariate
analysis, IMT correlated with elevated FFA (beta: 0.07, 95% CI: 0.02-0.12, P = 0.007), diabetes mellitus (P
= 0.05), older age (P < 0.002), and a body mass index >25 kg/m (P = 0.002).
Page 38
CONCLUSIONS: FFAs are associated with the development of IR and may be involved in the
pathogenesis of atherosclerosis in RTRs. Additional studies are required to explore these associations
further before considering whether an interventional trial aimed at lowering FFA would be a worthwhile
undertaking.
0 (Fatty Acids, Nonesterified).
Publication Type
Year of Publication
2005

<30>
Unique Identifier
15257035
Title
Adiponectin and risk of new-onset diabetes mellitus after kidney transplantation.
Source
Transplantation. 78(1):26-30, 2004 Jul 15.
VI 1
Record Owner
Status
MEDLINE
Authors
Bayes B; Lauzurica R; Granada ML; Serra A; Bonet J; Fontsere N; Salinas I; Romero R.
Authors Full Name
Bayes, Beatriz; Lauzurica, Ricardo; Granada, Maria Luisa; Serra, Assumpta; Bonet, Josep; Fontsere,
Nestor; Salinas, Isabel; Romero, Ramon.
Institution
Bayes, Beatriz. Department of Nephrology, Hospital Universitari "Germans Trias i Pujol", Autonomous
University of Barcelona, Spain. bbayes@teleline.es
Adiponectin
Adult
Blood Glucose
*Diabetes Mellitus, Type 2/ep [Epidemiology]
Female
Graft Rejection/dt [Drug Therapy]
Graft Survival
Humans
Immunosuppressive Agents/ad [Administration & Dosage]
Insulin/bl [Blood]
*Insulin Resistance
*Intercellular Signaling Peptides and Proteins
Leptin/bl [Blood]
Male
Middle Aged
Multivariate Analysis
Page 39
Postoperative Complications/bl [Blood]
*Proteins/me [Metabolism]
Risk Factors
Tacrolimus/ad [Administration & Dosage]
Abstract
BACKGROUND: New-onset diabetes mellitus after transplantation (NODAT) is a severe complication of
kidney transplantation (KTx) with negative effects upon patient and graft survival. Several risk factors for
NODAT have been described; however, the search for an early predictive marker is ongoing. It has recently
been demonstrated that high concentrations of adiponectin (APN), which is an adipocyte-derived peptide
with antiinflammatory and insulin-sensitizing properties, protect against future development of type 2
diabetes in healthy individuals. The purpose of this report was to study pretransplant insulin resistance and
analyze pretransplant serum leptin and APN levels as independent risk factors for the development of
NODAT.
METHODS: A total of 68 KTx patients were studied [mean age, 48 +/- 11 years; 70% males; body mass
index (BMI), 25 +/- 3 kg/m]; 31 KTx patients with NODAT and 37 KTx patients without NODAT (non-
NODAT) with similar age, sex, BMI, immunosuppression, and posttransplant time were studied. All
patients received prednisone and calcineurin inhibitors (75% tacrolimus and 25% cyclosporine A), and
76% of patients received mycophenolate mofetil. Family history of diabetes mellitus was recorded.
Pretransplant homeostasis model assessment for insulin resistance (HOMA-IR) index was calculated from
fasting plasma glucose and insulin. Pretransplant serum leptin and APN levels were determined by
radioimmunoassay.
RESULTS: NODAT patients showed higher pretransplant plasma insulin concentrations [NODAT, 13.4
(11-22.7) microIU/mL; non-NODAT, 10.05 (7.45-18.4) microIU/mL; P=0.049], HOMA-IR index
[NODAT, 4.18 (2.49-5.75); non-NODAT, 2.63 (1.52-4.68); P=0.043], and lower pretransplant serum APN
concentration [NODAT, 8.78 (7.2-11.38) microg/mL; non-NODAT, 11.4 (8.56-15.27) microg/mL,
P=0.012]. Inverse correlations between APN and BMI (r=-0.33; P=0.014) and APN and HOMA-IR index
(r=-0.39; P=0.002) and between APN and NODAT (r=-0.31; P=0.011) were observed. Multiple logistic
regression analysis showed the patients with lower pretransplant APN concentrations to be those at greater
risk of developing NODAT [Odds Ratio=0.832 (0.71-0.96); P=0.01].
CONCLUSION: Pretransplant serum APN concentration is an independent predictive factor for NODAT
development in kidney-transplanted patients.
0 (Adiponectin). 0 (Blood Glucose). 0 (Immunosuppressive Agents). 0 (Insulin). 0 (Intercellular Signaling
Peptides and Proteins). 0 (Leptin). 0 (Proteins). WM0HAQ4WNM (Tacrolimus).
Publication Type
Year of Publication
2004

<31>
Unique Identifier
15223906
Title
Effect of venous drainage site on insulin action after simultaneous pancreas-kidney transplantation.
Source
Page 40
Transplantation. 77(12):1875-9, 2004 Jun 27.
VI 1
Record Owner
Status
MEDLINE
Authors
Petruzzo P; Laville M; Badet L; Lefrancois N; Bin-Dorel S; Chapuis F; Andreelli F; Martin X.
Authors Full Name
Petruzzo, Palmina; Laville, Martine; Badet, Lionel; Lefrancois, Nicole; Bin-Dorel, Sylvie; Chapuis,
Francois; Andreelli, Fabrizio; Martin, Xavier.
Institution
Petruzzo, Palmina. Department of Surgery and Transplantation, University of Cagliari, Cagliari, Italy.
Adult
Diabetes Mellitus, Type 1/su [Surgery]
Diabetic Nephropathies/su [Surgery]
Drainage
Fasting
Female
Glucose Clamp Technique
Humans
Hyperinsulinism/ur [Urine]
*Kidney Transplantation/mt [Methods]
Lipids/bl [Blood]
Male
Middle Aged
*Pancreas Transplantation/mt [Methods]
Pancreas Transplantation/ph [Physiology]
*Portal Vein/su [Surgery]
Abstract
BACKGROUND: The aim of the present study was to determine the influence of the venous drainage site
on insulin homeostasis in simultaneous pancreas-kidney (SPK) transplant recipients.
METHODS: The study included 12 SPK patients with portal venous drainage (P) and 11 SPK patients
with systemic venous drainage (S) of pancreas allograft. All of the participants presented similar
characteristics. The euglycemic hyperinsulinemic clamp was performed using a 0.4-mU/kg/min insulin
infusion. An infusion of [6,6-(2)H2] glucose was used to determine glucose turnover at the basal state and
during the clamp to determine liver and peripheral tissue sensitivity to insulin.
RESULTS: Minor changes in glycemia and insulinemia were shown: fasting plasma glucose was
significantly higher in the SPK-P group and insulinemia was higher in the SPK-S group. Hepatic glucose
production was similar in both groups. During the clamp, insulin levels were higher in SPK-S recipients,
but hepatic glucose production was suppressed in both groups. Glucose use was lower in SPK-S recipients
than in SPK-P recipients, 3.32 +/-1.41 mg/kg/min and 4.70 +/-1.64 mg/kg/min, respectively (P<0.02).
Basal and under-clamp free fatty acid levels were similar. In addition, no significant difference in
cholesterol and low-density lipoprotein levels was shown, whereas high-density lipoprotein levels were
higher in the SPK-S group; triglycerides during fasting and under clamp were significantly higher in the
SPK-P group.
Page 41
CONCLUSIONS: In both groups, neither hepatic nor peripheral insulin resistance was detected. In SPK-
S recipients, the authors have showed only a lower insulin clearance and a slight decreased peripheral
responsiveness to insulin without modifications of lipid status.
0 (Blood Glucose). 0 (Lipids).
Publication Type
Year of Publication
2004

<32>
Unique Identifier
14529883
Title
Plasma adiponectin concentration before and after successful kidney transplantation.
Source
Transplantation Proceedings. 35(6):2186-9, 2003 Sep.
VI 1
Record Owner
Status
MEDLINE
Authors
Chudek J; Adamczak M; Karkoszka H; Budzinski G; Ignacy W; Funahashi T; Matsuzawa Y; Cierpka L;
Kokot F; Wiecek A.
Authors Full Name
Chudek, J; Adamczak, M; Karkoszka, H; Budzinski, G; Ignacy, W; Funahashi, T; Matsuzawa, Y;
Cierpka, L; Kokot, F; Wiecek, A.
Institution
Chudek, J. Department of Nephrology, Endocrinology, and Metabolic Diseases, Medical University of
Silesia, Katowice, Poland.
Adiponectin
Adult
*Biomarkers/bl [Blood]
Drug Therapy, Combination
Female
Humans
*Intercellular Signaling Peptides and Proteins
*Kidney Failure, Chronic/bl [Blood]
Kidney Transplantation/im [Immunology]
Male
Middle Aged
*Proteins/an [Analysis]
Reference Values
Page 42
*Renal Dialysis
Uremia/bl [Blood]
Uremia/su [Surgery]
Abstract
BACKGROUND: Adiponectin, a protein secreted exclusively by adipocytes, is presumed to be involved
in the pathogenesis of atherosclerosis and insulin resistance. An elevated plasma adiponectin concentration
was found in ESRD patients on hemodialysis (HD). However, the role of kidneys in adiponectin
biodegradation/elimination is unknown. Therefore, we assessed plasma adiponectin concentrations in
ESRD patients before and after successful kidney transplantation.
METHODS: Among 44 hemodialyzed patients (29 men, 15 women; mean age 39 +/- 11 years; mean
body mass index [BMI] 23.6 +/- 3.5 kg/m(2); mean duration of HD treatment before kidney transplantation
27 +/- 26 months), plasma adiponectin concentrations and insulin resistance indices (HOMA-R) were
measured twice: immediately before kidney transplantation (Tx) and 1-2 days before patient discharge from
the hospital with stable kidney transplant function (mean serum creatinine level 191 +/- 105 micromol/L).
The control group consisted of 22 normotensive healthy subjects (12 men, 10 women).
RESULTS: Among uremic patients, before Tx, plasma adiponectin concentrations were significantly
higher than in healthy subjects (20.8 +/- 8.3 vs 8.7 +/- 4.8 microg/mL; P <.001) After successful Tx, plasma
adiponectin concentrations decreased significantly (20.8 +/- 8.3 vs 15.7 +/- 7.0 microg/mL before and after
Tx, respectively; P <.001). Simultaneously, after successful kidney transplantation, an increase in HOMA-
R was observed (1.01 +/- 0.61 vs 1.43 +/- 0.83; P =.002). However, changes in adiponectinemia did not
significantly correlate with serum creatinine or HOMA-R.
CONCLUSION: The kidneys seem to play an important role in adiponectin biodegradation and/or
elimination.
0 (Adiponectin). 0 (Biomarkers). 0 (Immunosuppressive Agents). 0 (Intercellular Signaling Peptides and
Proteins). 0 (Proteins). AYI8EX34EU (Creatinine).
Publication Type
Year of Publication
2003

<33>
Unique Identifier
11889436
Title
Diabetogenic effect of tacrolimus in South African patients undergoing kidney transplantation1.
Source
Transplantation. 73(4):587-90, 2002 Feb 27.
VI 1
Record Owner
Status
MEDLINE
Authors
Panz VR; Bonegio R; Raal FJ; Maher H; Hsu HC; Joffe BI.
Authors Full Name
Panz, Vanessa R; Bonegio, Ramon; Raal, Frederick J; Maher, Heather; Hsu, Hon-Chun; Joffe, Barry I.
Page 43
Institution
Panz, Vanessa R. Carbohydrate & Lipid Metabolism Research Group, University of the Witwatersrand,
Johannesburg, South Africa.
Adult
African Continental Ancestry Group
Diabetes Mellitus/ci [Chemically Induced]
*Diabetes Mellitus/ep [Epidemiology]
European Continental Ancestry Group
Female
Homeostasis
Humans
*Immunosuppressive Agents/ae [Adverse Effects]
*Kidney Transplantation/im [Immunology]
Male
Middle Aged
Models, Biological
Regression Analysis
South Africa
*Tacrolimus/ae [Adverse Effects]
Time Factors
Abstract
BACKGROUND: Diabetes mellitus (DM) is a complication of tacrolimus therapy. This prospective study
evaluated the prevalence of DM in South African black and white patients receiving tacrolimus after kidney
transplantation and factors that could identify patients before transplantation who may be at risk of
developing DM.
METHODS: Fasting blood samples from 17 patients (11 black, 6 white) were analyzed immediately
pretransplantation and at 1 and 3 months posttransplantation for glucose, HbAIC, insulin, C-peptide, free
fatty acids, lipids, urea, and creatinine. Insulin resistance (IR) was calculated using the homeostasis model
assessment (HOMA) and quantitative insulin sensitivity check index (QUICKI) formulas.
RESULTS: Eight patients (47%) became diabetic (six black, two white), and nine patients (five black,
four white) remained nondiabetic. Mean glucose concentrations in the diabetic group were significantly
higher at 1 month (P=0.03) and 3 months (P=0.01). Mean insulin level was also significantly raised at 3
months (P=0.01) as was HbAIC (P=0.001). C-peptide concentrations did not change significantly in either
group. Significant correlations emerged between fasting glucose concentrations at 3 months
posttransplantation and initial HOMA (r=0.486; P=0.048) and initial QUICKI (r=-0.582; P=0.014).
CONCLUSIONS: Occurrence of DM was high and somewhat greater in black patients. IR was the main
mechanism involved, together with inadequate beta-cell compensation. IR pretransplantation predicts the
subsequent development of DM.
0 (Blood Glucose). 0 (C-Peptide). 0 (Glycated Hemoglobin A). 0 (Immunosuppressive Agents). 0
(Insulin). WM0HAQ4WNM (Tacrolimus).
Publication Type
Year of Publication
2002
Page 44
<34>
Unique Identifier
11391229
Title
beta-Cell dysfunction rather than insulin resistance is the main contributing factor for the development of
postrenal transplantation diabetes mellitus.
Source
Transplantation. 71(10):1417-23, 2001 May 27.
VI 1
Record Owner
Status
MEDLINE
Authors
Nam JH; Mun JI; Kim SI; Kang SW; Choi KH; Park K; Ahn CW; Cha BS; Song YD; Lim SK; Kim KR;
Lee HC; Huh KB.
Authors Full Name
Nam, J H; Mun, J I; Kim, S I; Kang, S W; Choi, K H; Park, K; Ahn, C W; Cha, B S; Song, Y D; Lim, S
K; Kim, K R; Lee, H C; Huh, K B.
Institution
Nam, J H. Division of Endocrinology and Metabolism, Yonsei University College of Medicine, 134
Shinchon-dong Seodaemun-ku, Seoul, 120-752, Korea.
Adult
Blood Glucose/an [Analysis]
Fasting/bl [Blood]
Female
Humans
Insulin/ph [Physiology]
*Insulin Resistance
*Islets of Langerhans/pp [Physiopathology]
Male
Middle Aged
Proinsulin/bl [Blood]
Abstract
BACKGROUND: Our study was undertaken to investigate the pathogenesis and possible risk factors for
postrenal transplantation diabetes mellitus (PTDM).
METHODS: We recruited 114 patients with normal glucose tolerance (NGT) and performed both 75-g
oral glucose tolerance tests (OGTT) and short insulin tolerance tests 1 week before and 9-12 months after
transplantation.
RESULTS: The subjects were classified into three groups by World Health Organization criteria on the
basis of OGTT after transplantation: (a) 36 (31.6%) subjects with normal glucose tolerance; (b) 51 (45.7%)
subjects with impaired glucose tolerance (IGT); and (c) 27 (23.7%) subjects with postrenal transplantation
diabetes mellitus. Dosages of steroid and cyclosporine were equivalent among the three groups. Before
transplantation, the fasting and 2-hr plasma glucose and proinsulin/insulin (PI/I) ratios were significantly
higher in the IGT and PTDM groups than in the NGT group, but the insulin sensitivity index (ISI) was not
Page 45
significantly different among the three groups. In addition, the area under the curve-insulin on OGTT was
significantly lower in the PTDM group than in the NGT group. After transplantation, however, the ISI was
increased in all groups. Furthermore, the ISI and PI/I ratios revealed significantly higher values in the
PTDM group than in the NGT group after transplantation.
CONCLUSIONS: These results revealed that fasting and 2-hr plasma glucose levels, as well as the
proinsulin/insulin ratio before transplantation, are both possible indicators of beta-cell dysfunction and may
be predictors for the development of PTDM. Furthermore, beta-cell dysfunction, rather than insulin
resistance, was proven to be the main factor for the pathogenesis of PTDM.
0 (Blood Glucose). 0 (Insulin). 9035-68-1 (Proinsulin).
Publication Type
Year of Publication
2001

<35>
Unique Identifier
10798747
Title
Insulin secretion and sensitivity after simultaneous pancreas-kidney transplantation estimated by
continuous infusion of glucose with model assessment.
Source
Transplantation. 69(7):1322-7, 2000 Apr 15.
VI 1
Record Owner
Status
MEDLINE
Authors
Smets YF; van der Pijl JW; Frolich M; Ringers J; de Fijter JW; Lemkes HH.
Authors Full Name
Smets, Y F; van der Pijl, J W; Frolich, M; Ringers, J; de Fijter, J W; Lemkes, H H.
Institution
Smets, Y F. Department of Endocrinology and Metabolic Diseases, Leiden University Medical Centre,
The Netherlands. smets@xs4all.nl
Adult
Female
*Glucose
Humans
Infusions, Intravenous
*Insulin/me [Metabolism]
*Insulin Resistance
Insulin Secretion
Male
Middle Aged
Prospective Studies
Page 46
Solutions
Abstract
BACKGROUND: Monitoring of insulin secretion and sensitivity after pancreas transplantation remains a
practical problem.
METHODS: We introduced the simple structural model, continuous infusion of glucose with model
assessment (CIGMA), to obtain insulin secretion and insulin sensitivity estimations after 35 successful
simultaneous pancreas-kidney transplantations. Eighteen non-diabetic kidney transplant recipients were
used as control group.
RESULTS: The baseline characteristics were equal between the two groups except for higher fasting
insulin levels in the pancreas transplant group. After the 1-hr CIGMA glucose load, the pancreas transplant
group reached a mean +/- SD blood glucose of 8.2+/-1.7 mmol/L compared with 7.3+/-1.0 mmol/L in the
control group (P = 0.05). Concurrent stimulated insulin and C-peptide levels were 48+/-28 mU/L and 2.3+/-
0.9 nmol/L in the pancreas transplant group compared with 36+/-21 mU/L and 2.9+/-1.1 nmol/L in the
control group (P = 0.1 and P = 0.03, respectively). Both the CIGMA estimation for secretion as well as the
CIGMA estimation for sensitivity were lower in pancreas transplant group (P = 0.003 and P = 0.01,
respectively). Mean +/- SE coefficients of variation for the model estimations were 15+/-4% for secretion
and 17+/-6% for sensitivity.
CONCLUSIONS: We conclude that CIGMA can be used clinically to evaluate carbohydrate metabolism
in pancreas-kidney transplant recipients. These patients have a reduction in insulin secretory capacity and
evidence of more insulin resistance than non-diabetic kidney transplant recipients.
0 (Insulin). 0 (Solutions). IY9XDZ35W2 (Glucose).
Publication Type
Journal Article.
Year of Publication
2000

<36>
Unique Identifier
9645815
Title
Successful long-term kidney-pancreas transplants in diabetic patients with high C-peptide levels.
Source
VI 1
Record Owner
Status
MEDLINE
Authors
Sasaki TM; Gray RS; Ratner RE; Currier C; Aquino A; Barhyte DY; Light JA.
Authors Full Name
Sasaki, T M; Gray, R S; Ratner, R E; Currier, C; Aquino, A; Barhyte, D Y; Light, J A.
Institution
Sasaki, T M. Transplantation Services, Washington Hospital Center, DC 20010, USA.
Adult
Page 47
African Continental Ancestry Group
*C-Peptide/bl [Blood]
*Diabetes Mellitus/bl [Blood]
Diabetes Mellitus/eh [Ethnology]
*Diabetes Mellitus/su [Surgery]
Female
Graft Survival/ph [Physiology]
Humans
Male
Middle Aged
Survival Analysis
Time Factors
Abstract
BACKGROUND: Pancreas transplants are rarely done in type 2 (noninsulin dependent) diabetic patients.
Most researchers believe that in type 2 diabetic patients, peripheral insulin resistance plays a central role
and also is associated with relative insulin deficiency or an insulin secretory defect. This suggests that in
patients receiving transplants, the new beta cells will be overstimulated, leading to beta cell "exhaustion"
and graft failure.
METHODS: Early in our experience, simultaneous pancreas-kidney transplant candidates were selected
using only clinical criteria for type 1 diabetes, i.e., early onset of diabetes and rapid onset of insulin use.
Pretransplant sera were available for C-peptide analysis in 70 of 94 of those patients. Forty-four percent
(31/70) were African American (AA).
RESULTS: Thirteen patients (12 AA) with a nonfasting C-peptide level >1.37 ng/ml were identified. In
these patients with high C-peptide levels, pancreas and kidney survival rates were 10O%. The results did
not differ statistically from the low C-peptide group (< or =1.37 ng/ ml). There were no differences
between patient and pancreas-kidney survival rates when the patients were separated into AA and non-AA
groups. The follow-up was 1-89 months, with a mean of 45.5 months.
CONCLUSIONS: Long-term pancreas graft function is attainable and beta cell "exhaustion" does not
occur in patients with high preoperative C-peptide (>1.37 ng/ ml) levels. AA and non-AA patients have
equivalent long-term patient, kidney, and pancreas-kidney graft survival rates.
0 (C-Peptide).
Publication Type
Journal Article.
Year of Publication
1998

<37>
Unique Identifier
8685947
Title
Clinical determinants of glucose homeostasis after pancreas transplantation.
Source
VI 1
Page 48
Record Owner
Status
MEDLINE
Authors
Nankivell BJ; Chapman JR; Bovington KJ; Spicer ST; O'Connell PJ; Allen RD.
Authors Full Name
Nankivell, B J; Chapman, J R; Bovington, K J; Spicer, S T; O'Connell, P J; Allen, R D.
Institution
Nankivell, B J. National Pancreas Transplant Unit, Westmead Hospital, Sydney, Australia.
Adult
C-Peptide/me [Metabolism]
Diabetes Mellitus, Type 1/su [Surgery]
Follow-Up Studies
*Homeostasis/ph [Physiology]
Humans
Insulin Secretion
Islets of Langerhans/me [Metabolism]
*Islets of Langerhans/ph [Physiology]
Liver/me [Metabolism]
Liver Glycogen/bi [Biosynthesis]
Longitudinal Studies
Middle Aged
Prospective Studies
Time Factors
Abstract
Although successful simultaneous pancreas and kidney transplantation (SPK) achieves normoglycemia in
the majority of diabetic recipients with end-stage renal disease, little is known about the factors that
influence long-term endocrine function. In this prospective study of 48 bladder-drained SPK patients, 209
oral glucose tolerance tests were performed between 3 months and 6 years after transplantation. Normal
fasting glucose levels and systemic hyperinsulinemia were stable for up to 6 years after SPK. Multivariate
analysis revealed that increased area-under-curve (AUC) levels of C-peptide 3 months after transplantation
were predicted by short surgical pancreas anastomosis time, greater recipient body weight, and total HLA
mismatch score. Episodes of acute pancreas rejection were not associated with reduced allograft insulin
output in the long term. Insulin output, stimulated by oral glucose tolerance tests and assessed by the ratio
of AUC insulin to AUC glucose, fell gradually after transplantation and was decreased by an elevated
serum calcium level and high cyclosporine dose. The ratio of fasting insulin to glucose, which acts as a
marker of peripheral insulin resistance, fell with time after transplantation and was increased by greater
body weight, higher prednisolone dose, and lower cyclosporine dose. The inhibitory effect of cyclosporine
on both fasting and postprandial insulin output was, however, minor when quantified by multivariate
analysis. Endocrine function of the transplanted pancreas was not correlated with its exocrine function
measured by urinary amylase excretion, nor was there a correlation with change in renal function measured
by isotopic glomerular filtration rate. In summary, simultaneous pancreas and kidney transplantation leads
to excellent long-term glucose homeostasis maintained at the expense of systemic hyperinsulinemia. The
key factors adversely affecting peripheral resistance in SPK were corticosteroid therapy, body weight, and
time after transplantation. The susceptibility of islets to ischemia-reperfusion injury, as quantitated by
surgical anastomosis time, may have implications for islet transplantation programs, as may the relative
Page 49
resistance of islets to allograft rejection. Glucose homeostasis after SPK, while remaining abnormal, may
be used as the standard against which islet transplantation must be measured.
0 (C-Peptide). 0 (Insulin). 0 (Liver Glycogen). IY9XDZ35W2 (Glucose).
Publication Type
Journal Article.
Year of Publication
1996

<38>
Unique Identifier
8623155
Title
The effect of (steroid) immunosuppression on skeletal muscle glycogen metabolism in patients after
kidney transplantation.
Source
Transplantation. 61(6):889-93, 1996 Mar 27.
VI 1
Record Owner
Status
MEDLINE
Authors
Ekstrand A; Schalin-Jantti C; Lofman M; Parkkonen M; Widen E; Franssila-Kallunki A; Saloranta C;
Koivisto V; Groop L.
Authors Full Name
Ekstrand, A; Schalin-Jantti, C; Lofman, M; Parkkonen, M; Widen, E; Franssila-Kallunki, A; Saloranta, C;
Koivisto, V; Groop, L.
Institution
Ekstrand, A. Department of Medicine, Helsinki University Hospital, Finland.
Adult
Female
Glycogen/bi [Biosynthesis]
*Glycogen/me [Metabolism]
Glycogen Synthase/me [Metabolism]
Humans
Insulin/ph [Physiology]
Male
*Methylprednisolone/ae [Adverse Effects]
Methylprednisolone/tu [Therapeutic Use]
Middle Aged
*Muscle, Skeletal/de [Drug Effects]
Muscle, Skeletal/en [Enzymology]
*Muscle, Skeletal/me [Metabolism]
Time Factors
Page 50
Abstract
To examine the mechanisms by which immunosuppression by steroids impairs glycogen synthesis in
human skeletal muscle, we measured glycogen synthase protein content and activity in muscle samples
from 14 patients receiving corticosteroid therapy after kidney transplantation and in 20 healthy control
subjects. A percutaneous muscle sample was taken before and at the end of a euglycemic hyperinsulinemic
insulin clamp. Insulin-stimulated glucose disposal was reduced by 33% in kidney transplant patients
compared with healthy controls (33.8 +/- 4.2 vs. 50.5 +/- 2.7 mumol (kg LBM)-1 min-1; P<0.01), primarily
due to a decrease in nonoxidative glucose metabolism (14.2 +/- 3.3 vs. 32.3 +/- 2.7 mumol (kg LBM)-1
min-1; P<0.001). Glycogen synthase activity measured at both 0.1 mmol/L (17.6 +/- 2.6 vs. 24.0 +/- 2.2
nmol min-1 mg protein-1; P<0.05), and at 10 mmol/L glucose 6-phosphate (24.1 +/- 3.5 vs. 33.7 +- 2.4
nmol min-1 mg protein-1; P<0.05) and glycogen synthase protein concentrations (8.8 +/- 1.8 vs. 18.9 +/-
1.9 relative units per ng DNA; P<0.01) were lower in kidney transplant patients compared with controls.
Glycogen synthase protein correlated with nonoxidative glucose metabolism (r=0.42; P=0.04). Alpha-
actinin (used as a control of general protein degradation) was lower in kidney transplant patients compared
with controls (4.4 +/- 0.8 vs. 9.6 +/- 1.1 cpm/ng DNA; P<0.01). In conclusion, corticosteroids cause insulin
resistance, which correlates with impaired activation of glycogen synthase and decreased enzyme protein
content. The decrease in glycogen synthase protein may reflect increased degradation rather than a defect in
translation.
0 (Blood Glucose). 0 (Immunosuppressive Agents). 0 (Insulin). 9005-79-2 (Glycogen). EC 2-4-1-11
(Glycogen Synthase). X4W7ZR7023 (Methylprednisolone).
Publication Type
Journal Article.
Year of Publication
1996

<39>
Unique Identifier
8333058
Title
Acute deterioration of pancreatic graft function presumably determined by steroid-induced insulin
resistance: a case report.
Source
Transplantation. 56(1):241-4, 1993 Jul.
VI 1
Record Owner
Status
MEDLINE
Authors
Martinenghi S; Secchi A; Luzi L; Battezzati A; DiCarlo V; Pozza G.
Authors Full Name
Martinenghi, S; Secchi, A; Luzi, L; Battezzati, A; DiCarlo, V; Pozza, G.
Institution
Martinenghi, S. Department of Internal Medicine, University of Milan, Scientific Institute H San Raffaele,
Italy.
Adult
Page 51
*Diabetes Mellitus, Type 1/pp [Physiopathology]
Drug Therapy, Combination
Female
Follow-Up Studies
Humans
*Immunosuppressive Agents/tu [Therapeutic Use]
*Insulin Resistance
*Methylprednisolone/ae [Adverse Effects]
Time Factors
Uremia/su [Surgery]
0 (Blood Glucose). 0 (Glycated Hemoglobin A). 0 (Immunosuppressive Agents). X4W7ZR7023
(Methylprednisolone).
Publication Type
Year of Publication
1993

<40>
Unique Identifier
3047926
Title
Impaired glucose tolerance in cyclosporine-prednisolone-treated renal graft recipients.
Source
Transplantation. 46(3):370-2, 1988 Sep.
VI 1
Record Owner
Status
MEDLINE
Authors
Ost L; Tyden G; Fehrman I.
Authors Full Name
Ost, L; Tyden, G; Fehrman, I.
Institution
Ost, L. Department of Transplantation Surgery, Karolinska Institute, Sweden.
*Cyclosporins/ae [Adverse Effects]
Humans
Immunosuppression/ae [Adverse Effects]
Page 52
Islets of Langerhans/de [Drug Effects]
Abstract
In 33 renal transplant patients, an intravenous glucose tolerance test (IVGTT) was performed, and fasting
plasma C-peptide concentrations analyzed. Nineteen of the patients were on treatment with cyclosporine-
prednisolone (CsA-Po), and 14 were treated with azathioprine-prednisolone (Aza-Po). In the Aza-Po group,
the K-values at IVGTT were normal in 13/14, but in the CsA-Po group they were only normal in 9/19 (P =
0.02). The fasting C-peptide levels were significantly higher in the CsA-Po group (P less than 0.001).
within this group, there was no correlation between C-peptide level and serum-creatinine concentration, i.e.
retention of C-peptide due to decreased renal function as judged by serum creatinine level was not
suspected. Intrinsic prednisolone clearance was determined in the CsA-Po patients and was found to be
lower than that previously described in Aza-Po patients. However, between those CsA-Po-treated patients
with a pathologic K-value at IVGTT and those with a normal K-value there was no difference in
prednisolone clearance, fasting C-peptide levels, CsA dose, or serum-creatinine concentrations. The
pathophysiology of the cyclosporine-induced glucose intolerance is uncertain, and increased insulin
resistance is possible.
0 (C-Peptide). 0 (Cyclosporins). 9PHQ9Y1OLM (Prednisolone). AYI8EX34EU (Creatinine).
IY9XDZ35W2 (Glucose).
Publication Type
Year of Publication
1988

<41>
Unique Identifier
1897023
Title
Cyclosporine's effect on insulin secretion in patients with kidney transplants.
Source
Transplantation. 52(3):500-3, 1991 Sep.
VI 1
Record Owner
Status
MEDLINE
Authors
Esmatjes E; Ricart MJ; Ferrer JP; Oppenhaimer F; Vilardell J; Casamitjana R.
Authors Full Name
Esmatjes, E; Ricart, M J; Ferrer, J P; Oppenhaimer, F; Vilardell, J; Casamitjana, R.
Institution
Esmatjes, E. Endocrinology and Diabetes Unit, Hospital Clinic, University of Barcelona, Spain.
Adult
C-Peptide/an [Analysis]
*Cyclosporins/ae [Adverse Effects]
Humans
Page 53
Insulin Secretion
*Islets of Langerhans/de [Drug Effects]
Middle Aged
Prednisone/ae [Adverse Effects]
Abstract
Adverse effects of cyclosporine on glucose metabolism have been reported in patients with kidney
transplantation, but steroids were present in all the immunosuppressive schedules evaluated. We have
studied endocrine pancreatic function (OGTT measuring plasma insulin [IRI] and c-peptide [CP]) in 3
groups of patients, matched for age and body-mass index, 16-66 months after functioning Ktx. Seven
patients were treated with CsA monotherapy (group I), 7 patients with CsA plus prednisone (group II), and
6 patients with azathioprine plus prednisone (group III). Seven healthy subjects formed the control group.
OGTT was normal in all patients, except one in group II (impaired glucose tolerance). There were no
significant differences between the 4 groups concerning fasting blood glucose and area under the glucose
curve, as well as basal insulin levels, peak insulin response to glucose, and area under the insulin curve.
Basal CP, peak CP response to glucose, and area under CP curve were lower in CG than in the 3 groups of
patients. Basal CP in group II (4.4 +/- 2.2 ng/ml) was higher than in group I (2.8 +/- 0.6 ng/ml, P less than
0.05). Glucose/IRI molar ratio in group II (5.7 +/- 1.4, P greater than 0.05) was lower than in group I (7.3
+/- 1.8) and CG (8.0 +/- 2.1, P less than 0.025). Our results suggest that CsA at normal dosage has no
clinically important effect on beta-cell function. The indirect evidence of insulin resistance observed in
patients treated with CsA plus prednisone is ascribable to corticosteroid treatment.
0 (Blood Glucose). 0 (C-Peptide). 0 (Cyclosporins). 0 (Insulin). VB0R961HZT (Prednisone).
Publication Type
Journal Article.
Year of Publication
1991

<42>
Unique Identifier
1549847
Title
Insulin resistance and insulin deficiency in the pathogenesis of posttransplantation diabetes in man.
Source
Transplantation. 53(3):563-9, 1992 Mar.
VI 1
Record Owner
Status
MEDLINE
Authors
Ekstrand AV; Eriksson JG; Gronhagen-Riska C; Ahonen PJ; Groop LC.
Authors Full Name
Ekstrand, A V; Eriksson, J G; Gronhagen-Riska, C; Ahonen, P J; Groop, L C.
Institution
Ekstrand, A V. Fourth Department of Medicine, Helsinki University Hospital, Finland.
Adult
B-Lymphocytes/ph [Physiology]
Page 54
Diabetes Mellitus/pp [Physiopathology]
Energy Metabolism
Female
Humans
*Insulin/df [Deficiency]
Male
Middle Aged
Abstract
Although steroids can induce insulin resistance, it is not known whether additional defects in insulin
secretion are necessary for the development of diabetes. To address this question, we measured insulin
sensitivity (euglycemic insulin clamp in combination with indirect calorimetry and infusion of tritiated
glucose) and insulin secretion (hyperglycemic clamp) in three groups of subjects: (1) 10 kidney transplant
patients with normal oral glucose tolerance, (2) 14 patients who developed diabetes after kidney
transplantation, and (3) 10 healthy controls. Glucose utilization, primarily storage of glucose as glycogen,
was reduced by 34% in kidney transplant patients with normal glucose tolerance when compared with
healthy control subjects (18.2 +/- 2.9 vs. 27.5 +/- 2.7 microM/L; P less than 0.05). Insulin secretion was
normal in relation to the degree of insulin resistance in transplanted non-diabetic patients, thus maintaining
a normal oral glucose tolerance. Development of transplantation diabetes was associated with only minor
further deterioration of glucose storage (14.7 +/- 2.7 microM/L; P less than 0.001 vs. control subjects),
whereas first-phase, second-phase, and glucagon-stimulated insulin secretion measured during
hyperglycemic clamping (incremental area under the insulin curve 287 +/- 120, 1275 +/- 419, and 3515 +/-
922 pM) became impaired as compared with nondiabetic kidney transplant patients (769 +/- 216, 3084 +/-
545, and 6293 +/- 533 pM; P less than 0.05). We conclude that both insulin resistance and insulin
deficiency are necessary for the development of diabetes in kidney transplant patients.
0 (Insulin). IY9XDZ35W2 (Glucose).
Publication Type
Year of Publication
1992

<43>
Unique Identifier
9723345
Title
Clinical use of the euglycemic hyperinsulinemic clamp for diagnosis of tacrolimus-induced insulin
resistance after combined pancreas-kidney transplantation.
Source
Transplantation Proceedings. 30(5):1944-5, 1998 Aug.
VI 1
Record Owner
Status
MEDLINE
Authors
Berweck S; Kahl A; Bechstein W; Platz K; Muller U; Neuhaus P; Frei U.
Page 55
Authors Full Name
Berweck, S; Kahl, A; Bechstein, W; Platz, K; Muller, U; Neuhaus, P; Frei, U.
Institution
Berweck, S. Department of Nephrology, Charite, Humboldt Universitat, Berlin, Germany.
Cyclosporine/tu [Therapeutic Use]
*Glucose Clamp Technique
Humans
Hyperinsulinism
Infusions, Intravenous
Insulin/ad [Administration & Dosage]
*Insulin
*Insulin Resistance
0 (Blood Glucose). 0 (Glycated Hemoglobin A). 0 (Immunosuppressive Agents). 0 (Insulin).
83HN0GTJ6D (Cyclosporine). WM0HAQ4WNM (Tacrolimus).
Publication Type
Journal Article.
Year of Publication
1998

<44>
Unique Identifier
9532203
Title
Insulin secretory capacity and peripheral sensitivity after pancreas-kidney transplantation estimated by
CIGMA.
Source
Transplantation Proceedings. 30(2):623, 1998 Mar.
VI 1
Record Owner
Status
MEDLINE
Authors
Smets YF; van der Pijl JW; Frolich M; Ringers J; de Fijter JW; Lemkes HH.
Authors Full Name
Smets, Y F; van der Pijl, J W; Frolich, M; Ringers, J; de Fijter, J W; Lemkes, H H.
Institution
Smets, Y F. Department of Endocrinology, Leiden University Medical Centre, The Netherlands.
Adult
*Diabetes Mellitus/me [Metabolism]
Page 56
Female
*Glucose/ad [Administration & Dosage]
Graft Survival
Humans
Insulin Resistance
Insulin Secretion
Male
Middle Aged
*Pancreas/me [Metabolism]
0 (Insulin). IY9XDZ35W2 (Glucose).
Publication Type
Journal Article.
Year of Publication
1998

<45>
Unique Identifier
22310786
Title
Impact of extrahepatic complications (diabetes and glomerulonephritis) associated with hepatitis C virus
infection after renal transplantation. [Review]
Source
Contributions to Nephrology. 176:108-116, 2012.
VI 1
Record Owner
Status
MEDLINE
Authors
Cruzado JM; Bestard O; Grinyo JM.
Authors Full Name
Cruzado, Josep M; Bestard, Oriol; Grinyo, Josep M.
Cryoglobulinemia/co [Complications]
*Glomerulonephritis, Membranoproliferative/co [Complications]
*Graft Survival
*Hepatitis C, Chronic/co [Complications]
Humans
Immunosuppression/ae [Adverse Effects]
Page 57
Abstract
Hepatitis C virus (HCV) infection is associated with some extrahepatic complications, like diabetes,
cryoglobulinemia, and membranoproliferative glomerulonephritis. Each of these complications has
important implications in the renal allograft recipient. Hence, HCV infection is strongly associated with a
lower patient and graft survival in renal transplantation. The increased risk of death in HCV-infected renal
allograft recipients has been attributed to cardiovascular mortality, linked someway to the insulin resistance
and high risk of new-onset diabetes, rather than to the progression of HCV-related liver disease. On the
other hand, graft survival is hampered by the occurrence of de novo HCV-related glomerulonephritis and
the higher risk of chronic humoral rejection in this population. Copyright © 2012 S. Karger AG, Basel.
Publication Type
Year of Publication
2012

<46>
Unique Identifier
7018745
Title
Fat clearances and hyperlipidaemia in renal allograft recipients--the role of insulin resistance.
Source
Clinica Chimica Acta. 114(1):61-7, 1981 Jul 18.
VI 1
Record Owner
Status
MEDLINE
Authors
Chan MK; Persaud JW; Varghese Z; Fernando ON; Moorhead JF.
Authors Full Name
Chan, M K; Persaud, J W; Varghese, Z; Fernando, O N; Moorhead, J F.
Adult
*Fats/me [Metabolism]
Female
Humans
*Hyperlipidemias/et [Etiology]
*Insulin Resistance
Lipoproteins, VLDL/bi [Biosynthesis]
Male
Middle Aged
Postoperative Complications
Triglycerides/bl [Blood]
Abstract
The mechanism of hyperlipidaemia in renal allograft recipients was investigated in 19 patients randomly
selected from a cohort of 54 patients with functioning renal allografts. Serum cholesterol, triglyceride and
high-density lipoprotein cholesterol concentrations as well as plasma immunoreactive insulin levels were
measured in fasting blood samples. Intravenous fat tolerance tests were performed before and 15 min after
heparin administration. Renal allograft recipients had reduced fractional clearance rates of Intralipid and a
Page 58
positive correlation was demonstrated between plasma immunoreactive insulin levels and serum
triglyceride concentrations. Plasma immunoreactive insulins also correlated inversely with fractional
clearance rates of Intralipid. It was concluded that both increased production and decreased removal of
lipoproteins contribute to the hyperlipidaemia and that insulin resistance due to corticosteroids was the
centre of the problem.
0 (Fats). 0 (Lipoproteins, VLDL). 0 (Triglycerides).
Publication Type
Year of Publication
1981

<47>
Unique Identifier
28848225
Title
Effect of Magnesium Supplements on Insulin Secretion After Kidney Transplantation: A Randomized
Controlled Trial.
Source
Annals of Transplantation. 22:524-531, 2017 Aug 29.
VI 1
Record Owner
Status
MEDLINE
Authors
Van Laecke S; Caluwe R; Huybrechts I; Nagler EV; Vanholder R; Peeters P; Van Vlem B; Van Biesen
W.
Authors Full Name
Van Laecke, Steven; Caluwe, Rogier; Huybrechts, Inge; Nagler, Evi V; Vanholder, Raymond; Peeters,
Patrick; Van Vlem, Bruno; Van Biesen, Wim.
Institution
Van Laecke, Steven. Renal Division, Department of Internal Medicine, Ghent University Hospital, Ghent,
Belgium.
Caluwe, Rogier. Renal Division, Onze-Lieve-Vrouwziekenhuis (OLV) Hospital, Aalst, Belgium.
Huybrechts, Inge. Department of Public Health, Ghent University, Ghent, Belgium.
Huybrechts, Inge. International Agency for Research on Cancer, Lyon, France.
Nagler, Evi V. Renal Division, Department of Internal Medicine, Ghent University Hospital, Ghent,
Belgium.
Vanholder, Raymond. Renal Division, Department of Internal Medicine, Ghent University Hospital,
Ghent, Belgium.
Peeters, Patrick. Renal Division, Department of Internal Medicine, Ghent University Hospital, Ghent,
Belgium.
Van Vlem, Bruno. Renal Division, Onze-Lieve-Vrouwziekenhuis (OLV) Hospital, Aalst, Belgium.
Van Biesen, Wim. Renal Division, Department of Internal Medicine, Ghent University Hospital, Ghent,
Belgium.
Adult
Aged
Page 59
*Dietary Supplements
Female
Glycated Hemoglobin A/me [Metabolism]
Graft Rejection/pc [Prevention & Control]
Humans
Insulin Secretion
*Magnesium/ad [Administration & Dosage]
Male
Middle Aged
Tacrolimus/tu [Therapeutic Use]
Treatment Outcome
Abstract
BACKGROUND Hypomagnesemia is associated with a disturbed glucose metabolism. Insulin hypo-
secretion predicts diabetes in the general population and in transplant recipients. We aimed to assess
whether magnesium improves insulin secretion and glycemic control after transplantation in prevalent
hypomagnesemic kidney transplant recipients. MATERIAL AND METHODS We conducted an open-
label, randomized, parallel-group study. Eligible participants were adults more than 4 months after kidney
transplantation on tacrolimus with persisting serum magnesium concentrations <1.8 mg/dL randomized to
magnesium oxide supplementation up to a maximum of 3 times 450 mg daily (N=26) or no supplements
(N=26). Insulin secretion was assessed by OGTT-derived, first-phase insulin secretion (FPIR). The primary
endpoint was the mean difference in FPIR between baseline and 6 months after randomization. Secondary
endpoints were differences in HbA1c and insulin resistance, measured by HOMA. Dietary magnesium was
assessed by a food-frequency questionnaire. All analyses were done on an intention-to-treat basis.
RESULTS Magnesium with a mean daily dose of 688+/-237mg in the treatment group failed to lead to
significant differences between the 2 groups in FPIR, fasting glucose, HbA1c, or HOMA-IR. Persisting
hypomagnesemia was very common and associated with more insulin hypo-secretion, glucose intolerance,
and lower dietary magnesium intake (142+/-56 versus 202+/-90 mg; p=0.015) as compared to patients with
a rise in serum magnesium over 6 months. CONCLUSIONS Magnesium supplementation does not
improve insulin secretion in stable hypomagnesemic kidney transplant recipients on tacrolimus. Persisting
hypomagnesemia is associated with impaired glucose tolerance, insulin hypo-secretion, and dietary factors.
0 (Blood Glucose). 0 (Glycated Hemoglobin A). 0 (Immunosuppressive Agents). 0 (Insulin). I38ZP9992A
(Magnesium). WM0HAQ4WNM (Tacrolimus).
Publication Type
Journal Article. Randomized Controlled Trial.
Year of Publication
2017

<48>
Unique Identifier
27980321
Title
Beta Cell Function and Insulin Resistance After Conversion from Tacrolimus Twice-Daily to Extended-
Release Tacrolimus Once-Daily in Stable Renal Transplant Recipients.
Source
Annals of Transplantation. 21:765-774, 2016 Dec 16.
VI 1
Page 60
Record Owner
Status
MEDLINE
Authors
Ruangkanchanasetr P; Sanohdontree N; Supaporn T; Sathavarodom N; Satirapoj B.
Authors Full Name
Ruangkanchanasetr, Prajej; Sanohdontree, Natthi; Supaporn, Thanom; Sathavarodom, Nattapol; Satirapoj,
Bancha.
Institution
Ruangkanchanasetr, Prajej. Division of Nephrology, Phramongkutklao Hospital and College of Medicine,
Bangkok, Thailand.
Sanohdontree, Natthi. Division of Nephrology, Phramongkutklao Hospital and College of Medicine,
Bangkok, Thailand.
Supaporn, Thanom. Division of Nephrology, Phramongkutklao Hospital and College of Medicine,
Bangkok, Thailand.
Sathavarodom, Nattapol. Division of Endocrinology, Phramongkutklao Hospital and College of
Medicine, Bangkok, Thailand.
Satirapoj, Bancha. Division of Nephrology, Phramongkutklao Hospital and College of Medicine,
Bangkok, Thailand.
Adult
Delayed-Action Preparations
Drug Administration Schedule
Female
Humans
*Immunosuppressive Agents/ad [Administration & Dosage]
*Insulin-Secreting Cells/de [Drug Effects]
Insulin-Secreting Cells/ph [Physiology]
Male
Middle Aged
Patient Satisfaction
Prospective Studies
*Tacrolimus/ad [Administration & Dosage]
Transplant Recipients
Abstract
BACKGROUND Post-transplantation diabetes mellitus is a major metabolic adverse effect of tacrolimus
(TAC). The objective of this study was to determine if the conversion from tacrolimus twice-daily (TAC-
BID) to extended-release tacrolimus once-daily (TAC-OD) in stable renal transplant recipients had any
effect on beta cell function (HOMA-b), insulin resistance (HOMA-IR), patient preference, and expense.
MATERIAL AND METHODS Twenty-eight renal transplant recipients were recruited and converted from
TAC-BID to TAC-OD at the same dose. Primary outcomes were beta cell function and insulin resistance in
stable renal transplant recipients at 4, 8, and 16 weeks after conversion. Secondary outcomes were patient
satisfaction and expense of medication. RESULTS No significant change in the HOMA-beta and HOMA-
IR was found in any of the 28 renal transplant recipients. However, HOMA-beta increased from 60 (37.33,
109.71) to 78.5 (44.3, 108.4) (p=0.02) in 15 patients who had the conversion within 4 years after renal
transplantation. In multivariate regression analysis, the conversion from TAC-BID to TAC-OD
significantly increased HOMA-b at 4 months at 1.21 mIU/mmol (95%CI 0.54-1.88 mIU/mmol, p=0.01) in
this subgroup. The renal transplant recipients reported the conversion was more satisfactory and cost of
treatment was comparable. CONCLUSIONS In short-term follow-up, conversion from TAC-BID to TAC-
OD is safe in stable renal transplant recipients and might be beneficial in term of improved beta cell
Page 61
function in the early years after renal transplantation. The conversion caused comparable cost and was
preferred by renal transplant recipients.
0 (Delayed-Action Preparations). 0 (Immunosuppressive Agents). WM0HAQ4WNM (Tacrolimus).
Publication Type
Journal Article.
Year of Publication
2016

<49>
Unique Identifier
27443824
Title
Facing the Metabolic Syndrome Epidemic in Living Kidney Donor Programs.
Source
Annals of Transplantation. 21:456-62, 2016 Jul 22.
VI 1
Record Owner
Status
MEDLINE
Authors
Mejia-Vilet JM; Cordova-Sanchez BM; Arreola-Guerra JM; Alberu J; Morales-Buenrostro LE.
Authors Full Name
Mejia-Vilet, Juan M; Cordova-Sanchez, Bertha M; Arreola-Guerra, Jose M; Alberu, Josefina; Morales-
Buenrostro, Luis E.
Institution
Mejia-Vilet, Juan M. Department of Nephrology and Mineral Metabolism, National Medical Sciences and
Nutrition Institute Salvador Zubiran, Mexico City, Mexico.
Cordova-Sanchez, Bertha M. Department of Nephrology and Mineral Metabolism, National Medical
Sciences and Nutrition Institute Salvador Zubiran, Mexico City, Mexico.
Arreola-Guerra, Jose M. Department of Nephrology and Mineral Metabolism, National Medical Sciences
and Nutrition Institute Salvador Zubiran, Mexico City, Mexico.
Alberu, Josefina. Department of Transplantation, National Medical Sciences and Nutrition Institute
Salvador Zubiran, Mexico City, Mexico.
Morales-Buenrostro, Luis E. Department of Nephrology and Mineral Metabolism, National Medical
Sciences and Nutrition Institute Salvador Zubiran, Mexico City, Mexico.
Adolescent
Adult
Aged
Donor Selection/sn [Statistics & Numerical Data]
*Donor Selection
Epidemics
Female
Humans
Kaplan-Meier Estimate
Kidney Failure, Chronic/mo [Mortality]
Page 62
*Living Donors
Male
Mexico/ep [Epidemiology]
Middle Aged
Tissue and Organ Procurement
Young Adult
Abstract
BACKGROUND Due to the shortage of organs for transplantation, there has been increased interest in
developing living-donor kidney transplantation (LDKT) programs. MATERIAL AND METHODS A total
of 668 potential living kidney donors (PLKD) for 496 intended recipients were evaluated in a LDKT
program between 2010 and 2014. Causes for PLKD exclusion were recorded, as well as patient survival.
RESULTS After evaluation, 250 (37.4%) PLKD were considered suitable for kidney donation, 331
(49.6%) were excluded for medical reasons, and 87 (13.0%) withdrew their consent. The main cause of
exclusion was metabolic syndrome and its components: 131 (39.6%) obesity, 37 (11.2%) new diagnosis of
diabetes mellitus, and 25 (7.6%) new diagnosis of hypertension. Sixty-three (19.0%) were excluded for
previously undetected renal diseases. Forty-six (13.9%) PLKD were excluded for immunological
incompatibility. A total of 158 patients (31.9%) were transplanted from living donors and 31 (6.3%) from
deceased donors (after the donor was considered non-suitable). Three-year patient survival was 99.4% for
transplanted patients and 41.4% for patients who remained on dialysis. CONCLUSIONS Metabolic
diseases constitute the main cause of donor exclusion in some LDKT programs. The high mortality rate of
patients whose donor is excluded renews the debate over expanding donor criteria against the long-term
risks they may pose to the living kidney donor.
Publication Type
Journal Article.
Year of Publication
2016

<50>
Unique Identifier
26644065
Title
Long-Term Effect of Renal Transplantation and Aging on Hemoglobin A1C Levels: A Case-Control
Study in 191 Non-Diabetic Deceased Donor Renal Transplant Recipients.
Source
Annals of Transplantation. 20:729-33, 2015 Dec 08.
VI 1
Record Owner
Status
MEDLINE
Authors
Tillmann FP; Hermsen D; Hemmrich K; Woznowski M; Rump LC; Quack I.
Authors Full Name
Tillmann, Frank-Peter; Hermsen, Derik; Hemmrich, Katrin; Woznowski, Magdalena; Rump, Lars
Christian; Quack, Ivo.
Institution
Tillmann, Frank-Peter. Department of Nephrology, Heinrich Heine University of Dusseldorf, Dusseldorf,
Germany.
Page 63
Hermsen, Derik. Central Institute of Clinical Chemistry and Laboratory Diagnostics, Heinrich Heine
University of Dusseldorf, Dusseldorf, Germany.
Hemmrich, Katrin. Department of Nephrology, Heinrich Heine University of Dusseldorf, Dusseldorf,
Germany.
Woznowski, Magdalena. Department of Nephrology, Heinrich Heine University of Dusseldorf,
Dusseldorf, Germany.
Rump, Lars Christian. Department of Nephrology, Heinrich Heine University of Dusseldorf, Dusseldorf,
Germany.
Quack, Ivo. Department of Nephrology, Heinrich Heine University of Dusseldorf, Dusseldorf, Germany.
Adult
*Aging/bl [Blood]
Cadaver
Case-Control Studies
*Creatinine/bl [Blood]
Databases, Factual
Female
Follow-Up Studies
Germany
*Glycated Hemoglobin A/me [Metabolism]
Graft Rejection
Graft Survival
Humans
Insulin Resistance/ph [Physiology]
Male
Middle Aged
Risk Assessment
Statistics, Nonparametric
Time Factors
Tissue Donors
Treatment Outcome
Abstract
BACKGROUND: Reduced renal function in patients with chronic kidney disease is linked to insulin
resistance; and impairments in glucose homeostasis, as measured by HbA1c levels, are related to
cardiovascular events. Recently, aging has been reported to affect HbA1c levels over time in non-diabetic
individuals. The objective of this study was to investigate the association between renal function and aging
in non-diabetic deceased-donor renal transplant recipients.
MATERIAL AND METHODS: A total of 191 patients were analyzed (mean age 50.6+/-12.2 years,
dialysis vintage 6.5+/-3.1 years, 53.4% male patients). HbA1-c levels were measured on the day of
transplantation and on follow-up. The mean follow-up time was 4.9+/-3.1 years.
RESULTS: Renal transplantation resulted in an increase in eGFR of 38.6+/-18.9 mL/min/1.73 m2 as

compared to baseline levels on dialysis and the mean eGFR on follow-up was 45.5+/-18.9 mL/min/1.73
m2. HbA1c levels increased significantly from the day of transplantation to the last follow-up (5.3+/-0.4%
to 5.6+/-0.4%, p<0.0001). Correlation analysis demonstrated non-significant associations between the
change in HbA1c levels and the parameters of age and renal transplant function.
CONCLUSIONS: In conclusion, we observed a significant increase in HbA1c levels over a 5-year post-
transplant follow-up period in non-diabetic deceased-donor renal transplant recipients. In contrast to the
non-diabetic general population, the increase in HbA1c observed in this cohort was greater but not
associated with aging.
Page 64
0 (Glycated Hemoglobin A). AYI8EX34EU (Creatinine).
Publication Type
Journal Article.
Year of Publication
2015

<51>
Unique Identifier
23018257
Title
Influence of conversion from cyclosporine A to tacrolimus on insulin sensitivity assessed by euglicaemic
hyperinsulinemic clamp technique in patients after kidney transplantation.
Source
Annals of Transplantation. 17(3):61-8, 2012 Jul-Sep.
VI 1
Record Owner
Status
MEDLINE
Authors
Bulanowski M; Chudek J; Wiecek A.
Authors Full Name
Bulanowski, Maciej; Chudek, Jerzy; Wiecek, Andrzej.
Institution
Bulanowski, Maciej. Department of Nephrology, Endocrinology, and Metabolic Diseases, Medical
University of Silesia, Francuska 20-24 Str., Katowice, Poland.
Adult
*Cyclosporine/tu [Therapeutic Use]
Female
Humans
Insulin/bl [Blood]
Male
Middle Aged
*Tacrolimus/tu [Therapeutic Use]
Abstract
BACKGROUND: Recent studies have shown diabetogenic properties of calcineurin inhibitors, but the
mechanism of more pronounced diabetogenic effect of tacrolimus (TAC) has not been completely
elucidated. The study was designed to answer 2 questions: Does conversion from CyA to TAC influence
tissue insulin sensitivity in patients after kidney transplantation? Are there any additional factors
influencing insulin sensitivity in these patients?
MATERIAL/METHODS: Fifteen non-diabetic kidney transplant recipients, receiving CyA-based

regimen were recruited to the study. Enrolled patients required conversion to TAC-based treatment due to
Page 65
CyA adverse effects. Euglicaemic-hyperinsulinemic clamp was performed shortly before and 3 months
after conversion from CyA to TAC.
RESULTS: Two out of 15 patients developed PTDM shortly after conversion. Mean insulin sensitivity
indices: glucose cell uptake (M value) and glucose cell uptake to insulin plasma concentration ratio (M/I)
did not change significantly after 3 months of TAC treatment compared to initial values. Significant
negative correlations between increase of body mass and both: changes of M values (-0.576; p=0.02) and
M/I ratios (-0.819; p<0.001) were observed. Similar correlations were observed between changes of BMI
and M values (-0.575; p=0.02) or M/I ratios (-0.800; p<0.001). A significant positive correlation between
changes of eGFR values and M/I ratios (0.591; p=0.03) was noted.
CONCLUSIONS: Tissue insulin sensitivity estimated by hyperinsulinemic, euglycaemic clamp technique

did not change significantly after conversion from CyA to TAC therapy in patients after kidney
transplantation. Weight gain and eGFR decrease are associated with decrease of insulin sensitivity in these
patients.
0 (C-Peptide). 0 (Immunosuppressive Agents). 0 (Insulin). 83HN0GTJ6D (Cyclosporine).
WM0HAQ4WNM (Tacrolimus).
Publication Type
Journal Article.
Year of Publication
2012

<52>
Unique Identifier
17598374
Title
Plasma adiponectin concentration in patients after successful kidney transplantation--a single-center,
observational study.
Source
Clinical Nephrology. 67(6):381-90, 2007 Jun.
VI 1
Record Owner
Status
MEDLINE
Authors
Adamczak M; Szotowska M; Chudek J; Karkoszka H; Cierpka L; Wiecek A.
Authors Full Name
Adamczak, M; Szotowska, M; Chudek, J; Karkoszka, H; Cierpka, L; Wiecek, A.
Institution
Adamczak, M. Department of Nephrology, Endocrinology and Metabolic Diseases, Medical University of
Silesia, Katowice, Poland.
*Adiponectin/bl [Blood]
Adult
Female
Follow-Up Studies
Humans
Page 66
Male
Middle Aged
Renal Dialysis
Time Factors
Abstract
BACKGROUND AND AIM: Adiponectin is an anti-inflammatory protein secreted almost exclusively by
adipocytes which improves insulin sensitivity and presents antiatherogenic properties. Plasma adiponectin
concentration is almost 3 times higher in hemodialysis patients and markedly decreased after successful
kidney transplantation. However, until now, there are no studies analyzing plasma adiponectin
concentration in kidney transplant patients (KTx) during the long-term period after transplantation.
Therefore, the aim of present study was to examine plasma adiponectin concentration in KTx patients
during the wide range of time after transplantation.
MATERIAL AND METHOD: Single center, cross-sectional study including 228 KTx adult recipients
(143 M and 85 F) with estimated glomerular filtration rate (eGFR) > or = 15 ml/min, 80 hemodialysis
patients (34 M and 46 F) and 52 healthy subjects (33 M and 19 F). Plasma adiponectin concentration was
estimated together with HOMA-IR (homeostasis model assessment insulin resistance index) and plasma
lipid profile.
RESULTS: In KTx patients plasma adiponectin concentration 14.0 (13.1-15.0) microg/ml was
significantly (p < 0.001), lower than in hemodialysis ones 29.0 (24.7-33.3) microg/ml, however,
significantly (p < 0.001) higher than in healthy subjects 10.1 (8.8-11.5) microg/ml. Among KTx patients
the highest plasma adiponectin concentration was observed in the subgroup of patients surviving with the
functioning graft more than 8 years after transplantation. In KTx patients, significant, negative correlations
were found between plasma adiponectin concentration and BMI (p = 0.017), HOMA-IR (p = 0.02) and
estimated GFR (p < 0.009), respectively. Multiple regression analysis performed in the group of KTx
patients, with plasma adiponectin concentration as the dependent variable and BMI, age, gender, estimated
GFR as independent variables showed that in this model (R2 = 0.09) plasma adiponectin concentration
significantly depends on BMI (p = 0.035), gender (p = 0.004) and eGFR (p = 0.023).
CONCLUSIONS: Patients with long-term renal graft survival are characterized by a higher plasma
adiponectin concentration. Kidney graft function (assessed as estimated GFR) is an important factor
influencing plasma adiponectin concentration.
0 (Adiponectin). 0 (Immunosuppressive Agents).
Publication Type
Year of Publication
2007

<53>
Unique Identifier
16505244
Title
IRS-1 serine phosphorylation and insulin resistance in skeletal muscle from pancreas transplant recipients.
Source
Diabetes. 55(3):785-91, 2006 Mar.
Page 67
VI 1
Record Owner
Status
MEDLINE
Authors
Bouzakri K; Karlsson HK; Vestergaard H; Madsbad S; Christiansen E; Zierath JR.
Authors Full Name
Bouzakri, Karim; Karlsson, Hakan K R; Vestergaard, Henrik; Madsbad, Sten; Christiansen, Erik; Zierath,
Juleen R.
Institution
Bouzakri, Karim. Karolinska Institute, Department of Molecular Medicine and Surgery, Section of
Integrative Physiology, Stockholm, Sweden.
Adult
Extracellular Signal-Regulated MAP Kinases/me [Metabolism]
Female
Humans
Insulin Receptor Substrate Proteins
*Insulin Resistance
Male
*Muscle, Skeletal/me [Metabolism]
Phosphatidylinositol 3-Kinases/me [Metabolism]
*Phosphoproteins/me [Metabolism]
Phosphorylation
Proto-Oncogene Proteins c-akt/me [Metabolism]
Serine/me [Metabolism]
Signal Transduction/ph [Physiology]
Abstract
Insulin-dependent diabetic recipients of successful pancreas allografts achieve self-regulatory insulin
secretion and discontinue exogenous insulin therapy; however, chronic hyperinsulinemia and impaired
insulin sensitivity generally develop. To determine whether insulin resistance is accompanied by altered
signal transduction, skeletal muscle biopsies were obtained from pancreas-kidney transplant recipients (n =
4), nondiabetic kidney transplant recipients (receiving the same immunosuppressive drugs; n = 5), and
healthy subjects (n = 6) before and during a euglycemic-hyperinsulinemic clamp. Basal insulin receptor
substrate (IRS)-1 Ser (312) and Ser (616) phosphorylation, IRS-1-associated phosphatidylinositol 3-kinase
activity, and extracellular signal-regulated kinase (ERK)-1/2 phosphorylation were elevated in pancreas-
kidney transplant recipients, coincident with fasting hyperinsulinemia. Basal IRS-1 Ser (312) and Ser (616)
phosphorylation was also increased in nondiabetic kidney transplant recipients. Insulin increased
phosphorylation of IRS-1 at Ser (312) but not Ser (616) in healthy subjects, with impairments noted in
nondiabetic kidney and pancreas-kidney transplant recipients. Insulin action on ERK-1/2 and Akt
phosphorylation was impaired in pancreas-kidney transplant recipients and was preserved in nondiabetic
kidney transplant recipients. Importantly, insulin stimulation of the Akt substrate AS160 was impaired in
nondiabetic kidney and pancreas-kidney transplant recipients. In conclusion, peripheral insulin resistance in
pancreas-kidney transplant recipients may arise from a negative feedback regulation of the canonical
insulin-signaling cascade from excessive serine phosphorylation of IRS-1, possibly as a consequence of
immunosuppressive therapy and hyperinsulinemia.
0 (Fatty Acids, Nonesterified). 0 (IRS1 protein, human). 0 (Immunosuppressive Agents). 0 (Insulin
Receptor Substrate Proteins). 0 (Phosphoproteins). 452VLY9402 (Serine). EC 2-7-1 (Phosphatidylinositol
Page 68
3-Kinases). EC 2-7-11-1 (Proto-Oncogene Proteins c-akt). EC 2-7-11-24 (Extracellular Signal-Regulated
MAP Kinases). IY9XDZ35W2 (Glucose).
Publication Type
Year of Publication
2006

<54>
Unique Identifier
16186274
Title
Validation of insulin resistance indexes in a stable renal transplant population.
Source
Diabetes Care. 28(10):2424-9, 2005 Oct.
VI 1
Record Owner
Status
MEDLINE
Authors
Oterdoom LH; de Vries AP; van Son WJ; van der Heide JJ; Ploeg RJ; Gansevoort RT; de Jong PE; Gans
RO; Bakker SJ.
Authors Full Name
Oterdoom, Leendert H; de Vries, Aiko P J; van Son, Willem J; van der Heide, Jaap J Homan; Ploeg,
Rutger J; Gansevoort, Ron T; de Jong, Paul E; Gans, Rijk O B; Bakker, Stephan J L.
Institution
Oterdoom, Leendert H. Renal Transplant Program, University of Groningen and University Medical
Center Groningen, P.O. Box 30.001, 9700 RB Groningen, Netherlands.
Adult
Body Mass Index
Fasting
Female
Glucose/pk [Pharmacokinetics]
Homeostasis
Humans
*Insulin/bl [Blood]
*Insulin Resistance
Male
*Metabolic Syndrome/di [Diagnosis]
Middle Aged
Risk Factors
Abstract
Page 69
OBJECTIVE: The purpose of this study was to investigate the validity of established insulin resistance
indexes, based on fasting blood parameters, in a stable renal transplant population.
RESEARCH DESIGN AND METHODS: Fasting insulin, homeostasis model assessment (HOMA), the
quantitative insulin sensitivity check index (QUICKI), and McAuley's index were assessed for correlation
and agreement with whole-body glucose uptake (M value) divided by prevailing serum insulin
concentrations (I value) assessed during a hyperinsulinemic-euglycemic clamp in 51 stable renal transplant
recipients, who were at a median of 7.5 years after transplant. Multivariate linear regression analyses were
used to determine independent risk factors for insulin resistance.
RESULTS: The M/I value correlated with fasting insulin concentration (r = -0.56), HOMA (r = -0.53),
QUICKI (r = 0.52), and McAuley's index (r = 0.61) (all P < 0.01). Linear regression showed agreement
between all indexes and insulin resistance. However, McAuley's index showed the strongest agreement
irrespective of age, sex, renal allograft function, and obesity. In multivariate analysis, fasting insulin
concentration (beta = -0.59, P = 0.002), fasting triglyceride concentration (beta = -0.33, P = 0.04), and BMI
(beta = -1.22, P = 0.05) were independently associated with the M/I value.
CONCLUSIONS: All investigated insulin resistance indexes were valid estimates of insulin resistance in
the long-term stable renal transplant population. However, correlation and agreement were strongest for
McAuley's index. In addition to fasting insulin and triglyceride concentrations, of which McAuley's index
is composed, only BMI seemed to be independently associated with insulin resistance in this population.
0 (Insulin). 0 (Triglycerides). IY9XDZ35W2 (Glucose).
Publication Type
Journal Article. Randomized Controlled Trial. Research Support, Non-U.S. Gov't. Validation Studies.
Year of Publication
2005

<55>
Unique Identifier
12663584
Title
High incidence of tacrolimus-associated posttransplantation diabetes in the Korean renal allograft
recipients according to American Diabetes Association criteria.
Source
Diabetes Care. 26(4):1123-8, 2003 Apr.
VI 1
Record Owner
Status
MEDLINE
Authors
Cho YM; Park KS; Jung HS; Jeon HJ; Ahn C; Ha J; Kim SJ; Rhee BD; Kim SY; Lee HK.
Authors Full Name
Cho, Young Min; Park, Kyong Soo; Jung, Hye Seung; Jeon, Hyun Jung; Ahn, Curie; Ha, Jongwon; Kim,
Sang Joon; Rhee, Byoung Doo; Kim, Seong Yeon; Lee, Hong Kyu.
Institution
Cho, Young Min. Department of Internal Medicine, Seoul National University College of Medicine,
Seoul, Korea.
Page 70
Adult
Cholesterol/bl [Blood]
Diabetes Mellitus/ci [Chemically Induced]
Female
Follow-Up Studies
Humans
Immunosuppressive Agents/ae [Adverse Effects]
Immunosuppressive Agents/bl [Blood]
Incidence
Insulin/bl [Blood]
Male
Societies, Medical
Tacrolimus/bl [Blood]
Time Factors
United States
Abstract
OBJECTIVE: The incidence of posttransplantation diabetes mellitus (PTDM) has been reported to vary
according to different study populations or different definitions. In this study, using American Diabetes
Association criteria, the incidence and clinical characteristics of PTDM in Korean renal allograft recipients
undergoing tacrolimus-based immunosuppression were examined.
RESEARCH DESIGN AND METHODS: A total of 21 patients taking tacrolimus as primary

immunosuppressant were recruited and tested with a serial 75-g oral glucose tolerance test at 0, 1, 3, and 6
months after renal transplantation.
RESULTS: The cumulative incidence of PTDM was 52.4% at 1 month and 57.1% at 3 and 6 months. The
baseline characteristics of the PTDM group were old age (especially >40 years), a high BMI, a high fasting
glucose level, a high plasma insulin level, and increased insulin resistance. Among these parameters, old
age was the only independent risk factor. The insulin secretory capacity in the PTDM group was maximally
suppressed 3 months after transplantation. Thereafter, it was gradually restored along with dose reduction
of tacrolimus.
CONCLUSIONS: Routine screening for PTDM is necessary in patients over 40 years of age who are
undergoing a relatively higher dose tacrolimus therapy during the early course of postrenal transplantation.
0 (C-Peptide). 0 (Immunosuppressive Agents). 0 (Insulin). 0 (Triglycerides). 97C5T2UQ7J (Cholesterol).
WM0HAQ4WNM (Tacrolimus).
Publication Type
Year of Publication
2003

<56>
Page 71
Unique Identifier
12087044
Title
Insulin resistance after renal transplantation.
Source
Diabetes Care. 25(7):1259-60; author reply 1260-1, 2002 Jul.
VI 1
Record Owner
Status
MEDLINE
Authors
de Vries AP; Bakker SJ.
Authors Full Name
de Vries, Aiko P J; Bakker, Stephan J L.
Comments
Comment on (CON)
Humans
*Insulin Resistance
0 (Blood Glucose).
Publication Type
Comment. Letter.
Year of Publication
2002

<57>
Unique Identifier
11723094
Title
Insulin resistance after renal transplantation: impact of immunosuppressive and antihypertensive therapy.
Source
Diabetes Care. 24(12):2121-6, 2001 Dec.
VI 1
Record Owner
Status
MEDLINE
Authors
Hjelmesaeth J; Midtvedt K; Jenssen T; Hartmann A.
Authors Full Name
Hjelmesaeth, J; Midtvedt, K; Jenssen, T; Hartmann, A.
Institution
Hjelmesaeth, J. Department of Medicine, Vestfold Central Hospital, Tonsberg, Norway. joran@online.no
Page 72
Comments
Comment in (CIN)
Adolescent
Adrenergic beta-Antagonists/tu [Therapeutic Use]
Adult
Aged
Aged, 80 and over
Antihypertensive Agents/tu [Therapeutic Use]
Body Mass Index
Cyclosporine/ad [Administration & Dosage]
Diuretics/tu [Therapeutic Use]
Female
Humans
Hyperinsulinism
Hypertension/dt [Drug Therapy]
Immunosuppressive Agents/ad [Administration & Dosage]
Insulin/bl [Blood]
*Insulin Resistance
Male
Middle Aged
Prednisolone/ad [Administration & Dosage]
Regression Analysis
Abstract
OBJECTIVE: The purpose of the present study was to validate various surrogate estimates of insulin
sensitivity (IS) in a renal transplant population and to assess the influence of immunosuppressive and
antihypertensive therapy on insulin resistance (IR) after renal transplantation.
RESEARCH DESIGN AND METHODS: A total of 167 consecutive renal transplant recipients without
previously known diabetes underwent a 75-g oral glucose tolerance test (OGTT) 3 months after renal
transplantation. A total of 43 patients also underwent a euglycemic-hyperinsulinemic glucose clamp study.
Six OGTT-derived IS indexes were validated against the euglycemic-hyperinsulinemic glucose clamp-
derived IS index (ISI(CLAMP)).
RESULTS: The OGTT-derived ISI(TX) correlated closely with the ISI(CLAMP) (r = 0.58, P < 0.001).
The other surrogate estimates of IS were also significantly but less well correlated with the ISI(CLAMP)
(Spearman's correlation; r = -0.45 to 0.41, P = 0.003-0.050). In the univariate model, BMI, daily
prednisolone dose, creatinine clearance, hypertension, number of antihypertensive agents, and use of
diuretics or beta-blockers were negatively associated with ISI(TX) (P < 0.05). After multiple regression
analysis, BMI (P < 0.001), daily prednisolone dose (P < 0.001), cytomegalovirus infection (P = 0.030), and
triglycerides (P = 0.034) were shown to be independent predictors of posttransplant IR.
CONCLUSIONS: The OGTT-derived ISI(TX) may be a useful estimate of IS in Caucasian renal

transplant recipients. Increasing daily prednisolone dose is an independent predictor of IR after renal
transplantation. Hypertension and the use of beta-blockers and diuretics may also deteriorate IR in this
group of patients.
0 (Adrenergic beta-Antagonists). 0 (Antihypertensive Agents). 0 (Blood Glucose). 0 (Diuretics). 0
(Immunosuppressive Agents). 0 (Insulin). 83HN0GTJ6D (Cyclosporine). 9PHQ9Y1OLM (Prednisolone).
Publication Type
Page 73
Year of Publication
2001

<58>
Unique Identifier
11375342
Title
The effect of systemic versus portal insulin delivery in pancreas transplantation on insulin action and
VLDL metabolism.
Source
Diabetes. 50(6):1402-13, 2001 Jun.
VI 1
Record Owner
Status
MEDLINE
Authors
Carpentier A; Patterson BW; Uffelman KD; Giacca A; Vranic M; Cattral MS; Lewis GF.
Authors Full Name
Carpentier, A; Patterson, B W; Uffelman, K D; Giacca, A; Vranic, M; Cattral, M S; Lewis, G F.
Institution
Carpentier, A. Department of Medicine, University of Toronto, Toronto, Ontario, Canada.
Adult
Apolipoproteins B/bl [Blood]
Fasting/me [Metabolism]
Female
Forecasting
Glucose/ad [Administration & Dosage]
Glucose/pd [Pharmacology]
Humans
*Iliac Vein
Injections, Intravenous
Insulin/bl [Blood]
*Insulin/ph [Physiology]
Kinetics
*Lipoproteins, VLDL/bl [Blood]
Liver/me [Metabolism]
Male
Osmolar Concentration
*Portal System
Abstract
Combined kidney-pancreas transplantation (KPT) with anastomosis of the pancreatic vein to the systemic
circulation (KPT-S) or to the portal circulation (KPT-P) provides a human model in which the chronic
effects of portal versus systemic insulin delivery on glucose and VLDL metabolism can be examined.
Despite similar plasma glucose and C-peptide levels, KPT-S (n = 9) had an approximate twofold elevation
Page 74
of fasting and intravenous glucose-stimulated plasma insulin levels compared with both KPT-P (n = 7) and
healthy control subjects (n = 15). The plasma free fatty acid (FFA) levels were elevated in both transplant
groups versus control subjects, but the plasma insulin elevation necessary to lower plasma FFA by 50%
was approximately two times higher in KPT-S versus KPT-P and control subjects. Endogenous glucose
production was similar in KPT-S and KPT-P, despite approximately 35% higher hepatic insulin levels in
the latter, and was suppressed to a greater extent during a euglycemic-hyperinsulinemic clamp in KPT-S
versus KPT-P. Total-body glucose utilization during the euglycemic-hyperinsulinemic clamp was
approximately 40% lower in KPT-S versus KPT-P, indicating peripheral tissue but not hepatic insulin
resistance in KPT-S versus KPT-P. Both transplant groups had an approximate twofold elevation of
triglyceride (TG)-rich lipoprotein apolipoprotein B (apoB) and lipids versus control subjects. Elevation of
VLDL-apoB and VLDL-TG in both transplant groups was entirely explained by an approximately 50%
reduction in clearance of VLDL compared with healthy control subjects. In the presence of increased FFA
load but in the absence of hepatic overinsulinization and marked hepatic insulin resistance, there was no
elevation of VLDL secretion in KPT-S versus KPT-P and control subjects. These findings suggest that
chronic systemic hyperinsulinemia and peripheral tissue insulin resistance with the consequent elevation of
plasma FFA flux are insufficient per se to cause VLDL overproduction and that additional factors, such as
hepatic hyperinsulinemia and/or gross insulin resistance, may be an essential prerequisite in the
pathogenesis of VLDL overproduction in the common form of the insulin resistance syndrome.
0 (Apolipoproteins B). 0 (Insulin). 0 (Lipoproteins, VLDL). 0 (Triglycerides). IY9XDZ35W2 (Glucose).
Publication Type
Year of Publication
2001

<59>
Unique Identifier
8742568
Title
Continued insulin dependence despite normal range insulin sensitivity and insulin connecting peptide
levels in a kidney/islet transplant patient.
Source
Diabetes Care. 19(3):236-40, 1996 Mar.
VI 1
Record Owner
Status
MEDLINE
Authors
Atkison PR; Zucker P; Hramiak I; Paul TL; Dupre J; Behme MT; Scharp DW; Lacy PE; Olack BJ; Stiller
CR.
Authors Full Name
Atkison, P R; Zucker, P; Hramiak, I; Paul, T L; Dupre, J; Behme, M T; Scharp, D W; Lacy, P E; Olack, B
J; Stiller, C R.
Institution
Atkison, P R. University of Western Ontario, London, Canada.
Adult
*C-Peptide/bl [Blood]
Page 75
*Diabetes Mellitus, Type 1/dt [Drug Therapy]
Female
Follow-Up Studies
Humans
Immunosuppression
Insulin/bl [Blood]
*Insulin/tu [Therapeutic Use]
*Islets of Langerhans Transplantation
Abstract
OBJECTIVE: The majority of islet transplant recipients remain insulin-requiring, although many have
near-normal connecting peptide (CP) levels. Insulin resistance may be one possible cause of the continuing
need for exogenous insulin in islet transplant recipients. To assess this, we have studied the insulin
sensitivity index (S1) in one patient with near-normal CP levels after islet transplant who remained insulin-
requiring.
RESEARCH DESIGN AND METHODS: The islet transplant recipient is a 36-year-old woman with no
residual CP who received a kidney transplant, followed 7 days later by an islet transplant. The islets were
infused into the liver via the umbilical vein. Induction immunosuppression consisted of OKT3, prednisone,
cyclosporin A, and azathioprine, with maintenance on the latter three.
RESULTS: Maximum CP levels after a standardized Sustacal meal were 2.09, 1.18, 0.85, and 0.81 nmol/l
at 1,6,18, and 24 months posttransplant, respectively. Insulin requirements at the same times were 0.27,
0.45, 0.49, and 0.62 U.kg(-1).d(-1), while S1 was 36.3, 53.3, and 13.2 min (-1).nmol(-1).ml at 6,18, and 24
months, respectively. This compares with S1 values of 43.3+/- 10.0 min (-1).nmol(-1).ml for normal
subjects.
CONCLUSIONS: This patient had near-normal S1 and CP levels, but she was unable to discontinue
insulin therapy, suggesting that other factors are critical. Despite this, she maintained normal or near-
normal glycated hemoglobins, indicating metabolic benefit from the islet transplant.
0 (Blood Glucose). 0 (C-Peptide). 0 (Insulin).
Publication Type
Case Reports. Comparative Study. Journal Article.
Year of Publication
1996

<60>
Unique Identifier
2642863
Title
Effects of pancreas transplantation on metabolic and hormonal profiles in IDDM patients.
Source
Diabetes. 38 Suppl 1:88-93, 1989 Jan.
VI 1
Record Owner
Status
Page 76
MEDLINE
Authors
Ostman J; Bolinder J; Gunnarsson R; Brattstrom C; Tyden G; Wahren J; Groth CG.
Authors Full Name
Ostman, J; Bolinder, J; Gunnarsson, R; Brattstrom, C; Tyden, G; Wahren, J; Groth, C G.
Institution
Ostman, J. Department of Medicine, Huddinge Hospital, Karolinska Institute, Stockholm, Sweden.
3-Hydroxybutyric Acid
Adult
Circadian Rhythm
*Diabetes Mellitus, Type 1/bl [Blood]
Female
*Hormones/bl [Blood]
Humans
Hydroxybutyrates/bl [Blood]
Insulin Resistance
Male
Urea/bl [Blood]
Abstract
The diurnal patterns of relevant metabolites and hormones in five pancreas-kidney-transplanted patients
(aged 36 +/- 2 yr, mean +/- SD) with insulin-dependent diabetes mellitus (IDDM) were compared with
those in five kidney-transplanted nondiabetic patients (aged 28 +/- 2 yr). The groups were matched for
body mass and current dose and type of immunosuppressive treatment. The serum creatinine levels did not
differ between the two study groups, but the serum urea level in the nondiabetic patients was slightly but
significantly higher than in the diabetic patients. In the pancreas-kidney-transplanted group the
investigation was performed 8-47 mo posttransplantation; in the kidney-transplanted nondiabetic patients,
12-18 mo posttransplantation. The mean 24-h levels and rhythms of blood glucose, free fatty acid, 3-
hydroxybutyrate, and alanine did not differ between the groups. The mean 24-h levels of blood lactate and
glycerol were moderately but significantly higher in the pancreas-kidney-transplanted diabetic patients. At
fasting, the level of serum immunoreactive insulin was more than twice as high in the pancreas-kidney-
transplanted patients, whereas the plasma C-peptide levels did not differ significantly between the two
groups. The meal-induced increases in serum insulin as well as in the plasma C-peptide levels were more
marked in the pancreas-kidney-transplanted patients. The findings suggest that the hyperinsulinemia in
these patients was due to both the systemic delivery of insulin and an increase in insulin resistance, the
latter being particularly apparent in the postprandial phase.(ABSTRACT TRUNCATED AT 250 WORDS)
0 (Blood Glucose). 0 (Fatty Acids, Nonesterified). 0 (Hormones). 0 (Hydroxybutyrates). 8W8T17847W
(Urea). AYI8EX34EU (Creatinine). TZP1275679 (3-Hydroxybutyric Acid).
Publication Type
Year of Publication
1989

Page 77
<61>
Unique Identifier
10344369
Title
Polycystic kidney disease as a risk factor for post-transplant diabetes mellitus.
Source
Nephrology Dialysis Transplantation. 14(5):1244-6, 1999 May.
VI 1
Record Owner
Status
MEDLINE
Authors
Ducloux D; Motte G; Vautrin P; Bresson-Vautrin C; Rebibou JM; Chalopin JM.
Authors Full Name
Ducloux, D; Motte, G; Vautrin, P; Bresson-Vautrin, C; Rebibou, J M; Chalopin, J M.
Institution
Ducloux, D. Department of Nephrology and Renal Transplantation, Hopital Saint Jacques, Besancon,
France.
Adult
Female
Humans
Insulin Resistance
Kidney Failure, Chronic/et [Etiology]
Male
Middle Aged
*Polycystic Kidney, Autosomal Dominant/co [Complications]
*Polycystic Kidney, Autosomal Dominant/su [Surgery]
Risk Factors
Abstract
BACKGROUND: Insulin resistance with compensatory hyperinsulinaemia has been reported in adult
polycystic kidney disease (APKD) patients. Diabetes mellitus is a common complication following
transplantation and previous studies have demonstrated that inadequate insulin secretion was a prerequisite
for the development of post-transplant diabetes mellitus (PTDM). We conducted a retrospective study to
determine whether APKD is a risk factor for PTDM.
METHODS: Twenty-six consecutive patients transplanted because of end-stage renal disease due to
APKD were studied. A control patient matched for age, gender, immunosuppressive therapy and transplant
year was selected for each APKD patient. PTDM was defined by fasting glycaemia exceeding 7.8 mmol/l
and the need for insulin or oral antidiabetic therapy.
RESULTS: Age, renal function, immunosuppressive regimen, number of acute rejection, cumulative dose
of steroids and haemodialysis duration before transplantation were similar in both groups. PTDM occured
in 10 APKD patients and four controls (34.6% vs 15.3%; P < 0.005). Among diabetic patients, six APKD
patients and two controls required insulin therapy (60% vs 50%; P = n.s.). Diabetic patients were
significantly older (55.8 +/- 7 years vs 50.2 +/- 11 years; P < 0.05).
CONCLUSION: Although retrospective, this study suggests that APKD confers an increased risk of
PTDM.
Publication Type
Page 78
Journal Article.
Year of Publication
1999

<62>
Unique Identifier
10069196
Title
Leptin in CAPD patients: serum concentrations and peritoneal loss.
Source
Nephrology Dialysis Transplantation. 14(2):400-5, 1999 Feb.
VI 1
Record Owner
Status
MEDLINE
Authors
Kagan A; Haran N; Leschinsky L; Shuali N; Rapoport J.
Authors Full Name
Kagan, A; Haran, N; Leschinsky, L; Shuali, N; Rapoport, J.
Institution
Kagan, A. Department of Nephrology and Hypertension, Kaplan Medical Center, Rehovot, Israel.
Adult
*Ascitic Fluid/ch [Chemistry]
Body Mass Index
Female
Humans
Leptin
Male
Middle Aged
*Peritoneal Dialysis, Continuous Ambulatory
Postoperative Period
*Proteins/an [Analysis]
Reference Values
Renal Dialysis
Abstract
BACKGROUND: To determine whether serum leptin concentrations in patients undergoing continuous
ambulatory peritoneal dialysis (CAPD) are influenced by peritoneal loss of leptin and to compare serum
leptin levels of normal subjects with those of patients receiving renal replacement therapy such as
haemodialysis (HD), CAPD, or kidney transplantation.
SUBJECTS AND METHODS: Eighty-four individuals were investigated: six females and 14 males on
standard CAPD; 13 females and 13 males on chronic HD; 10 female and eight male kidney transplant
recipients, and 10 female and 10 male subjects as controls. Morning serum, 8-h and 24-h samples of
peritoneal fluid concentrated to 6-20-fold by Centricon 3 (cutoff 3000 daltons), and 24-h urinary
concentrations of leptin were measured with commercial RIA (Linco Research, Inc., USA). Venous blood
Page 79
and peritoneal fluid samples of albumin, beta2-microglobulin, glucose, urea, and creatinine were
determined by standard laboratory techniques. Serum insulin levels were measured by radioimmunoassay.
RESULTS: Patients (men and women) on CAPD and after kidney transplantation exhibited significantly
higher serum concentrations of leptin and leptin/BMI ratios than control subjects. These increased values
did not reach statistical significance in HD patients. Serum leptin concentrations were correlated very
significantly with BMI in all cases (r=0.380, P<0.001). Moreover, in CAPD patients (r=0.630, P<0.007)
and in HD patients (r=0.668, P<0.005), but not in kidney transplant recipients or control subjects,
significant correlations were observed between serum leptin and insulin concentrations. Residual renal
function (RRF) in the range 0-12.8 ml/min and serum beta2-microglobulin levels in the range 7.9-47.1 mg/l
did not influence serum leptin levels in CAPD and HD patients. As expected, leptin was detected in the
peritoneal fluid of CAPD patients. Twenty-four-hour peritoneal loss (30.95+/-21.05 ng/min) and 24-h
peritoneal clearance (0.01+/-0.01 ml/kg/min) of leptin account for only 3.9% of estimated whole-body
leptin production rate and 0.7% of leptin clearance from plasma respectively. Twenty-four-hour urinary
losses of leptin in CAPD patients were negligible, accounting for 5.6+/-1.8% (range 0.3-15.2%) of total
(peritoneal and urinary) loss of this hormone.
CONCLUSIONS: These findings suggest that serum leptin levels are not affected by continuous
peritoneal loss of leptin during CAPD and that insulin resistance and hyperinsulinaemia contribute to
elevated serum leptin concentrations in CAPD and HD patients. The aetiology of increased serum leptin
levels in kidney transplant recipients is probably different from that in dialysis patients.
0 (Leptin). 0 (Proteins).
Publication Type
Year of Publication
1999

<63>
Unique Identifier
9509457
Title
Insulin resistance is a common denominator of post-transplant diabetes mellitus and impaired glucose
tolerance in renal transplant recipients.
Source
VI 1
Record Owner
Status
MEDLINE
Authors
Midtvedt K; Hartmann A; Hjelmesaeth J; Lund K; Bjerkely BL.
Authors Full Name
Midtvedt, K; Hartmann, A; Hjelmesaeth, J; Lund, K; Bjerkely, B L.
Institution
Midtvedt, K. Department of Internal Medicine, National Hospital, University of Oslo, Norway.
Adult
*Diabetes Mellitus/pp [Physiopathology]
Page 80
Female
*Glucose Intolerance
Humans
Insulin/bl [Blood]
*Insulin Resistance
Male
Middle Aged
Reference Values
Abstract
BACKGROUND: Post-transplant diabetes mellitus is a known complication of steroid therapy in renal
transplant recipients. Both insulin resistance and insulin deficiency have been shown to be necessary for
development of post-transplant diabetes mellitus. It is not known whether recipients with impaired glucose
tolerance have similar degree of insulin resistance or deficient insulin response as recipients with post-
transplant diabetes mellitus.
METHOD: To address this question, we used an oral glucose tolerance test to categorize 46 renal
transplant recipients on triple immunosuppressive medication to groups with normal glucose tolerance,
impaired glucose tolerance or post-transplant diabetes mellitus. Insulin sensitivity was measured using a
hyperinsulinaemic euglycaemic clamp. Insulin response was calculated from the increase in serum insulin
concentration during the oral glucose tolerance test.
RESULTS: Twenty-five were categorized to normal glucose tolerance, 15 to impaired glucose tolerance
and six to post-transplant diabetes mellitus. There were no statistically significant differences between the
groups regarding prednisolone dose, azathioprine dose, use of beta-blocker, age, gender, weight, waist-hip
ratio, body mass index, donor source, smoking habits, or first-degree relatives with histories of diabetes
mellitus. The impaired glucose tolerance and post-transplant diabetes mellitus groups showed a significant
reduction in insulin-stimulated glucose disposal rate (mg/kg.min) compared to the normal glucose tolerance
group (4.6 +/- 1.6 and 3.4 +/- 1.3 respectively vs 7.1 +/- 2.4, P < 0.05). The insulin response (picomol/l)
was not different between the normal glucose tolerance and impaired glucose tolerance groups but was
significantly reduced in the post-transplant diabetes mellitus group (448 +/- 310 and 450 +/- 291
respectively vs 170 +/- 128, P < 0.05).
CONCLUSION: Insulin resistance is a common denominator of post-transplant diabetes mellitus and

impaired glucose tolerance in renal transplant recipients.
0 (Insulin).
Publication Type
Journal Article.
Year of Publication
1998

<64>
Unique Identifier
9132657
Page 81
Title
Transient diabetes mellitus and peripheral insulin resistance following Tacrolimus intoxication in a child
after renal transplantation.
Source
VI 1
Record Owner
Status
MEDLINE
Authors
Filler G; Amendt P; von Bredow MA; Ehrich JH.
Authors Full Name
Filler, G; Amendt, P; von Bredow, M A; Ehrich, J H.
Institution
Filler, G. Department of Paediatric Nephrology, Charite Children's Hospital, Humboldt University, Berlin,
Germany.
Adolescent
C-Peptide/an [Analysis]
*Diabetes Mellitus/ci [Chemically Induced]
Female
Humans
*Immunosuppressive Agents/po [Poisoning]
*Insulin Resistance
*Tacrolimus/po [Poisoning]
0 (C-Peptide). 0 (Immunosuppressive Agents). WM0HAQ4WNM (Tacrolimus).
Publication Type
Year of Publication
1997

<65>
Unique Identifier
20724958
Title
Association of metabolic syndrome with development of new-onset diabetes after transplantation.
Source
Transplantation. 90(8):861-6, 2010 Oct 27.
VI 1
Record Owner
Status
MEDLINE
Authors
Bayer ND; Cochetti PT; Anil Kumar MS; Teal V; Huan Y; Doria C; Bloom RD; Rosas SE.
Authors Full Name
Page 82
Bayer, Nathaniel D; Cochetti, Philip T; Anil Kumar, Mysore S; Teal, Valerie; Huan, Yonghong; Doria,
Cataldo; Bloom, Roy D; Rosas, Sylvia E.
Institution
Bayer, Nathaniel D. Department of Medicine, University of Pennsylvania, Philadelphia, PA, USA.
Comments
Comment in (CIN)
Comment in (CIN)
Fasting
Female
Humans
Male
*Metabolic Syndrome/et [Etiology]
Middle Aged
Polycystic Kidney Diseases/ep [Epidemiology]
Prevalence
Regression Analysis
Abstract
BACKGROUND: New-onset diabetes after transplantation (NODAT) is a major posttransplant
complication associated with lower allograft and recipient survival. Our objective was to determine
whether metabolic syndrome pretransplant is independently associated with NODAT development.
METHODS: We recruited 640 consecutive incident nondiabetic renal transplant recipients from three
academic centers between 1999 and 2004. NODAT was defined as the use of hypoglycemic medication, a
random plasma glucose level more than 200 mg/dL, or two fasting glucose levels more than or equal to 126
mg/dL beyond 30 days posttransplant.
RESULTS: Metabolic syndrome was common pretransplant (57.2%). NODAT developed in 31.4% of
recipients 1 year posttransplant. Participants with metabolic syndrome were more likely to develop
NODAT compared with recipients without metabolic syndrome (34.4% vs. 27.4%, P=0.057). Recipients
with increasing number of positive metabolic syndrome components were more likely to develop NODAT
(metabolic syndrome score prevalence at 1 year: 0 components-0.0%, 1-24.2%, 2-29.3%, 3-31.0%, 4-
34.8%, and 5-73.7%, P=0.001). After adjustment for demographics, age by decade (hazard ratio [HR] 1.34
[1.20-1.50], P<0.0001), African American race (HR 1.35 [1.01-1.82], P=0.043), cumulative prednisone
dosage (HR 1.18 [1.07-1.30], P=0.001), and metabolic syndrome (HR 1.34 [1.00-1.79], P=0.047) were
independent predictors of development of NODAT at 1 year posttransplant. In a multivariable analysis
incorporating the individual metabolic syndrome components themselves as covariates, the only
pretransplant metabolic syndrome component to remain an independent predictor of NODAT was low
high-density lipoprotein (hazard ratio [HR] 1.37 [1.01-1.85], P=0.042).
CONCLUSIONS: Metabolic syndrome is an independent predictor for NODAT and is a possible target
for intervention to prevent NODAT. Future studies to evaluate whether modification of metabolic
syndrome factors pretransplant reduces NODAT development are needed.
0 (Blood Glucose). 0 (Immunosuppressive Agents). WM0HAQ4WNM (Tacrolimus).
Publication Type
Journal Article. Research Support, N.I.H., Extramural. Research Support, U.S. Gov't, Non-P.H.S..
Page 83
Year of Publication
2010

<66>
Unique Identifier
18791455
Title
Metabolic syndrome and coronary artery calcification in renal transplant recipients.
Source
Transplantation. 86(5):728-32, 2008 Sep 15.
VI 1
Record Owner
Status
MEDLINE
Authors
Adeseun GA; Rivera ME; Thota S; Joffe M; Rosas SE.
Authors Full Name
Adeseun, Gbemisola A; Rivera, Maria E; Thota, Subhashini; Joffe, Marshall; Rosas, Sylvia E.
Institution
Adeseun, Gbemisola A. Renal, Electrolyte, and Hypertension Division, Department of Medicine,
University of Pennsylvania, Philadelphia, PA, USA.
Adult
Body Mass Index
Calcinosis/bl [Blood]
Calcinosis/co [Complications]
*Calcinosis/ep [Epidemiology]
Coronary Disease/bl [Blood]
Coronary Disease/co [Complications]
*Coronary Disease/ep [Epidemiology]
Humans
Lipids/bl [Blood]
Metabolic Syndrome/co [Complications]
Obesity/ep [Epidemiology]
Prevalence
Abstract
BACKGROUND: Coronary artery calcification (CAC) and metabolic syndrome (MS) have been
associated with increased cardiovascular risk. The study objective was to examine the association of MS
with CAC presence and progression in renal transplant recipients.
METHODS: We measured the CAC progression in asymptomatic recipients who had no prior history of
coronary artery disease.
Page 84
RESULTS: MS was common (55.4%). Median CAC scores were 0, 33.1, 98, and 261.9 for patients with
one, two, three, and four or more positive components of the MS, respectively. Severe CAC scores were
more common in recipients with MS (P=0.04). Although recipients with MS had higher mean CAC scores
at baseline and significant CAC progression (483 [590.6] vs. 619 [813.8], P=0.01), MS was not an
independent predictor of annualized rate of CAC change in a multivariate model.
CONCLUSION: Future studies to evaluate if MS treatment improves cardiovascular outcomes are

imperative.
0 (Lipids). 0 (Triglycerides).
Publication Type
Journal Article. Research Support, N.I.H., Extramural. Research Support, Non-U.S. Gov't.
Year of Publication
2008

<67>
Unique Identifier
26093730
Title
Relationships Between Metabolic Syndrome, Microalbuminuria, and C-Reactive Protein in Turkish
Kidney Transplant Recipients.
Source
Transplantation Proceedings. 47(5):1408-12, 2015 Jun.
VI 1
Record Owner
Status
MEDLINE
Authors
Sipahioglu MH; Unal A; Yazgac H; Tunca O; Arikan T; Kocyigit I; Tokgoz B; Oymak O.
Authors Full Name
Sipahioglu, M H; Unal, A; Yazgac, H; Tunca, O; Arikan, T; Kocyigit, I; Tokgoz, B; Oymak, O.
Institution
Sipahioglu, M H. Department of Nephrology, Erciyes University Medical Faculty, Kayseri, Turkey.
Electronic address: murathsipahioglu@yahoo.com.
Unal, A. Department of Nephrology, Erciyes University Medical Faculty, Kayseri, Turkey.
Yazgac, H. Department of Internal Medicine, Erciyes University Medical Faculty, Kayseri, Turkey.
Tunca, O. Department of Nephrology, Erciyes University Medical Faculty, Kayseri, Turkey.
Arikan, T. Department of Nephrology, Erciyes University Medical Faculty, Kayseri, Turkey.
Kocyigit, I. Department of Nephrology, Erciyes University Medical Faculty, Kayseri, Turkey.
Tokgoz, B. Department of Nephrology, Erciyes University Medical Faculty, Kayseri, Turkey.
Oymak, O. Department of Nephrology, Erciyes University Medical Faculty, Kayseri, Turkey.
Adult
Albuminuria/bl [Blood]
*Albuminuria/ep [Epidemiology]
Blood Pressure
*C-Reactive Protein/me [Metabolism]
Cardiovascular Diseases/et [Etiology]
Page 85
Fasting/bl [Blood]
Female
Humans
Logistic Models
Male
Metabolic Syndrome/ur [Urine]
Middle Aged
Odds Ratio
Prevalence
Risk Factors
Turkey/ep [Epidemiology]
Abstract
AIM: The aims of this study were to report the prevalence of metabolic syndrome (MS) in a cohort of
Turkish kidney transplant recipients and to define the relationships between MS, microalbuminuria and C-
reactive protein (CRP), which are cardiovascular risk factors, in kidney transplant setting.
METHODS: This cross sectional study included 170 adult renal transplantation recipients with a mean
follow-up of 53.1 +/- 49.9 months. The diagnosis of MS was made according to the National Cholesterol
Education Program-Adult Treatment Panel III (NCEP-ATP III) criteria. Microalbuminuria was defined as a
urinary albumin/creatinine ratio of 30-300 mg/g. CRP levels >=6.0 were classified as high CRP.
RESULTS: Mean age was 39.3 +/- 11 years. The prevalence of MS was 45.8% (n = 78). The prevalence
of microalbuminuria was not different in patients with MS compared to those without MS (39.7% vs 37%,
P = .428). In multivariate logistic regression analyses, systolic blood pressure (SBP) (odds ratio 1.68; 95%
confidence interval [CI] 1.12-2.52; P = .011) and high fasting glucose (odds ratio 2.82; 95% confidence
interval [CI] 1.16-6.86; P = .022) were significantly associated with microalbuminuria. When patients with
MS and high CRP were compared with patients with normal CRP and without MS, microalbuminuria did
not differ between the groups (P = .213).
CONCLUSION: The prevalence of MS in our kidney recipient cohort was found to be increased
compared to general population. MS was not related to increased prevalence of microalbuminuria, even
when combined with high CRP. Microalbuminuria was associated with elevated SBP and hyperglycemic
status. Copyright © 2015 Elsevier Inc. All rights reserved.
0 (Blood Glucose). 9007-41-4 (C-Reactive Protein).
Publication Type
Journal Article.
Year of Publication
2015

<68>
Unique Identifier
26735686
Title
Conversion from Tacrolimus to Cyclosporine A Improves Glucose Tolerance in HCV-Positive Renal
Transplant Recipients.
Page 86
Source
PLoS ONE [Electronic Resource]. 11(1):e0145319, 2016.
VI 1
Record Owner
Status
MEDLINE
Authors
Handisurya A; Kerscher C; Tura A; Herkner H; Payer BA; Mandorfer M; Werzowa J; Winnicki W;
Reiberger T; Kautzky-Willer A; Pacini G; Saemann M; Schmidt A.
Authors Full Name
Handisurya, Ammon; Kerscher, Corinna; Tura, Andrea; Herkner, Harald; Payer, Berit Anna; Mandorfer,
Mattias; Werzowa, Johannes; Winnicki, Wolfgang; Reiberger, Thomas; Kautzky-Willer, Alexandra;
Pacini, Giovanni; Saemann, Marcus; Schmidt, Alice.
Institution
Handisurya, Ammon. Department of Internal Medicine III, Division of Nephrology and Dialysis, Medical
University of Vienna, Vienna, Austria.
Kerscher, Corinna. Department of Internal Medicine III, Division of Nephrology and Dialysis, Medical
Tura, Andrea. Institute of Neurosciences, CNR, Padova, Italy.
Herkner, Harald. Department of Emergency Medicine, Medical University of Vienna, Vienna, Austria.
Payer, Berit Anna. Department of Internal Medicine III, Division of Gastroenterology and Hepatology,
Medical University of Vienna, Vienna, Austria.
Mandorfer, Mattias. Department of Internal Medicine III, Division of Gastroenterology and Hepatology,
Werzowa, Johannes. Department of Internal Medicine III, Division of Nephrology and Dialysis, Medical
Winnicki, Wolfgang. Department of Internal Medicine III, Division of Nephrology and Dialysis, Medical
Reiberger, Thomas. Department of Internal Medicine III, Division of Gastroenterology and Hepatology,
Kautzky-Willer, Alexandra. Department of Internal Medicine III, Division of Endocrinology and
Metabolism, Medical University of Vienna, Vienna, Austria.
Pacini, Giovanni. Institute of Neurosciences, CNR, Padova, Italy.
Saemann, Marcus. Department of Internal Medicine III, Division of Nephrology and Dialysis, Medical
Schmidt, Alice. Department of Internal Medicine III, Division of Nephrology and Dialysis, Medical
Adult
Diabetes Mellitus, Type 2/et [Etiology]
*Graft Rejection/pc [Prevention & Control]
Hepatitis C/co [Complications]
*Hepatitis C/dt [Drug Therapy]
Hepatitis C/ge [Genetics]
*Hepatitis C/pa [Pathology]
Humans
Insulin Resistance
Liver/pp [Physiopathology]
Page 87
Middle Aged
Prospective Studies
RNA, Viral/an [Analysis]
Risk Factors
Abstract
BACKGROUND: Calcineurin-inhibitors and hepatitis C virus (HCV) infection increase the risk of post-
transplant diabetes mellitus. Chronic HCV infection promotes insulin resistance rather than beta-cell
dysfunction. The objective was to elucidate whether a conversion from tacrolimus to cyclosporine A affects
fasting and/or dynamic insulin sensitivity, insulin secretion or all in HCV-positive renal transplant
recipients.
METHODS: In this prospective, single-center study 10 HCV-positive renal transplant recipients

underwent 2h-75g-oral glucose tolerance tests before and three months after the conversion of
immunosuppression from tacrolimus to cyclosporine A. Established oral glucose tolerance test-based
parameters of fasting and dynamic insulin sensitivity and insulin secretion were calculated. Data are
expressed as median (IQR).
RESULTS: After conversion, both fasting and challenged glucose levels decreased significantly. This
was mainly attributable to a significant amelioration of post-prandial dynamic glucose sensitivity as
measured by the oral glucose sensitivity-index OGIS [422.17 (370.82-441.92) vs. 468.80 (414.27-488.57)
mL/min/m2, p = 0.005), which also resulted in significant improvements of the disposition index (p =
0.017) and adaptation index (p = 0.017) as markers of overall glucose tolerance and beta-cell function.
Fasting insulin sensitivity (p = 0.721), insulinogenic index as marker of first-phase insulin secretion [0.064
(0.032-0.106) vs. 0.083 (0.054-0.144) nmol/mmol, p = 0.093) and hepatic insulin extraction (p = 0.646)
remained unaltered. No changes of plasma HCV-RNA levels (p = 0.285) or liver stiffness (hepatic fibrosis
and necroinflammation, p = 0.463) were observed after the conversion of immunosuppression.
CONCLUSIONS: HCV-positive renal transplant recipients show significantly improved glucose-

stimulated insulin sensitivity and overall glucose tolerance after conversion from tacrolimus to
cyclosporine A. Considering the HCV-induced insulin resistance, HCV-positive renal transplant recipients
may benefit from a cyclosporine A-based immunosuppressive regimen.
TRIAL REGISTRATION: ClinicalTrials.gov NCT02108301.

0 (Blood Glucose). 0 (Immunosuppressive Agents). 0 (Insulin). 0 (RNA, Viral). 83HN0GTJ6D
(Cyclosporine). WM0HAQ4WNM (Tacrolimus).
Publication Type
Clinical Trial. Journal Article.
Year of Publication
2016

<69>
Unique Identifier
30450927
Title
[Diabetology and solid organ transplantation]. [Review] [Hungarian]
Original Title
Diabetologia es szervatultetes.
Page 88
Source
Orvosi Hetilap. 159(46):1930-1939, 2018 11.
VI 1
Record Owner
Status
MEDLINE
Authors
Wagner L; Wittmann I; Piros L; P Szabo R; Szakaly P.
Authors Full Name
Wagner, Laszlo; Wittmann, Istvan; Piros, Laszlo; P Szabo, Reka; Szakaly, Peter.
Institution
Wagner, Laszlo. Transzplantacios es Sebeszeti Klinika, Semmelweis Egyetem, Altalanos Orvostudomanyi
Kar Budapest, Baross u. 23., 1082.
Wittmann, Istvan. II. Belgyogyaszati Klinika es Nephrologiai Centrum, Pecsi Tudomanyegyetem,
Altalanos Orvostudomanyi Kar, Klinikai Kozpont Pecs.
Piros, Laszlo. Transzplantacios es Sebeszeti Klinika, Semmelweis Egyetem, Altalanos Orvostudomanyi
Kar Budapest, Baross u. 23., 1082.
P Szabo, Reka. Klinikai Kozpont, Sebeszeti Intezet, Szervtranszplantacios Nem Onallo Tanszek,
Debreceni Egyetem, Altalanos Orvostudomanyi Kar Debrecen.
Szakaly, Peter. Sebeszeti Klinika, Pecsi Tudomanyegyetem, Altalanos Orvostudomanyi Kar, Klinikai
Kozpont Pecs.
Diabetic Nephropathies/pp [Physiopathology]
Humans
Kidney Failure, Chronic/et [Etiology]
*Kidney Failure, Chronic/su [Surgery]
Kidney Transplantation/sn [Statistics & Numerical Data]
Living Donors
Pancreas Transplantation/sn [Statistics & Numerical Data]
Peripheral Vascular Diseases/et [Etiology]
Peripheral Vascular Diseases/su [Surgery]
Keyword Heading
*diabetes mellitus
*hasnyalmirigy-atultetes
*kidney transplantation
*pancreas transplantation
*posttransplantation diabetes mellitus
*poszttranszplantacios diabetes mellitus
*veseatultetes
Abstract
Diabetes increases the risk of different kidney diseases. The most important is diabetic nephropathy,
however, ischemic kidney disease, chronic pyleonephritis and papilla necrosis may also develop. The
prognosis of diabetic nephropathy has improved recently, however, it is still the primary cause of dialysis
and transplantation. Cardiovascular diseases predict mostly mortality in diabetic patients, however,
cerebrovascular insults and peripheral obstructive arterial diseases necessitating lower limb amputations are
also important. Diabetic retinopathy is almost always present with diabetic nephropathy. Diabetic
neuropathy may also develop, furthermore vascular complications often combine. All these urge complex
workup, follow-up and early treatment. If transplantation is indicated, preemptive operation should be
preferred, and living donation shows the best outcomes. Different forms of carbohydrate disorder may
occur after transplantation: new-onset diabetes or diabetes known before transplantation may progress.
Renal transplantation with pancreas transplantation may be indicated in type 1 diabetes with end-stage
diabetic nephropathy, most often simultaneously. This may result in normoglycemia and insulin-
independence and the progression of other complications may also halt. Transplant associated
Page 89
hyperglycemia occurs in most of the patients early, however, it is often transitory. Despite stabilization of
the patient and of the immunosuppressive therapy, about one third of the patients may develop
posttransplant diabetes. Insulin secretion disorder is the primary cause, but insulin resistance is also needed.
Insulin administration may help, however, other antidiabetics can also be useful. Carbohydrate metabolism
should be checked in both cadaveric and living donors. The authors make an attempt to summarize the
above conditions with Hungarian relevance as well. Orv Hetil. 2018; 159(46): 1930-1939.
Other Abstract
Publisher: Absztrakt: A cukorbetegseg szamos vesebetegseg kockazatat noveli. A legjelentosebb a
diabeteses nephropathia, de ischaemias vesebetegseget, kronikus pyelonephritist es papillanecrosist is
okozhat. A diabeteses nephropathia prognozisa a ma alkalmazott kezeles mellett sokat javult, ennek
ellenere meg az egyik leggyakoribb oka a dializisnek es a veseatultetesnek. A diabetes tovabbi
szovodmenyei kozul elsosorban a cardiovascularis betegsegek hatarozzak meg a mortalitast, de a
cerebrovascularis esemenyek es az also vegtagi amputaciot igenylo obstruktiv veroerbetegseg is
megemlitendo. A diabeteses retinopathia szinte mindig fennall diabeteses nephropathia eseten, de a
neuropathia is gyakori, illetve az erkarosodasok gyakran kombinaltan allnak fenn. Ezek miatt a betegek
komplex kivizsgalast, kovetest es korai kezelest igenyelnek. Ha transzplantacio indokolt, akkor erdemesebb
azt preemptiv modon vegezni, illetve a legjobb eredmenyek az elodonoros veseatultetestol varhatok. A
szenhidrathaztartas zavaranak kulonbozo formaival talalkozhatunk transzplantacio kapcsan: uj keletu
poszttranszplantacios diabetes alakulhat ki, de a recipiens diabetese is progredialhat transzplantaciot
kovetoen. A veseatultetes mellett hasnyalmirigy-atultetesre 1-es tipusu diabetes okozta vegstadiumu
veseelegtelensegben kerulhet sor, a leggyakrabban szimultan modon, mely normoglykaemiat es
inzulinindependenciat is eredmenyezhet, illetve a diabetes tobb masodlagos szovodmenyenek progresszioja
is megallhat. A szervatultetest kozvetlenul koveto nehany hetben a betegek jelentos reszeben
transzplantaciohoz asszocialt hyperglykaemia alakul ki, ennek oka sokszor atmeneti, azonban az
immunszuppressziv kezeles es a beteg allapotanak stabilizalodasa ellenere a betegek akar harmadanal
megmaradhat. Patogeneziseben elsosorban inzulinszekrecios zavar jatszik szerepet, de kifejlodesehez
inzulinrezisztencia is kell. Megelozeseben es kezeleseben elsosorban inzulinkezeles segithet, de mas
antidiabetikumok is szoba johetnek. Mind a kadaver, mind a vese-elodonorok eseten fontos a szenhidrat-
anyagcsere felmerese. A szerzok a fenti allapotok magyar vonatkozasairol is beszamolnak
osszefoglalojukban. Orv Hetil. 2018; 159(46): 1930-1939.; Language: Hungarian
Publication Type
Year of Publication
2018

<70>
Unique Identifier
28838898
Title
Protocol for a pilot randomised controlled trial of metformin in pre-diabetes after kidney transplantation:
the Transplantation and Diabetes (Transdiab) study.
Source
BMJ Open. 7(8):e016813, 2017 Aug 23.
VI 1
Record Owner
Status
MEDLINE
Authors
Alnasrallah B; Pilmore H; Manley P.
Page 90
Author NameID
Alnasrallah, Basil; ORCID: http://orcid.org/0000-0003-1973-0030
Authors Full Name
Alnasrallah, Basil; Pilmore, Helen; Manley, Paul.
Institution
Alnasrallah, Basil. Department of Nephrology, Auckland City Hospital, Auckland, New Zealand.
Pilmore, Helen. Department of Nephrology, Auckland City Hospital, Auckland, New Zealand.
Pilmore, Helen. Department of Medicine, University of Auckland, Auckland, New Zealand.
Manley, Paul. Department of Nephrology, Auckland City Hospital, Auckland, New Zealand.
Blood Glucose/de [Drug Effects]
Glucose Intolerance/dt [Drug Therapy]
Humans
*Hypoglycemic Agents/ad [Administration & Dosage]
Insulin Resistance
Linear Models
*Metformin/ad [Administration & Dosage]
New Zealand
Pilot Projects
Postoperative Complications/dt [Drug Therapy]
*Postoperative Complications/pc [Prevention & Control]
*Prediabetic State/pc [Prevention & Control]
Research Design
Keyword Heading
NODAT
PTDM
metformin
prevention
randomised-controlled trial
Abstract
INTRODUCTION: Post-transplant diabetes mellitus (PTDM) is a common complication of kidney
transplantation and is associated with significant morbidity and mortality. In the general population,
metformin has been used for diabetes prevention in high-risk individuals. Improving insulin sensitivity is
one of many proven favourable effects of metformin. Despite the high incidence of PTDM in kidney
transplant recipients, there is a lack of evidence for the role of metformin in the prevention of diabetes in
this setting. METHODS AND ANALYSIS: Transplantation and Diabetes (Transdiab) is a single-centre,
unblinded, pilot randomised controlled trial assessing the feasibility, tolerability and efficacy of metformin
after renal transplantation in patients with impaired glucose tolerance (IGT). Participants will undergo an
oral glucose tolerance test in the 4-12 weeks post-transplantation; those with IGT will be randomised to
standard care or standard care and metformin 500 mg twice daily, and followed up for 12 months. The
primary outcomes of the study will be the feasibility of recruitment, the tolerability of metformin assessed
using the Gastrointestinal Symptom Rating Scale at 3 and 12 months, and the efficacy of metformin
assessed by morning glucose and glycated haemoglobin at 3, 6, 9 and 12 months.
ETHICS AND DISSEMINATION: Despite the significant morbidity and mortality of PTDM, there are
currently no randomised clinical trials assessing pharmacological interventions for its prevention after
kidney transplantation. The Transdiab trial will thus provide important data on the feasibility, safety,
tolerability and efficacy of metformin after renal transplantation in patients with IGT; this will facilitate
undertaking larger multicentre trials of interventions to reduce the incidence or severity of diabetes after
kidney transplantation. This study has been approved by the Northern B Health and Disability Ethics
Page 91
Committee of the Ministry of Health in New Zealand. On study completion, results are expected to be
published in a peer-reviewed journal.
TRIAL REGISTRATION NUMBER: Australian New Zealand Clinical Trials Registry Number:
ACTRN12614001171606. Copyright © Article author(s) (or their employer(s) unless otherwise stated in
the text of the article) 2017. All rights reserved. No commercial use is permitted unless otherwise expressly
granted.
0 (Blood Glucose). 0 (Glycated Hemoglobin A). 0 (Hypoglycemic Agents). 9100L32L2N (Metformin).
Publication Type
Journal Article. Randomized Controlled Trial.
Year of Publication
2017

<71>
Unique Identifier
21116317
Title
Metabolic syndrome, insulin resistance, and chronic allograft dysfunction. [Review]
Source
Kidney International - Supplement. (119)S42-6, 2010 Dec.
VI 1
Record Owner
Status
MEDLINE
Authors
Porrini E; Delgado P; Torres A.
Authors Full Name
Porrini, Esteban; Delgado, Patricia; Torres, Armando.
Institution
Porrini, Esteban. Nephrology Section and Research Unit, Hospital Universitario de Canarias, University
of La Laguna, Tenerife, Canary Islands, Spain.
Animals
Chronic Disease
*Graft Rejection/et [Etiology]
Graft Rejection/pp [Physiopathology]
Humans
*Insulin Resistance
*Kidney/pp [Physiopathology]
*Kidney Diseases/et [Etiology]
Kidney Diseases/pp [Physiopathology]
*Metabolic Syndrome/et [Etiology]
Risk Assessment
Risk Factors
Treatment Outcome
Page 92
Abstract
Metabolic syndrome (MS) is a cluster of cardiovascular (CV) risk factors (hypertension, dyslipidemia,
obesity, and glucose homeostasis alterations), and insulin resistance (IR) is suggested to be a common
pathogenic background. In the general population, MS and IR have been proven to be risk factors for
diabetes, CV disease, and chronic kidney disease. In the renal transplant setting, few studies have analyzed
the relevance of MS and IR. According to the few data available, the prevalence of MS in renal transplant
patients has been described as 22.6% at 12 months, 37.7% at 36 months, and 64% at 6 years after
transplantation. Importantly, MS has been shown to be an independent risk factor for chronic allograft
dysfunction (CAD), graft failure, new-onset diabetes, and CV disease. Also, persistent hyperinsulinemia
during the first posttransplant year has been related to an increase in glomerular filtration rate, probably
reflecting glomerular hyperfiltration as observed in prediabetes and early type 2 diabetes. Importantly,
prediabetes (impaired fasting glucose and impaired glucose tolerance), a state hallmarked by IR, proved to
be highly frequent among stable renal transplant recipients (30%), which is nearly three times its incidence
in the general population. Posttransplant IR has been associated with subclinical atheromatosis as assessed
by carotid intima-media thickness, and with chronic subclinical inflammation. In conclusion, MS and IR
are important modifiable risk factors in renal transplant recipients, and prompt interventions to avoid its
deleterious effects at the metabolic, CV, and graft function levels are needed.
Publication Type
Year of Publication
2010

<72>
Unique Identifier
20706225
Title
The metabolic syndrome following kidney transplantation. [Review]
Source
Kidney International - Supplement. (118)S8-14, 2010 Sep.
VI 1
Record Owner
Status
MEDLINE
Authors
Goldsmith D; Pietrangeli CE.
Authors Full Name
Goldsmith, David; Pietrangeli, Carolynn E.
Institution
Goldsmith, David. Renal and Transplantation Department, Guy's and St Thomas' Hospital, Great Maze
Pond, London, UK. david.goldsmith@gstt.nhs.uk
Humans
Incidence
Male
Page 93
Prevalence
Abstract
The metabolic syndrome is a constellation of defined cardiovascular risk factors occurring simultaneously
in a single individual. The result of dysregulated glucose and vascular metabolism, the syndrome has been
identified as a significant risk factor for cardiovascular morbidity in the general population. More recently,
a relatively high prevalence of the metabolic syndrome has been recognized among kidney transplant
recipients. The prevalence, risk factors, pathophysiology, and potential consequences of the metabolic
syndrome in the general population and in kidney transplant recipients are reviewed. The definitions and
clinical utility of the metabolic syndrome as a medical condition continue to be debated. Nevertheless, the
burden of risk increases with the presence of multiple components, including insulin resistance, abdominal
obesity, and dysregulated lipid metabolism. Risk factors specific to transplant recipients include the
duration of pretransplant dialysis and posttransplant immunosuppression and weight gain. The metabolic
syndrome is emerging as a significant surveillance target following kidney transplantation. Control of body
mass index, blood glucose and lipid levels, as well as blood pressure, is required to prevent the
consequences of the metabolic syndrome, including cardiovascular events and cardiovascular death.
Immunosuppressive regimens should be designed to limit exacerbation of components of the metabolic
syndrome.
Publication Type
Case Reports. Journal Article. Review.
Year of Publication
2010

<73>
Unique Identifier
30299895
Title
Preserved insulin secretion and kidney function in recipients with functional pancreas grafts 1 year after
transplantation: a single-center prospective observational study.
Source
European Journal of Endocrinology. 179(4):251-259, 2018 10 01.
VI 1
Record Owner
Status
MEDLINE
Authors
Nordheim E; Birkeland KI; Asberg A; Hartmann A; Horneland R; Jenssen T.
Authors Full Name
Nordheim, Espen; Birkeland, Kare I; Asberg, Anders; Hartmann, Anders; Horneland, Rune; Jenssen,
Trond.
Institution
Nordheim, Espen. Department of Transplantation Medicine, Section of Nephrology, Oslo University
Hospital, Rikshospitalet, Oslo, Norway
Nordheim, Espen. Faculty of Medicine, University of Oslo, Oslo, Norway
Birkeland, Kare I. Department of Transplantation Medicine, Section of Nephrology, Oslo University
Birkeland, Kare I. Faculty of Medicine, University of Oslo, Oslo, Norway
Asberg, Anders. Department of Transplantation Medicine, Section of Nephrology, Oslo University
Asberg, Anders. School of Pharmacy, University of Oslo, Oslo, Norway
Page 94
Hartmann, Anders. Department of Transplantation Medicine, Section of Nephrology, Oslo University
Hartmann, Anders. Faculty of Medicine, University of Oslo, Oslo, Norway
Horneland, Rune. Department of Transplantation Medicine, Section of Transplantation Surgery, Oslo
University Hospital, Rikshospitalet, Oslo, Norway
Jenssen, Trond. Department of Transplantation Medicine, Section of Nephrology, Oslo University
Jenssen, Trond. Metabolic and Renal Research Group, Faculty of Health Sciences, UiT- The Arctic
University of Norway, Tromso, Norway
Local Messages
Titulo en Biblioteca "Dr J.J. IZQUIERDO", " 1994 - "
Adult
Diabetes Mellitus, Type 1/co [Complications]
Diabetes Mellitus, Type 1/me [Metabolism]
Female
*Graft Rejection/pc [Prevention & Control]
Graft Survival
Humans
Insulin Resistance
Insulin Secretion
Male
Middle Aged
Mycophenolic Acid/ae [Adverse Effects]
Mycophenolic Acid/tu [Therapeutic Use]
Prednisolone/ae [Adverse Effects]
Prospective Studies
Tacrolimus/ae [Adverse Effects]
Abstract
Objective: Successful simultaneous pancreas and kidney transplantation (SPK) or pancreas transplantation
alone (PTA) restores glycemic control. Diabetes and impaired kidney function are common side effects of
immunosuppressive therapy. This study addresses glucometabolic parameters and kidney function during
the first year.
Methods: We examined 67 patients with functioning grafts (SPK n = 30, PTA n = 37) transplanted
between September 2011 and November 2016 who underwent repeated oral glucose tolerance tests
(OGTTs) 8 and 52 weeks after transplantation. Another 19 patients lost their graft the first year post-
transplant and 28 patients did not undergo repeated OGTTs and could not be studied. All patients received
ATG induction therapy plus tacrolimus, mycophenolate and prednisolone. Glomerular filtration rate was
measured before and 8 and 52 weeks after transplantation by serum clearance methods.
Page 95
Results: From week 8 to 52 after transplantation, mean fasting glucose decreased (SPK: 5.4 +/- 0.7 to 5.1
+/- 0.8 mmol/L, PTA: 5.4 +/- 0.6 to 5.2 +/- 0.7 mmol/L; both P < 0.05), and also 120-min post-OGTT
glucose (SPK: 6.9 +/- 2.9 to 5.7 +/- 2.2 mmol/L; P = 0.07, PTA: 6.5 +/- 1.7 to 5.7 +/- 1.2 mmol/L; P <
0.05). Fasting C-peptide levels also decreased (SPK: 1500 +/- 573 to 1078 +/- 357 pmol/L, PTA: 1210 +/-
487 to 1021 +/- 434 pmol/L, both P < 0.005). Measured GFR decreased from enlistment to 8 weeks post
transplant in PTA patients (94 +/- 22 to 78 +/- 19 mL/min/1.73 m2; P < 0.005), but did not deteriorate from
week 8 to week 52 (SPK: 55.0 +/- 15.1 vs 59.7 +/- 11.3 ml/min/1.73 m2; P = 0.19, PTA: 76 +/- 19 vs 77 +/-
19 mL/min/1.73 m2; P = 0.74).
Conclusion: Glycemic control and kidney function remain preserved in recipients with functioning SPK
and PTA grafts 1 year after transplantation. Copyright © 2018 European Society of Endocrinology
0 (Blood Glucose). 0 (Immunosuppressive Agents). 0 (Insulin). 9PHQ9Y1OLM (Prednisolone).
HU9DX48N0T (Mycophenolic Acid). WM0HAQ4WNM (Tacrolimus).
Publication Type
Journal Article. Observational Study.
Year of Publication
2018

<74>
Unique Identifier
19765444
Title
Insulin resistance and insulin secretion changes in kidney transplant recipients with normal graft function
compared with those with delayed graft function early after transplantation.
Source
Transplantation Proceedings. 41(7):2817-9, 2009 Sep.
VI 1
Record Owner
Status
MEDLINE
Authors
Hekmat R; Javan ML; Javadi Z.
Authors Full Name
Hekmat, R; Javan, M L; Javadi, Z.
Institution
Hekmat, R. Department of Nephrology, Mashhad University of Medical Sciences, Ghaem Hospital,
Mashhad, Iran. drhekmatreza@yahoo.com
Adult
Atherosclerosis/ep [Epidemiology]
Delayed Graft Function/ep [Epidemiology]
Delayed Graft Function/pp [Physiopathology]
Female
Humans
Insulin/bl [Blood]
Insulin Secretion
Page 96
Insulin-Secreting Cells/me [Metabolism]
Male
Middle Aged
Postoperative Complications/bl [Blood]
Reference Values
Risk Factors
Young Adult
Abstract
INTRODUCTION: We compared insulin resistance (IR) and insulin secretion (IS) among kidney
transplant recipients with normal versus delayed graft function (DGF) early after transplantation.
METHODS: We selected 55 kidney transplant recipients without a history of clinical diabetes mellitus.
The basal values of glucose (G) and insulin (I) were used to calculate indices of IR and IS before, on the
third day, as well as at the end of the first, second, and third weeks after transplantation.
RESULTS: Before transplantation IR was more prevalent (62.5%) than impaired IS (20%; P = .012).
Three weeks after engraftment, IR was significantly reduced (P < .001), whereas the reduction in the IS
was not significant (P = .17). Splitting the results between normal and delayed functioning grafts showed a
significant difference in both IR and IS between the 2 groups on the third day after transplantation (P = .
018 and .024, respectively). Regression models showed that only cumulative administered cyclosporine
dose and plasma creatinine were significantly (or near significantly) associated with IR (P = .04 and .07,
respectively).
CONCLUSION: Among patients with DGF there was a significantly greater prevalence of IR and IS
compared with successfully engrafted patients in the middle of the first week after transplantation. With
resumption of normal kidney function among the DGF group, this difference disappeared at the end of the
third week after transplantation.
0 (Insulin).
Publication Type
Journal Article.
Year of Publication
2009

<75>
Unique Identifier
15999750
Title
[Kidney transplantation in patients with diabetic nephropathy]. [Review] [15 refs] [Japanese]
Source
Nippon Rinsho - Japanese Journal of Clinical Medicine. 63 Suppl 6:447-52, 2005 Jun.
VI 1
Record Owner
Status
MEDLINE
Page 97
Authors
Babazono T; Inoue A; Teraoka S.
Authors Full Name
Babazono, Tetsuya; Inoue, Aiko; Teraoka, Satoshi.
Institution
Babazono, Tetsuya. Department of Medicine, Diabetes Center, Tokyo Women's Medical University.
Antibodies, Monoclonal/tu [Therapeutic Use]
Basiliximab
Diabetic Nephropathies/di [Diagnosis]
Graft Survival
Humans
Insulin Resistance
Insulin Secretion
Prognosis
Recombinant Fusion Proteins/tu [Therapeutic Use]
Secondary Prevention
0 (Antibodies, Monoclonal). 0 (Immunosuppressive Agents). 0 (Insulin). 0 (Recombinant Fusion
Proteins). 9927MT646M (Basiliximab).
Publication Type
Year of Publication
2005

<76>
Unique Identifier
18675079
Title
New-onset diabetes mellitus after kidney transplantation: the role of immunosuppression.
Source
Transplantation Proceedings. 40(6):1885-7, 2008 Jul-Aug.
VI 1
Record Owner
Status
MEDLINE
Authors
Veroux M; Corona D; Giuffrida G; Gagliano M; Sorbello M; Virgilio C; Tallarita T; Zerbo D; Giaquinta
A; Fiamingo P; Macarone M; Li Volti G; Caglia P; Veroux P.
Authors Full Name
Veroux, M; Corona, D; Giuffrida, G; Gagliano, M; Sorbello, M; Virgilio, C; Tallarita, T; Zerbo, D;
Giaquinta, A; Fiamingo, P; Macarone, M; Li Volti, G; Caglia, P; Veroux, P.
Institution
Page 98
Veroux, M. Department of Surgery, Transplantation and Advanced Technologies-Organ Transplant Unit,
University Hospital of Catania, Catania, Italy. veroux@unict.it
Cyclosporine/ae [Adverse Effects]
Diabetes Mellitus/im [Immunology]
Humans
*Immunosuppression/ae [Adverse Effects]
Insulin/df [Deficiency]
Insulin Resistance
Insulin Secretion
Middle Aged
Mycophenolic Acid/aa [Analogs & Derivatives]
*Postoperative Complications/im [Immunology]
Abstract
BACKGROUND: Complications related to posttransplantation immunosuppressive therapy remain
common. New-onset diabetes mellitus after transplantation (PTDM) is a well-recognized complication
associated with reduced graft and patient survival. The type of immunosuppression may be responsible for
more than two thirds of PTDM. We retrospectively reviewed our experience in a population of 284 kidney
transplant recipients, evaluating the incidence of PTDM with regard to the type of immunosuppression.
PATIENTS AND METHODS: From January 2001 to December 2005, 284 kidney transplantations were
performed using tacrolimus-based (TAC) immunosuppression in 192 patients and a cyclosporine-based
(CyA) regimen in 62 patients, whereas 30 patients received sirolimus-based immunosuppression.
RESULTS: The overall incidence of PTDM was 4.9%. Among the immunosuppression protocols, 8
patients (4.1%) received TAC and 6 patients (9.6%) received CyA, whereas no patients treated with
sirolimus developed PTDM. Graft and patient survival rates were 93% and 100%, respectively.
CONCLUSIONS: The overall risk of PTDM with recent immunosuppressive protocols is low, but it is
increased among calcineurin inhibitor (CNI)-treated kidney transplant recipients. Sirolimus did not increase
the risk of PTDM, allowing potential clinical application in diabetic recipients and in patients affected by
PTDM.
0 (Immunosuppressive Agents). 0 (Insulin). 83HN0GTJ6D (Cyclosporine). 9PHQ9Y1OLM
(Prednisolone). HU9DX48N0T (Mycophenolic Acid).
Publication Type
Journal Article.
Year of Publication
2008

<77>
Page 99
Unique Identifier
11181807
Title
Influence of tacrolimus on glucose metabolism before and after renal transplantation: a prospective study.
Source
Journal of the American Society of Nephrology. 12(3):583-8, 2001 Mar.
VI 1
Record Owner
Status
MEDLINE
Authors
Duijnhoven EM; Boots JM; Christiaans MH; Wolffenbuttel BH; Van Hooff JP.
Authors Full Name
Duijnhoven, E M; Boots, J M; Christiaans, M H; Wolffenbuttel, B H; Van Hooff, J P.
Institution
Duijnhoven, E M. Department of Internal Medicine, University Hospital Maastricht, Maastricht, The
Netherlands.
Adult
Animals
Diabetes Mellitus/et [Etiology]
Female
Humans
Insulin Resistance
Insulin Secretion
Male
Middle Aged
Prospective Studies
Abstract
Most studies concerning the influence of tacrolimus on glucose metabolism have been performed either in
animals or after organ transplantation. These clinical studies have largely been transversal with patients
who were using steroids. Therefore, this prospective, longitudinal study investigated the influence of
tacrolimus on glucose metabolism before and after transplantation. Eighteen Caucasian dialysis patients
underwent an intravenous glucose tolerance test before and 5 d after the start of tacrolimus. Insulin
sensitivity index (k(G)), insulin resistance (insulin/glucose ratio and homeostasis model assessment), and
C-peptide and insulin secretion were calculated. Trough levels of tacrolimus were measured. After
transplantation, the occurrence of posttransplantation diabetes mellitus (PTDM) was prospectively
monitored. Statistical analysis was performed using the Wilcoxon signed ranks test and Spearman's rho for
correlation. Before tacrolimus, k(G) was indeterminate in three patients. During tacrolimus, k(G) decreased
in 16 of 18 patients, from a median of 1.74 mmol/L per min to 1.08 mmol/L per min (P<0.0001). The
correlation between C-peptide and insulin data was excellent. Insulin secretion decreased from 851.0 mU x
min/L to 558.0 mU x min/L (P = 0.014), whereas insulin resistance did not change. Insulin sensitivity
correlated negatively with tacrolimus trough level. After transplantation, three patients developed PTDM;
before tacrolimus, two had an indeterminate and one a low normal k(G). During tacrolimus administration,
k(G) decreased in almost all patients as a result of a diminished insulin secretion response to a glucose load,
whereas insulin resistance did not change. Patients with an abnormal or indeterminate k(G) seem to be at
risk of developing PTDM while on tacrolimus.
Page 100
0 (Immunosuppressive Agents). 0 (Insulin). IY9XDZ35W2 (Glucose). WM0HAQ4WNM (Tacrolimus).
Publication Type
Year of Publication
2001

<78>
Unique Identifier
19461501
Title
Insulin, glucose, and glomerular filtration rate.
Source
Transplantation. 87(10):1592-3, 2009 May 27.
VI 1
Record Owner
Status
MEDLINE
Authors
Sharif A.
Authors Full Name
Sharif, Adnan.
Comments
Comment on (CON)
Female
*Glomerular Filtration Rate
Homeostasis
Humans
Hyperinsulinism/et [Etiology]
Hyperinsulinism/me [Metabolism]
Insulin Secretion
Male
0 (Blood Glucose). 0 (Insulin).
Publication Type
Letter. Comment.
Year of Publication
2009

Page 101
<79>
Unique Identifier
17327329
Title
Risk factors associated with the onset and progression of posttransplantation diabetes in renal allograft
recipients.
Source
Diabetes Care. 30(3):609-15, 2007 Mar.
VI 1
Record Owner
Status
MEDLINE
Authors
Hur KY; Kim MS; Kim YS; Kang ES; Nam JH; Kim SH; Nam CM; Ahn CW; Cha BS; Kim SI; Lee HC.
Authors Full Name
Hur, Kyu Yeon; Kim, Myoung Soo; Kim, Yu Seun; Kang, Eun Seok; Nam, Jae Hyun; Kim, So Hun;
Nam, Chung Mo; Ahn, Chul Woo; Cha, Bong Soo; Kim, Soon Il; Lee, Hyun Chul.
Institution
Hur, Kyu Yeon. Department of Internal Medicine, Yonsei University College of Medicine, 134 Shinchon-
Dong Seodaemun-Gu, Seoul, 120-752, Korea.
Adult
Age Factors
Diabetes Mellitus/ge [Genetics]
Female
Humans
Incidence
Insulin Secretion
Living Donors/sn [Statistics & Numerical Data]
Male
Middle Aged
Risk Factors
Time Factors
Transplantation, Homologous/ae [Adverse Effects]
Abstract
OBJECTIVE: The aim of this study was to assess the incidence of posttransplantation diabetes mellitus
(PTDM) in renal allograft recipients and to investigate factors contributing to the onset and progression of
PTDM and its underlying pathogenic mechanism(s).
RESEARCH DESIGN AND METHODS: A total of 77 patients with normal glucose tolerance (NGT)
were enrolled in this study. An oral glucose tolerance test was performed 1 week before transplantation and
repeated at 1 and 7 years after transplantation.
RESULTS: The overall incidence of PTDM was 39% at 1 year and 35.1% at 7 years posttransplantation.
The incidence for each category of PTDM was as follows: persistent PTDM (P-PTDM) (patients who
developed diabetes mellitus within 1 year of transplantation and remained diabetic during 7 years), 23.4%;
transient PTDM (T-PTDM) (patients who developed diabetes mellitus during the 1st year after
transplantation but eventually recovered to have NGT), 15.6%; late PTDM (L-PTDM) (patients who
Page 102
developed diabetes mellitus later than 1 year after transplantation), 11.7%; and non-PTDM during 7 years
(N-PTDM7) (patients who did not develop diabetes mellitus during 7 years), 49.3%. Older age (> or = 40
years) at transplantation was a higher risk factor for P-PTDM, whereas a high BMI (> or = 25 kg/m2) and
impaired fasting glucose (IFG) at 1 year posttransplantation were higher risk factors for L-PTDM. Impaired
insulin secretion rather than insulin resistance was significantly associated with the development of P- and
L-PTDM.
CONCLUSIONS: Impaired insulin secretion may be the main mechanism for the development of PTDM.
Older age at transplantation seems to be associated with P-PTDM, whereas a high BMI and IFG at 1 year
after transplantation were associated with L-PTDM.
Publication Type
Year of Publication
2007

<80>
Unique Identifier
19845589
Title
Impaired insulin sensitivity as an underlying mechanism linking hepatitis C and posttransplant diabetes
mellitus in kidney recipients.
Source
American Journal of Transplantation. 9(12):2777-84, 2009 Dec.
VI 1
Record Owner
Status
MEDLINE
Authors
Baid-Agrawal S; Frei U; Reinke P; Schindler R; Kopp MA; Martus P; Berg T; Juergensen JS; Anker SD;
Doehner W.
Authors Full Name
Baid-Agrawal, S; Frei, U; Reinke, P; Schindler, R; Kopp, M A; Martus, P; Berg, T; Juergensen, J S;
Anker, S D; Doehner, W.
Institution
Baid-Agrawal, S. Division of Nephrology and Medical Intensive Care, Department of Medicine, Berlin,
Germany. seema.baid-agrawal@charite.de
Adult
*Diabetes Mellitus, Type 2/et [Etiology]
Female
*Hepatitis C, Chronic/co [Complications]
Humans
*Insulin Resistance
Insulin Secretion
Page 103
Male
Middle Aged
Abstract
Aim of this study was to investigate the mechanism/s associating hepatitis C virus (HCV) infection and
posttransplant diabetes mellitus in kidney recipients. Twenty HCV-positive and 22 HCV-negative kidney
recipients, 14 HCV-positive nontransplant patients and 24 HCV-negative nontransplant (healthy) subjects
were analyzed. A 3-h intravenous glucose tolerance test was performed; peripheral insulin sensitivity was
assessed by minimal modeling. Pancreatic insulin secretion, hepatic insulin uptake, pancreatic antibodies
and proinflammatory cytokines in serum (tumor necrosis factor-alpha, intereukin-6, high-sensitive C-
reactive protein) were also assessed. HCV-positive recipients showed a significantly lower insulin
sensitivity as compared to HCV-negative recipients (3.0 +/- 2.1 vs. 4.9 +/- 3.0 min(-1).microU.mL(-
1).10(4), p = 0.02), however, insulin secretion and hepatic insulin uptake were not significantly different.
Pancreatic antibodies were negative in all. HCV status was an independent predictor of impaired insulin
sensitivity (multivariate analysis, p = 0.008). The decrease of insulin sensitivity due to HCV was
comparable for transplant and non-transplant subjects. No significant correlation was found between any of
the cytokines and insulin sensitivity. Our results suggest that impaired peripheral insulin sensitivity is
associated with HCV infection irrespective of the transplant status, and is the most likely pathogenic
mechanism involved in the development of type 2 diabetes mellitus associated with HCV infection.
0 (Insulin).
Publication Type
Year of Publication
2009

<81>
Unique Identifier
15615809
Title
Short-term treatment with rosiglitazone improves glucose tolerance, insulin sensitivity and endothelial
function in renal transplant recipients.
Source
VI 1
Record Owner
Status
MEDLINE
Authors
Voytovich MH; Simonsen C; Jenssen T; Hjelmesaeth J; Asberg A; Hartmann A.
Authors Full Name
Voytovich, Monica Hagen; Simonsen, Cathrine; Jenssen, Trond; Hjelmesaeth, Joran; Asberg, Anders;
Hartmann, Anders.
Institution
Voytovich, Monica Hagen. Department of Medicine, Section of Nephrology, Laboratory for Renal
Physiology, Rikshospitalet University Hospital, 0027 Oslo, Norway. monica.hagen@rikshospitalet.no
Blood Glucose/de [Drug Effects]
Page 104
*Endothelium, Vascular/de [Drug Effects]
Female
*Glucose Intolerance/dt [Drug Therapy]
Humans
Hypoglycemic Agents/tu [Therapeutic Use]
Insulin/bl [Blood]
*Insulin Resistance
Insulin Secretion
Male
PPAR gamma/ai [Antagonists & Inhibitors]
Rosiglitazone
*Thiazolidinediones/tu [Therapeutic Use]
Abstract
BACKGROUND: Insulin resistance (IR) contributes to the development of glucose intolerance (post-
transplant diabetes mellitus or impaired glucose tolerance) following renal transplantation. Furthermore,
endothelial dysfunction (ED) is associated with IR. Glucose intolerance, IR and ED are all independent risk
factors for cardiovascular disease. Therefore, treatment with insulin sensitizers may benefit glucose-
intolerant renal transplant recipients. The main objectives of the present study were to investigate the effect
of 4 weeks' treatment with the PPAR-gamma agonist rosiglitazone on insulin sensitivity, plasma glucose
and endothelial function in renal transplant recipients with glucose intolerance. Safety parameters were also
addressed.
METHODS: A total of 10 glucose-intolerant renal transplant recipients were treated with rosiglitazone
(initially 4 mg/day increasing to 8 mg/day after 1 week). A hyperinsulinaemic euglycaemic glucose clamp,
an oral glucose tolerance test and endothelial function assessment with laser Doppler flowmetry were
performed both at baseline and at follow-up.
RESULTS: Treatment with rosiglitazone was followed by a significantly improved mean glucose
disposal rate (from 6.5 to 9.1 g/kg/min; P = 0.02) and a significant decline in fasting and 2 h plasma
glucose (from 6.4 to 5.8 mmol/l, P = 0.01 and from 14.2 to 10.6 mmol/l, P = 0.03, respectively).
Furthermore, a significant improvement in endothelial function was demonstrated (AUC(ACh); from 389
to 832 AU x min, P = 0.04). No serious adverse events or hypoglycaemic episodes were observed.
CONCLUSIONS: Four weeks' treatment with rosiglitazone was associated with increased insulin
sensitivity, lowered fasting and 2 h plasma glucose and improved endothelial function in renal transplant
recipients with glucose intolerance. The drug was well tolerated and may be a good alternative for treating
these patients.
0 (Blood Glucose). 0 (Hypoglycemic Agents). 0 (Insulin). 0 (PPAR gamma). 0 (Thiazolidinediones).
05V02F2KDG (Rosiglitazone).
Publication Type
Clinical Trial. Journal Article. Research Support, Non-U.S. Gov't.
Year of Publication
2005

<82>
Unique Identifier
Page 105
23726615
Title
Insulin resistance and insulin secretion in renal transplant recipients with hepatitis C.
Source
Transplantation Proceedings. 45(4):1540-3, 2013 May.
VI 1
Record Owner
Status
MEDLINE
Authors
Uchida J; Iwai T; Machida Y; Kuwabara N; Kabei K; Kumada N; Nakatani T.
Authors Full Name
Uchida, J; Iwai, T; Machida, Y; Kuwabara, N; Kabei, K; Kumada, N; Nakatani, T.
Institution
Uchida, J. Department of Urology, Osaka City University Graduate School of Medicine, Osaka, Japan.
m9492120@msic.med.osaka-cu.ac.jp
Adult
Female
*Hepatitis C/su [Surgery]
Humans
*Insulin Resistance
Insulin Secretion
Islets of Langerhans/pp [Physiopathology]
Male
Abstract
BACKGROUND: Several reports have suggested an association between hepatitis C virus (HCV)
infection and new-onset diabetes after transplantation (NODAT). NODAT is a common complication after
renal transplantation, and it has been associated with increased long-term morbidity and mortality. HCV-
positive recipients may have abnormal glucose metabolism, even though NODAT has never been
previously diagnosed. The aim of this study was to analyze the pathogenic factors responsible for glucose
metabolism in a series of HCV-positive renal transplant recipients.
METHODS: The study population comprised 16 renal transplant patients who received their grafts from
deceased or living donors with anti-HCV antibodies. HCV-negative transplant recipients were individually
matched with these HCV-positive recipients by year of transplantation, sex, age, serum creatinine levels,
and type of calcineurin inhibitors. None of the patients had been diagnosed with diabetes. Insulin secretion
and insulin resistance were determined by a 75-g oral glucose tolerance test (OGTT) and compared
between the 2 groups. Categories of glucose tolerance were defined according to World Health
Organization criteria.
RESULTS: Glucose intolerance (impaired fasting glucose, impaired glucose tolerance, diabetes mellitus)
as assessed by OGTT was detected in 7 of the HCV-positive recipients (43.8%) and 3 of the HCV-negative
recipients. The homeostasis model assessment of insulin resistance was greater in the HCV-positive
recipients than in the HCV-negative recipients. The homeostasis model assessment of beta-cell function
was higher in the HCV-positive recipients than in the HCV-negative recipients.
CONCLUSIONS: The frequency of glucose intolerance tended to be higher in HCV-positive recipients.

Furthermore, insulin resistance was greater and insulin secretion higher in HCV-positive recipients, which
indicated that the increase in insulin secretion compensated for insulin resistance observed in these patients.
However, HCV-positive renal transplant recipients may ultimately develop NODAT as this compensation
diminishes with time. Copyright © 2013 Elsevier Inc. All rights reserved.
Page 106
0 (Insulin).
Publication Type
Journal Article.
Year of Publication
2013

<83>
Unique Identifier
20354482
Title
Impending hyperglycemia in normoglycemic renal transplant recipients--an experimental predictive
surrogate.
Source
VI 1
Record Owner
Status
MEDLINE
Authors
Sharif A; Ravindran VK; Dunseath G; Luzio SD; Owens DR; Baboolal K.
Authors Full Name
Sharif, Adnan; Ravindran, Vinod K; Dunseath, Gareth; Luzio, Steve D; Owens, David R; Baboolal,
Keshwar.
Institution
Sharif, Adnan. Department of Nephrology and Transplantation, Renal Institute of Birmingham, University
Hospital Birmingham, Edgbaston, Birmingham, United Kingdom. sharif_adnan@hotmail.com
Diabetes Mellitus/bl [Blood]
Fasting
Glucose Intolerance/bl [Blood]
Humans
*Hyperglycemia/dt [Drug Therapy]
Insulin/bl [Blood]
Insulin Secretion
Lipids/bl [Blood]
Abstract
BACKGROUND: beta-Cell dysfunction and insulin resistance combine to cause new-onset diabetes after
transplantation. The product of these two parameters, quantitatively measured as disposition index (DI), is a
mathematical constant in normoglycemia and declines in advance of impending hyperglycemia. The aim of
Page 107
this study was to derive a simple surrogate for the DI to expose predysglycemic abnormalities
posttransplantation.
METHODS: First-phase insulin secretion and sensitivity were determined by mathematical minimal
model analysis of 58 frequently sampled, intravenous glucose tolerance tests in 58 non-diabetic renal
transplant recipients and correlated against surrogate indexes based on fasting blood samples. Products of
insulin secretion/resistance indexes were correlated against calculated DI, regression analysis performed for
hyperbolic compatibility, autocorrelation studies conducted, and surrogates tested in various subgroups of
renal transplant recipients to ensure robustness in a heterogeneous group.
RESULTS: The best correlation was achieved with "HOMA(sec) (first-phase insulin
secretion)xMcAuley's index (insulin resistance)" (r=0.594, P<0.001). Regression analysis was consistent
with a mathematical hyperbola (ln HOMA(sec) vs. ln McAuley's index, r=-0.639 [95% confidence interval,
-1.772 to -0.950]), statistical autocorrelation was excluded (in a subset of 20 patients with repeat metabolic
investigations), and the surrogate remained valid in different subgroups of transplant recipients.
CONCLUSIONS: Our surrogate "HOMA(sec)xMcAuley's index," requiring only fasting glucose, insulin,
and triglycerides, is a simple and noninvasive surrogate for the DI. Its predictive utility for identifying
impending hyperglycemia posttransplantation should be investigated further to ascertain whether its
experimental nature can translate to clinical validity.
0 (Blood Glucose). 0 (Insulin). 0 (Lipids).
Publication Type
Journal Article.
Year of Publication
2010

<84>
Unique Identifier
11520309
Title
Metabolic and hormonal effects of tacrolimus (FK506) or cyclosporin immunosuppression following renal
transplantation.
Source
Diabetes, Obesity & Metabolism. 3(4):287-92, 2001 Aug.
VI 1
Record Owner
Status
MEDLINE
Authors
Dmitrewski J; Krentz AJ; Mayer AD; Buckels JA; Barnes AD; Smith J; Nattrass M.
Authors Full Name
Dmitrewski, J; Krentz, A J; Mayer, A D; Buckels, J A; Barnes, A D; Smith, J; Nattrass, M.
Institution
Dmitrewski, J. Transplantation Unit, Queen Elizabeth Hospital, Birmingham, UK.
Alanine/bl [Blood]
Page 108
Follow-Up Studies
Glycerol/bl [Blood]
Humans
Insulin/bl [Blood]
Insulin Resistance/im [Immunology]
Insulin Secretion
Ketone Bodies/bl [Blood]
Lactates/bl [Blood]
Postprandial Period
Pyruvates/me [Metabolism]
Reference Values
Time Factors
Abstract
Twelve renal transplant recipients randomised to receive immunosuppression with either tacrolimus
(FK506) or cyclosporin underwent oral glucose tolerance tests (OGTT) a median of 8 months (range 7-9)
after transplantation. Six healthy subjects acted as controls. Compared with the controls, both transplant
groups had significantly elevated fasting (p < 0.05 for both groups) and postprandial (p < 0.001 for
tacrolimus and p < 0.05 for cyclosporin) blood glucose concentrations. Fasting hyperinsulinaemia was
observed in both transplant groups (p < 0.05) relative to the control subjects. Glucose-stimulated plasma
immunoreactive insulin concentrations in the tacrolimus-treatment group were significantly higher than in
the cyclosporin group (p < 0.05) and the controls (p < 0.001). Postprandial blood alanine concentrations
were also significantly elevated in the tacrolimus group compared with both the controls (p < 0.001) and
cyclosporin-treated patients (p < 0.001). The raised insulin concentrations with normal or increased blood
glucose concentrations after renal transplantation suggests that insulin resistance was more marked in
patients receiving tacrolimus-based immunosuppression.
0 (Blood Glucose). 0 (C-Peptide). 0 (Fatty Acids, Nonesterified). 0 (Immunosuppressive Agents). 0
(Insulin). 0 (Ketone Bodies). 0 (Lactates). 0 (Pyruvates). 83HN0GTJ6D (Cyclosporine). OF5P57N2ZX
(Alanine). PDC6A3C0OX (Glycerol). WM0HAQ4WNM (Tacrolimus).
Publication Type
Clinical Trial. Comparative Study. Journal Article. Multicenter Study. Randomized Controlled Trial.
Research Support, Non-U.S. Gov't.
Year of Publication
2001

<85>
Unique Identifier
28720321
Title
No evidence for progressive deterioration in stimulated insulin secretion in renal transplant recipients after
12years tacrolimus exposure.
Source
Page 109
Journal of Diabetes & its Complications. 31(9):1384-1388, 2017 Sep.
VI 1
Record Owner
Status
MEDLINE
Authors
Gelens MACJ; van Hooff JP; Usvyat L; Christiaans MH.
Authors Full Name
Gelens, Marielle A C J; van Hooff, Johannes P; Usvyat, Len; Christiaans, Maarten H.
Institution
Gelens, Marielle A C J. Department of Internal Medicine, Maastricht University Medical Centre, PO-box
5800, 6202 AZ Maastricht, The Netherlands. Electronic address: m.gelens@mumc.nl.
van Hooff, Johannes P. Department of Internal Medicine, Maastricht University Medical Centre, PO-box
5800, 6202 AZ Maastricht, The Netherlands. Electronic address: hooffvan@xs4all.nl.
Usvyat, Len. Renal Research Institute, 315E 62nd ST, New York, NY 10065, USA; Fresenius Medical
Care North America, 950 Winter St, Waltham, MA 02451, USA. Electronic address: Len.Usvyat@fmc-
na.com.
Christiaans, Maarten H. Department of Internal Medicine, Maastricht University Medical Centre, PO-box
5800, 6202 AZ Maastricht, The Netherlands. Electronic address: m.christiaans@mumc.nl.
Adult
Aged
Disease Progression
Female
Humans
Insulin Resistance
Insulin Secretion
*Insulin-Secreting Cells/de [Drug Effects]
Insulin-Secreting Cells/pa [Pathology]
Male
Middle Aged
Time Factors
*Transplant Recipients
Young Adult
Keyword Heading
Insulin resistance
Insulin secretion
NODAT
Post transplantation diabetes mellitus (PTDM)
Renal transplantation
Tacrolimus (Tac)
Abstract
AIMS: Tacrolimus (Tac) inhibits insulin secretion in a Tac-trough blood level dependent way early post-
transplant in renal transplant recipients (Rtx). It is unknown whether long-term exposure results into a
progressive beta cells dysfunction.
METHODS: Two independent cohorts of Tac-treated non-diabetic Rtx, previously participating in

glucose metabolism studies using intravenous Glucose Tolerance Test (ivGTT) were included: Fifty-eight
Page 110
Rtx were tested by ivGTT cross-sectional between 0.25 and 12.6years post-transplant. Factors related to
glucose metabolism parameters were explored by multilinear regression analysis. Eighteen non-diabetic
Rtx tested by ivGTT 6months post-transplant were retested at 12years. The glucose metabolism outcome
parameters were also adjusted according to the results of the cross-sectional study.
RESULTS: Multivariate analysis showed 'Age', 'BMI' and 'use of steroids' to be significantly related, in
different combinations, to the glucose metabolism parameters 'insulin resistance', 'fasting insulin level' and
'stimulated insulin secretion'. However 'time on tacrolimus' wasn't related to any parameter. In the
longitudinal study, none of the glucose metabolism parameters (either analyzed crude or adjusted)
deteriorated clinically or statistically significant. Numerically, 'stimulated insulin secretion' even increased.
CONCLUSIONS: Chronic Tac exposure does NOT lead to a progressive decrease in 'stimulated insulin
secretion' between 6months and 12years post renal transplant in our population of 18 patients. Copyright ©
2017 Elsevier Inc. All rights reserved.
0 (Immunosuppressive Agents). 0 (Insulin). WM0HAQ4WNM (Tacrolimus).
Publication Type
Journal Article.
Year of Publication
2017

<86>
Unique Identifier
13679495
Title
A 6-year prospective study on new onset diabetes mellitus, insulin release and insulin sensitivity in renal
transplant recipients.
Source
Nephrology Dialysis Transplantation. 18(10):2154-9, 2003 Oct.
VI 1
Record Owner
Status
MEDLINE
Authors
Hagen M; Hjelmesaeth J; Jenssen T; Morkrid L; Hartmann A.
Authors Full Name
Hagen, Monica; Hjelmesaeth, Joran; Jenssen, Trond; Morkrid, Lars; Hartmann, Anders.
Institution
Hagen, Monica. Department of Medicine, Section of Nephrology, Rikshospitalet, 0027 Oslo, Norway.
monica.hagen@rikshospitalet.no
Adult
Age Distribution
Age of Onset
*Blood Glucose/an [Analysis]
Cohort Studies
*Diabetes Mellitus/di [Diagnosis]
Diabetes Mellitus/dt [Drug Therapy]
Page 111
Female
Humans
Hypoglycemic Agents/ad [Administration & Dosage]
Incidence
Insulin/an [Analysis]
Insulin Resistance
Insulin Secretion
Male
Middle Aged
Probability
Prognosis
Prospective Studies
Risk Assessment
Sex Distribution
Time Factors
Treatment Outcome
Abstract
BACKGROUND: It is well known that both insulin resistance and insulin deficiency are involved in the
pathogenesis of post-transplant diabetes mellitus (PTDM), but the relative importance of the two different
mechanisms is still under debate. The present prospective longitudinal study was performed over 6 years to
investigate the impact of impaired insulin secretion (ISec) and insulin sensitivity (IS) in the development of
PTDM in renal transplant recipients.
METHODS: A total of 95 non-diabetic patients underwent a 75 g oral glucose tolerance test (OGTT) 10
weeks post-transplant. Six years later, 63 of these recipients were re-examined, the majority (n = 58) with
an OGTT. Fasting, 1- and 2-h insulin and glucose levels were measured and used to estimate the insulin
secretory response and IS both at baseline and at follow-up.
RESULTS: The proportion of recipients with normal glucose tolerance (NGT) rose from 46% (baseline)
to 65% (follow-up) (P = 0.008), and median fasting and 2-h serum glucose were reduced by 0.7 mmol/l (P
< 0.001) and 1.3 mmol/l (P = 0.039), respectively. The recipients with PTDM at follow-up had a significant
decline in the estimated median first and second phase ISec (-58 and -47%, respectively, P = 0.005 for
both). The patients who normalized their glucose tolerance from PTDM or IGT at baseline to NGT at
follow-up increased their IS significantly (68%, P = 0.002) without significant alterations in ISec.
CONCLUSIONS: Impaired ISec seems to be the dominant mechanism in the development of PTDM
after renal transplantation. In contrast, normalization of glucose intolerance is associated with improved IS.
0 (Blood Glucose). 0 (Hypoglycemic Agents). 0 (Insulin).
Publication Type
Comparative Study. Journal Article. Research Support, Non-U.S. Gov't.
Year of Publication
2003

Page 112
<87>
Unique Identifier
17627237
Title
The dynamics of glucose metabolism under calcineurin inhibitors in the first year after renal
transplantation in nonobese patients.
Source
Transplantation. 84(1):50-5, 2007 Jul 15.
VI 1
Record Owner
Status
MEDLINE
Authors
David-Neto E; Lemos FC; Fadel LM; Agena F; Sato MY; Coccuza C; Pereira LM; de Castro MC; Lando
VS; Nahas WC; Ianhez LE.
Authors Full Name
David-Neto, Elias; Lemos, Francine C; Fadel, Luciana M; Agena, Fabiana; Sato, Melissa Y; Coccuza,
Christiano; Pereira, Lilian M; de Castro, M Cristina R; Lando, Valeria S; Nahas, William C; Ianhez, Luiz
E.
Institution
David-Neto, Elias. Renal Transplantation Unit, Hospital das Clinicas, University of Sao Paulo School of
Medicine, Sao Paulo, Brazil. elias.david.neto@attglobal.net
Adult
*Calcineurin Inhibitors
Fasting/bl [Blood]
Female
Homeostasis
Humans
Immunosuppressive Agents/pk [Pharmacokinetics]
Insulin Resistance
Insulin Secretion
Male
Metabolic Diseases/ci [Chemically Induced]
Metabolic Diseases/et [Etiology]
Middle Aged
Mycophenolic Acid/aa [Analogs & Derivatives]
Prospective Studies
Steroids/tu [Therapeutic Use]
Time Factors
Abstract
BACKGROUND: The incidence of glucose metabolism disturbances after transplantation often is based
on the use of hypoglycemic agents and not on the results of glucose tolerance tests (GTTs), which may
Page 113
camouflage the real incidence. A lack of information also exists regarding the profile of glucose
metabolism during the first year after transplant.
METHODS: Oral GTT along with insulin measurements and drugs pharmacokinetics were prospectively
performed at days 30, 60, 180, and 360 after transplant to diagnose disturbances of glucose metabolism
after renal transplantation, in nonobese patients receiving either tacrolimus (n=55) or cyclosporine (n=29),
along with mycophenolate mofetil and steroids.
RESULTS: The incidence of impaired glucose tolerance or diabetes mellitus reached a peak at 60 days
and decreased at 1 year. It could not be adequately diagnosed using fasting plasma glucose in a decreased
abnormal (>99 ng/mL) range. In both groups, insulin secretion, evaluated by the Homeostasis Model
Assesment (HoMA-beta), decreased (P<0.005) from the condition of normal GTT (101+/-56%) to impaired
glucose tolerance (72+/-35%) and diabetes mellitus (54+/-25%). In the cyclosporine group, insulin
secretion was normal and stable throughout the study period, but in the tacrolimus group, insulin secretion
recovered over time and was inversely correlated with tacrolimus exposure. Insulin resistance (HoMA-IR)
did not change.
CONCLUSIONS: This study shows the need to perform an oral GTT at 60 days and at the end of the first
year of renal transplantation to adequately diagnose impaired glucose metabolism.
0 (Blood Glucose). 0 (Calcineurin Inhibitors). 0 (Immunosuppressive Agents). 0 (Insulin). 0 (Steroids).
83HN0GTJ6D (Cyclosporine). HU9DX48N0T (Mycophenolic Acid). WM0HAQ4WNM (Tacrolimus).
Publication Type
Year of Publication
2007

<88>
Unique Identifier
20199368
Title
Family history of diabetes as a new determinant of insulin sensitivity and secretion in patients who have
undergone a simultaneous pancreas-kidney transplant.
Source
Experimental & Clinical Transplantation: Official Journal of the Middle East Society for Organ
Transplantation. 8(1):29-37, 2010 Mar.
VI 1
Record Owner
Status
MEDLINE
Authors
Rangel EB; Melaragno CS; Neves MD; Dib SA; Gonzalez AM; Linhares MM; Pacheco-Silva A; Sa JR.
Authors Full Name
Rangel, Erika B; Melaragno, Claudio S; Neves, Maria Deolinda F; Dib, Sergio A; Gonzalez, Adriano M;
Linhares, Marcelo M; Pacheco-Silva, Alvaro; Sa, Joao R.
Institution
Rangel, Erika B. Division of Nephrology, Universidade Federal de Sao Paulo, Sao Paulo, Brazil.
erikabr@uol.com.br
Page 114
Adult
Body Mass Index
*Diabetes Mellitus/ge [Genetics]
Diabetes Mellitus/me [Metabolism]
Diabetes Mellitus/pp [Physiopathology]
Female
Homeostasis/ph [Physiology]
Humans
Insulin Secretion
Male
Models, Biological
*Pedigree
Prednisone/tu [Therapeutic Use]
Abstract
OBJECTIVES: We used homeostasis model assessment to investigate insulin sensitivity and secretion
after a simultaneous pancreas-kidney transplant or kidney transplant alone. In that model, fasting plasma
glucose and C-peptide levels are used to evaluate insulin sensitivity and beta-cell function.
MATERIALS AND METHODS: Factors (eg, age, sex, race, delayed kidney allograft function) were
correlated with homeostasis model assessment of beta-cell function and homeostasis model assessment of
insulin sensitivity values after simultaneous pancreas-kidney transplant (n=89) or kidney transplant alone
(n=68), and the results were compared with those in healthy subjects (n=49).
RESULTS: Homeostasis model assessment of beta-cell function values were similar in patients who
underwent kidney transplant alone or a simultaneous pancreas-kidney transplant, and were higher than
homeostasis model assessment of beta cell function values in healthy subjects. The homeostasis model
assessment of insulin sensitivity showed intermediate values for patients who underwent a simultaneous
pancreas-kidney transplant and correlated with prednisone dosages (in those who underwent kidney
transplant alone) and tacrolimus levels (in patients who underwent a simultaneous pancreas-kidney
transplant). Homeostasis model assessment of beta-cell function values correlated with prednisone dosages
in both groups and with tacrolimus levels in only those who underwent a simultaneous pancreas-kidney
transplant. The body mass index of subjects who underwent kidney transplant alone correlated with both
homeostasis model assessment of beta-cell function results and homeostasis model assessment of insulin
sensitivity results. A family history of diabetes in subjects who underwent a simultaneous pancreas-kidney
transplant correlated with homeostasis model assessment of beta-cell function results and homeostasis
model assessment of insulin sensitivity results.
CONCLUSIONS: Immunosuppressive regimen and body mass index were linked with reduced insulin
sensitivity after kidney transplant. A family history of diabetes was linked with higher values of insulin
secretion and lower insulin sensitivity in patients who underwent a simultaneous pancreas-kidney
transplant.
0 (Blood Glucose). 0 (C-Peptide). 0 (Immunosuppressive Agents). 0 (Insulin). VB0R961HZT
(Prednisone). WM0HAQ4WNM (Tacrolimus).
Publication Type
Page 115
Year of Publication
2010

<89>
Unique Identifier
29619563
Title
Post-transplantation diabetes in kidney transplant recipients: an update on management and prevention.
[Review]
Source
Acta Diabetologica. 55(8):763-779, 2018 Aug.
VI 1
Record Owner
Status
MEDLINE
Authors
Conte C; Secchi A.
Author NameID
Conte, Caterina; ORCID: http://orcid.org/0000-0001-7066-5292
Authors Full Name
Conte, Caterina; Secchi, Antonio.
Institution
Conte, Caterina. I.R.C.C.S. Ospedale San Raffaele, Via Olgettina 60, 20132, Milan, Italy.
conte.caterina@hsr.it.
Secchi, Antonio. I.R.C.C.S. Ospedale San Raffaele, Via Olgettina 60, 20132, Milan, Italy.
Secchi, Antonio. Vita-Salute San Raffaele University, Via Olgettina 58, 20132, Milan, Italy.
Diabetes Mellitus/pc [Prevention & Control]
*Diabetes Mellitus/th [Therapy]
Humans
Hyperglycemia/ep [Epidemiology]
Hyperglycemia/th [Therapy]
Hypertension/co [Complications]
Hypertension/th [Therapy]
Postoperative Complications/pc [Prevention & Control]
*Postoperative Complications/th [Therapy]
Risk Factors
Keyword Heading
Page 116
Hyperglycaemia
Insulin resistance
Kidney transplantation
Obesity
Post-transplantation diabetes
Abstract
Post-transplantation diabetes mellitus (PTDM) may severely impact both short- and long-term outcomes
of kidney transplant recipients in terms of graft and patient survival. However, PTDM often goes
undiagnosed is underestimated or poorly managed. A diagnosis of PTDM should be delayed until the
patient is on stable maintenance doses of immunosuppressive drugs, with stable kidney graft function and
in the absence of acute infections. Risk factors for PTDM should be assessed during the pre-transplant
evaluation period, in order to reduce the likelihood of developing diabetes. The oral glucose tolerance test
is considered as the gold standard for diagnosing PTDM, whereas HbA1c is not reliable during the first
months after transplantation. Glycaemic targets should be individualised, and comorbidities such as
dyslipidaemia and hypertension should be treated with drugs that have the least possible impact on glucose
metabolism, at doses that do not interact with immunosuppressants. While insulin is the preferred agent for
treating inpatient hyperglycaemia in the immediate post-transplantation period, little evidence is available
to guide therapeutic choices in the management of PTDM. Metformin and incretins may offer some
advantage over other glucose-lowering agents, particularly with respect to risk of hypoglycaemia and
weight gain. Tailoring immunosuppressive regimens may be of help, although maintenance of good kidney
function should be prioritised over prevention/treatment of PTDM. The aim of this narrative review is to
provide an overview of the available evidence on management and prevention of PTDM, with a focus on
the available therapeutic options.
0 (Blood Glucose). 0 (Immunosuppressive Agents). 0 (Insulin).
Publication Type
Year of Publication
2018

<90>
Unique Identifier
29499059
Title
Progranulin serum levels in human kidney transplant recipients: A longitudinal study.
Source
PLoS ONE [Electronic Resource]. 13(3):e0192959, 2018.
VI 1
Record Owner
Status
MEDLINE
Authors
Nicoletto BB; Pedrollo EF; Carpes LS; Coloretti NG; Krolikowski TC; Souza GC; Goncalves LFS;
Manfro RC; Canani LH.
Author NameID
Nicoletto, Bruna Bellincanta; ORCID: https://orcid.org/0000-0001-9378-1130
Authors Full Name
Page 117
Nicoletto, Bruna Bellincanta; Pedrollo, Elis Forcellini; Carpes, Larissa Salomoni; Coloretti, Natalia
Gomes; Krolikowski, Thaiana Cirino; Souza, Gabriela Correa; Goncalves, Luiz Felipe Santos; Manfro,
Roberto Ceratti; Canani, Luis Henrique.
Institution
Nicoletto, Bruna Bellincanta. Faculdade de Medicina, Universidade Federal do Rio Grande do Sul
(UFRGS), Porto Alegre, Brazil.
Nicoletto, Bruna Bellincanta. Life Science Knowledge Area, Universidade de Caxias do Sul (UCS),
Caxias do Sul, Brazil.
Pedrollo, Elis Forcellini. Faculdade de Medicina, Universidade Federal do Rio Grande do Sul (UFRGS),
Porto Alegre, Brazil.
Carpes, Larissa Salomoni. Faculdade de Medicina, Universidade Federal do Rio Grande do Sul
Coloretti, Natalia Gomes. Faculdade de Medicina, Universidade Federal do Rio Grande do Sul (UFRGS),
Krolikowski, Thaiana Cirino. Faculdade de Medicina, Universidade Federal do Rio Grande do Sul
Souza, Gabriela Correa. Department of Nutrition, Faculdade de Medicina, Universidade Federal do Rio
Grande do Sul (UFRGS), Porto Alegre, Brazil.
Goncalves, Luiz Felipe Santos. Division of Nephrology, Hospital de Clinicas de Porto Alegre, Porto
Alegre, Brazil.
Manfro, Roberto Ceratti. Division of Nephrology, Hospital de Clinicas de Porto Alegre, Porto Alegre,
Brazil.
Canani, Luis Henrique. Faculdade de Medicina, Universidade Federal do Rio Grande do Sul (UFRGS),
Canani, Luis Henrique. Division of Endocrinology, Hospital de Clinicas de Porto Alegre, Porto Alegre,
Brazil.
Female
Humans
*Intercellular Signaling Peptides and Proteins/bl [Blood]
Kidney Failure, Chronic/bl [Blood]
*Kidney Failure, Chronic
Male
Middle Aged
Progranulins
Time Factors
Abstract
BACKGROUND: The adipokine progranulin has metabolic proprieties, playing a role in obesity and
insulin resistance. Its levels seems to be dependent of renal function, since higher progranulin concentration
is observed in patients with end-stage kidney disease. However, the effect of kidney transplantation on
progranulin remains unknown.
OBJECTIVE: To assess the serum progranulin levels in kidney transplant recipients before and after
kidney transplantation.
METHODS: Forty-six prospective kidney transplant recipients were included in this longitudinal study.
They were evaluated before transplantation and at three and twelve months after transplantation. Clinical,
anthropometric and laboratorial measurements were assessed. Progranulin was determined with enzyme-
linked immunosorbent assays.
RESULTS: Serum progranulin significantly decreased in the early period after transplantation (from
72.78 +/- 2.86 ng/mL before transplantation to 40.65 +/- 1.49 ng/mL at three months; p<0.01) and
Page 118
increased at one year (53.15 +/- 2.55 ng/mL; p<0.01 vs. three months), remaining significantly lower than
before transplantation (p<0.01) (pover time<0.01). At one year after transplantation, there was a significant
increase in body mass index, trunk fat and waist circumference compared to immediate period after
transplantation. Progranulin was associated with waist circumference and fasting plasma glucose after
adjusted for age, gender, study period, glomerular filtration rate, interleukin-6, high sensitivity C reactive
protein and adiponectin.
CONCLUSION: Progranulin serum levels are increased before transplantation and a reduction is
observed in the early period after transplantation, possibly attributed to an improvement in renal function.
At one year after transplantation, an increment in progranulin is observed, seems to be independent of
glomerular filtration, and remained significantly lower than before transplantation.
0 (GRN protein, human). 0 (Intercellular Signaling Peptides and Proteins). 0 (Progranulins).
Publication Type
Clinical Trial. Journal Article. Research Support, Non-U.S. Gov't.
Year of Publication
2018

<91>
Unique Identifier
29432668
Title
Reply to: Correspondence regarding the impact of kidney transplantation on insulin sensitivity.
Source
Transplant International. 31(4):458-459, 2018 04.
VI 1
Record Owner
Status
MEDLINE
Authors
Jorgensen MB; Hornum M; van Hall G; Bistrup C; Hansen JM; Mathiesen ER; Feldt-Rasmussen B.
Author NameID
Jorgensen, Morten B; ORCID: https://orcid.org/0000-0001-9681-3134
Authors Full Name
Jorgensen, Morten B; Hornum, Mads; van Hall, Gerrit; Bistrup, Claus; Hansen, Jesper M; Mathiesen,
Elisabeth R; Feldt-Rasmussen, Bo.
Institution
Jorgensen, Morten B. Department of Nephrology, Rigshospitalet, University of Copenhagen,
Copenhagen, Denmark.
Hornum, Mads. Department of Nephrology, Rigshospitalet, University of Copenhagen, Copenhagen,
Denmark.
van Hall, Gerrit. Clinical Metabolomics Core Facility, Clinical Biochemistry, Rigshospitalet, University
of Copenhagen, Copenhagen, Denmark.
Bistrup, Claus. Department of Nephrology, Odense University Hospital, Odense, Denmark.
Hansen, Jesper M. Department of Nephrology, Herlev Hospital, University of Copenhagen, Copenhagen,
Denmark.
Mathiesen, Elisabeth R. Department of Endocrinology, Rigshospitalet, University of Copenhagen,
Page 119
Feldt-Rasmussen, Bo. Department of Nephrology, Rigshospitalet, University of Copenhagen,
Comments
Comment on (CON)
Comment on (CON)
Blood Glucose
Diabetes Mellitus, Type 1
Humans
Insulin
*Insulin Resistance
Pancreas Transplantation
Publication Type
Letter. Comment.
Year of Publication
2018

<92>
Unique Identifier
29377325
Title
Correspondence regarding the impact of kidney transplantation on insulin sensitivity.
Source
Transplant International. 31(4):456-457, 2018 04.
VI 1
Record Owner
Status
MEDLINE
Authors
Bergfeld L; Werzowa J; Saemann M; Hecking M.
Author NameID
Bergfeld, Leon; ORCID: https://orcid.org/0000-0002-7827-7064
Authors Full Name
Bergfeld, Leon; Werzowa, Johannes; Saemann, Marcus; Hecking, Manfred.
Institution
Bergfeld, Leon. Charite Universitatsmedizin Berlin Medizinische Klinik mit Schwerpunkt Nephrologie
und Internistische Intensivmedizin, Berlin, Germany.
Werzowa, Johannes. Universitatsklinik fur Innere Medizin III, Medizinische Universitat Wien, Klinische
Abteilung fur Nephrologie & Dialyse, Vienna, Austria.
Saemann, Marcus. Universitatsklinik fur Innere Medizin III, Medizinische Universitat Wien, Klinische
Hecking, Manfred. Universitatsklinik fur Innere Medizin III, Medizinische Universitat Wien, Klinische
Comments
Comment on (CON)
Comment in (CIN)
Page 120
Blood Glucose
Diabetes Mellitus, Type 1
Humans
Insulin
*Insulin Resistance
Pancreas Transplantation
Publication Type
Letter. Comment.
Year of Publication
2018

<93>
Unique Identifier
29251576
Title
Pretransplant HbA1c and Glucose Metabolism Parameters in Predicting Posttransplant Diabetes Mellitus
and Their Course in the First 6 Months After Living-Donor Renal Transplant.
Source
Experimental & Clinical Transplantation: Official Journal of the Middle East Society for Organ
Transplantation. 16(4):446-454, 2018 08.
VI 1
Record Owner
Status
MEDLINE
Authors
Rao N; Rathi M; Sharma A; Ramachandran R; Kumar V; Kohli HS; Gupta KL; Sakhuja V.
Authors Full Name
Rao, Namrata; Rathi, Manish; Sharma, Ashish; Ramachandran, Raja; Kumar, Vivek; Kohli, Harbir Singh;
Gupta, Krishan Lal; Sakhuja, Vinay.
Institution
Rao, Namrata. From the Department of Nephrology, Postgraduate Institute of Medical Education &
Research, Chandigarh, India 160012.
Adult
Diabetes Mellitus/bl [Blood]
Diabetes Mellitus/di [Diagnosis]
Female
*Glucose Metabolism Disorders/bl [Blood]
Glucose Metabolism Disorders/co [Complications]
Glucose Metabolism Disorders/di [Diagnosis]
*Glycated Hemoglobin A/me [Metabolism]
Humans
Page 121
Insulin/bl [Blood]
*Insulin Resistance
Insulin-Secreting Cells/me [Metabolism]
Kidney Failure, Chronic/di [Diagnosis]
*Living Donors
Male
Risk Factors
Time Factors
Treatment Outcome
Abstract
OBJECTIVES: Posttransplant diabetes mellitus is a common and serious metabolic complication after
renal transplant. Patients with uremia are known to have abnormal glucose metabolism characterized by
insulin resistance and defects in insulin secretion, which are ameliorated to some extent with renal
replacement therapy and more so with renal transplant. However, the diabetogenicity of calcineurin
inhibitors compounds this state of dysglycemia and promotes the development of diabetes in some patients.
It is not clear whether pretransplant dysglycemia is a risk factor for posttransplant diabetes mellitus and, if
so, which between insulin resistance and pancreatic beta-cell dysfunction is a major determinant in
predicting posttransplant diabetes mellitus. Here, we examined the roles of the pretransplant oral glucose
tolerance test, glycated hemoglobin (HbA1c) levels, and homeostatic model assessment-derived insulin
resistance and beta-cell function in the prediction of posttransplant diabetes mellitus and the course of these
indexes posttransplant. Our aim was to examine the correlations between these factors and their changes
posttransplant with the development of posttransplant diabetes mellitus.
MATERIALS AND METHODS: Pretransplant fasting blood was drawn from patients for plasma
glucose, insulin, C-peptide, and HbA1c levels, which was followed by a 2-hour oral glucose tolerance test.
After transplant, patients were followed for 6 months to detect posttransplant diabetes mellitus. Serum
insulin, C-peptide, and glycated hemoglobin levels were reexamined in patients with posttransplant
diabetes mellitus at 1 and 6 months.
RESULTS: Twenty-one patients (29%) developed posttransplant diabetes mellitus. Pretransplant HbA1c
was associated with development of posttransplant diabetes mellitus (odds ratio 27.04) on logistic
regression. Homeostatic model assessment-derived insulin resistance improved significantly at 6 months
posttransplant, whereas beta-cell function remained lower than pretransplant levels in patients with
posttransplant diabetes mellitus.
CONCLUSIONS: Pretransplant HbA1c may be used as a predictive marker for posttransplant diabetes
mellitus. Insulin resistance but not beta-cell function improves in patients with posttransplant diabetes
mellitus at 6 months posttransplant.
0 (Biomarkers). 0 (Blood Glucose). 0 (Glycated Hemoglobin A). 0 (Insulin). 0 (hemoglobin A1c protein,
human).
Publication Type
Journal Article.
Year of Publication
2018

Page 122
<94>
Unique Identifier
28882358
Title
Impact of screening for metabolic syndrome on the evaluation of obese living kidney donors.
Source
American Journal of Surgery. 215(1):144-150, 2018 Jan.
VI 1
Record Owner
Status
MEDLINE
Authors
Marcusa DP; Schaubel DE; Woodside KJ; Sung RS.
Authors Full Name
Marcusa, Daniel P; Schaubel, Douglas E; Woodside, Kenneth J; Sung, Randall S.
Institution
Marcusa, Daniel P. Department of Surgery, University of Michigan, Ann Arbor, MI, USA.
Schaubel, Douglas E. Department of Biostatistics, University of Michigan, Ann Arbor, MI, USA.
Woodside, Kenneth J. Department of Surgery, University of Michigan, Ann Arbor, MI, USA.
Sung, Randall S. Department of Surgery, University of Michigan, Ann Arbor, MI, USA. Electronic
address: rssung@umich.edu.
Local Messages
Titulo en Biblioteca "Dr J.J. IZQUIERDO", " 1966 - "
Adult
*Donor Selection/mt [Methods]
Donor Selection/td [Trends]
Female
Humans
Living Donors/sn [Statistics & Numerical Data]
*Living Donors
Logistic Models
Male
Metabolic Syndrome/et [Etiology]
*Obesity/co [Complications]
Practice Guidelines as Topic
Risk Assessment
Risk Factors
Keyword Heading
Complex kidney donor
Kidney transplant
Living kidney donation
Metabolic syndrome
Obesity
Abstract
BACKGROUND: We report our experience with metabolic syndrome screening for obese living kidney
donor candidates to mitigate the long-term risk of CKD.
Page 123
METHODS: We retrospectively reviewed 814 obese (BMI>=30) and 993 nonobese living kidney donor
evaluations over 12 years. Using logistic regression, we explored interactions between social/clinical
variables and candidate acceptance before and after policy implementation.
RESULTS: Obese donor candidate acceptance decreased after metabolic syndrome screening began
(56.3%, 46.3%, p < 0.01), while nonobese candidate acceptance remained similar (59.6%, 59.2%, p =
0.59). Adjusting for age, gender, race, BMI, and number of prior evaluations, acceptance of obese
candidates decreased significantly more than nonobese (p = 0.025). In candidates without metabolic
syndrome, there was no significant change in how age, sex, race, or BMI affected a donor candidate's
probability of acceptance.
CONCLUSION: Metabolic syndrome screening is a simple stratification tool for centers with liberal
absolute BMI cut-offs to exclude potentially higher-risk obese candidates. Copyright © 2017 Elsevier Inc.
All rights reserved.
Publication Type
Journal Article.
Year of Publication
2018

<95>
Unique Identifier
27653449
Title
Do metabolic derangements in end-stage polycystic kidney disease differ versus other primary kidney
diseases?.
Source
Nephrology. 23(1):31-36, 2018 Jan.
VI 1
Record Owner
Status
MEDLINE
Authors
Jankowska M; Qureshi AR; Barany P; Heimburger O; Stenvinkel P; Lindholm B.
Authors Full Name
Jankowska, Magdalena; Qureshi, Abdul Rashid; Barany, Peter; Heimburger, Olof; Stenvinkel, Peter;
Lindholm, Bengt.
Institution
Jankowska, Magdalena. Division of Renal Medicine and Baxter Novum, Karolinska Institutet, Stockholm,
Sweden.
Jankowska, Magdalena. Department of Nephrology, Transplantology and Internal Medicine, Medical
University of Gdansk, Poland.
Qureshi, Abdul Rashid. Division of Renal Medicine and Baxter Novum, Karolinska Institutet,
Stockholm, Sweden.
Barany, Peter. Division of Renal Medicine and Baxter Novum, Karolinska Institutet, Stockholm, Sweden.
Heimburger, Olof. Division of Renal Medicine and Baxter Novum, Karolinska Institutet, Stockholm,
Sweden.
Stenvinkel, Peter. Division of Renal Medicine and Baxter Novum, Karolinska Institutet, Stockholm,
Sweden.
Page 124
Lindholm, Bengt. Division of Renal Medicine and Baxter Novum, Karolinska Institutet, Stockholm,
Sweden.
Adult
Aged
Bone Density
Female
Humans
Inflammation Mediators/bl [Blood]
Insulin/bl [Blood]
Insulin Resistance
Insulin-Like Growth Factor I/me [Metabolism]
Kaplan-Meier Estimate
*Kidney Failure, Chronic/et [Etiology]
Kidney Failure, Chronic/mo [Mortality]
Male
Middle Aged
Nutritional Status
Phenotype
Polycystic Kidney, Autosomal Dominant/bl [Blood]
*Polycystic Kidney, Autosomal Dominant/co [Complications]
Polycystic Kidney, Autosomal Dominant/mo [Mortality]
Polycystic Kidney, Autosomal Dominant/th [Therapy]
Renal Dialysis
Risk Factors
Time Factors
Treatment Outcome
Young Adult
Keyword Heading
Autosomal dominant polycystic kidney disease
end-stage renal disease
inflammation
insulin resistance
Abstract
AIM: Autosomal dominant polycystic kidney disease (ADPKD), a systemic disorder caused by mutation
in genes encoding polycystins, has been reported to lead to metabolic derangements including new-onset
diabetes mellitus after kidney transplantation. We analyzed markers of insulin resistance (IR),
inflammation, nutritional status and insulin-like growth factor-1 (IGF-1) in end-stage renal disease (ESRD)
patients with ADPKD and ESRD patients with other primary kidney diseases.
METHODS: In a post hoc cross-sectional analysis in 254 non-diabetic CKD 5 patients starting on
dialysis, glucose metabolism (insulin, IGF-1, homeostasis model assessment of IR, HOMA-IR),
inflammation (high sensitivity C-reactive protein, interleukin-6, and tumour necrosis factor), nutritional
status, and bone mineral density (BMD), were assessed. Survival was recorded for median time of 28
months (IQR 15-48 months).
RESULTS: Neither indices of IR, nor IGF-1, inflammatory status, nutritional status, or BMD were
different in patients with ADPKD as compared to other aetiologies of ESRD. Kaplan-Meier curves showed
better survival among the ADPKD group versus other aetiologies, even after an exclusion of diabetic
patients.
Page 125
CONCLUSIONS: The ESRD phenotype did not differ in ADPKD versus other primary kidney diseases
in terms of markers of IR, inflammation, and nutritional status. This argues against the proposition that
ADPKD patients are more prone to develop metabolic derangements beyond those generally observed in
advanced CKD. However, additional studies are warranted to further elucidate systemic metabolic aspects
of ADPKD. Copyright © 2016 Asian Pacific Society of Nephrology.
0 (Biomarkers). 0 (Blood Glucose). 0 (IGF1 protein, human). 0 (Inflammation Mediators). 0 (Insulin).
67763-96-6 (Insulin-Like Growth Factor I).
Publication Type
Comparative Study. Journal Article. Observational Study.
Year of Publication
2018

<96>
Unique Identifier
29333450
Title
RBP4: A Culprit for Insulin Resistance in End Stage Renal Disease That Can Be Cleared by
Hemodiafiltration.
Source
BioMed Research International. 2017:7270595, 2017.
VI 1
Record Owner
Status
MEDLINE
Authors
Grosjean F; Esposito P; Maccarrone R; Libetta C; Dal Canton A; Rampino T.
Author NameID
Grosjean, Fabrizio; ORCID: https://orcid.org/0000-0001-8367-3806
Esposito, Pasquale; ORCID: https://orcid.org/0000-0002-0834-5586
Authors Full Name
Grosjean, Fabrizio; Esposito, Pasquale; Maccarrone, Rosario; Libetta, Carmelo; Dal Canton, Antonio;
Rampino, Teresa.
Institution
Grosjean, Fabrizio. Nephrology, Dialysis, Transplant, Fondazione IRCCS Policlinico San Matteo and
University of Pavia, Pavia, Italy.
Esposito, Pasquale. Nephrology, Dialysis, Transplant, Fondazione IRCCS Policlinico San Matteo and
Maccarrone, Rosario. Nephrology, Dialysis, Transplant, Fondazione IRCCS Policlinico San Matteo and
Libetta, Carmelo. Nephrology, Dialysis, Transplant, Fondazione IRCCS Policlinico San Matteo and
Dal Canton, Antonio. Nephrology, Dialysis, Transplant, Fondazione IRCCS Policlinico San Matteo and
Rampino, Teresa. Nephrology, Dialysis, Transplant, Fondazione IRCCS Policlinico San Matteo and
Adult
Page 126
Blood Glucose
Female
Gene Expression Regulation/ge [Genetics]
*Glucose Transporter Type 4/bl [Blood]
Hemodiafiltration
Humans
*Insulin Resistance/ge [Genetics]
*Kidney Failure, Chronic/bl [Blood]
Male
Middle Aged
Renal Dialysis
Retinol-Binding Proteins, Plasma/ge [Genetics]
*Retinol-Binding Proteins, Plasma/me [Metabolism]
Abstract
Introduction: Retinol Binding Protein 4 (RBP4) is mainly excreted by the kidney and plays a pivotal role
in insulin resistance (IR). In our study, we evaluated the association between RBP4 and IR in hemodialysis
subjects (HD). We also assessed how circulating RBP4 could be influenced by kidney transplant or
different dialytic techniques.
Methods: RBP4 serum levels were evaluated in HD (n = 16) and matched healthy controls (C; n = 16).
RBP4 and glucose transporter type 4 (GLUT4) mRNA expressions were also determined in adipose tissue.
Circulating RBP4 was evaluated after kidney transplant (n = 7) and in hemodialysis patients (n = 10)
enrolled in a cross-over study treated with standard bicarbonate dialysis (BD) or hemodiafiltration (HDF).
Results: HOMA index (P < 0.05) and serum RBP4 (P < 0.005) were higher in HD compared to C. RBP4
levels positively correlated with fasting serum glucose (P < 0.05). RBP4 mRNA was lower in HD
compared to C (P < 0.05) and positively correlated with kidney function (P < 0.05) and GLUT4 mRNA (P
< 0.001). Transplant or HDF reduced circulating RBP4 (P < 0.01 and P < 0.05, resp.). Our results
demonstrate that IR is associated with high circulating RBP4 and that suppressed RBP4 adipose tissue
expression is accompanied by reduced GLUT4 expression in HD. Renal transplantation or HDF are
effective in lowering serum RBP4 levels.
0 (Blood Glucose). 0 (Glucose Transporter Type 4). 0 (RBP4 protein, human). 0 (Retinol-Binding
Proteins, Plasma). 0 (SLC2A4 protein, human).
Publication Type
Journal Article.
Year of Publication
2017

<97>
Unique Identifier
29207225
Title
[ASSOCIATION BETWEEN VERTEBRAL FRACTURES AND VASCULAR CALCIFICATIONS].
[Review] [Italian]
Original Title
Associazione tra fratture vertebrali e calcificazioni vascolari.
Source
Giornale Italiano di Nefrologia. 34(Nov-Dec), 2017 Dec 05.
Page 127
VI 1
Record Owner
Status
MEDLINE
Authors
Piscopo G; Morrone L.
Authors Full Name
Piscopo, Giovanni; Morrone, Luigi.
Institution
Piscopo, Giovanni. UOC Nefrologia, Dialisi e Trapianto, AOU Policlinico, Bari.
Morrone, Luigi. UOC Nefrologia e Dialisi, Ospedale SS Annunziata, Taranto.
Aged
Aged, 80 and over
*Aortic Diseases/ep [Epidemiology]
*Calcinosis/ep [Epidemiology]
Cardiovascular Diseases/ep [Epidemiology]
Causality
Chronic Kidney Disease-Mineral and Bone Disorder/et [Etiology]
Comorbidity
Female
*Fractures, Spontaneous/ep [Epidemiology]
Fractures, Spontaneous/et [Etiology]
Humans
Male
Middle Aged
Multicenter Studies as Topic
Osteoporosis/ep [Epidemiology]
Prospective Studies
Renal Dialysis/ae [Adverse Effects]
*Renal Insufficiency, Chronic/ep [Epidemiology]
Renal Insufficiency, Chronic/th [Therapy]
Risk
*Spinal Fractures/ep [Epidemiology]
Spinal Fractures/et [Etiology]
Keyword Heading
Chronic Kidney Disease
Vertebral fractures
mortality
vascular calcifications
Abstract
Several cross-sectional and prospective studies highlight the existence of an association between bone
fractures and abdominal aortic calcifications, especially if particularly severe and independent from
confounders such as aging, smoking habits and diabetes. This phenomenon affects not only the general
population but also patients with chronic kidney disease in which cortical bone lesions are prevalent.
Moreover, bone fractures and aortic calcifications have been proved to be linked to increased
cardiovascular morbidity and mortality, both in the general populations and in patients with chronic kidney
disease, who notoriously show elevated cardiovascular risks. Therefore, diagnostic investigations about
bone fractures and abdominal aortic calcifications, particularly in patients with chronic kidney disease, may
represent a useful tool for identification of patients with a higher cardiovascular risk in order to optimize
therapies for bone metabolism disorders. Copyright by Societa Italiana di Nefrologia SIN, Rome, Italy.
Publication Type
Page 128
Year of Publication
2017

<98>
Unique Identifier
29131248
Title
Body mass index and metabolic syndrome impact differently on major clinical events in renal transplant
patients.
Source
European Review for Medical & Pharmacological Sciences. 21(20):4654-4660, 2017 Oct.
VI 1
Record Owner
Status
MEDLINE
Authors
De Giorgi A; Storari A; Forcellini S; Manfredini F; Lamberti N; Todeschini P; La Manna G; Manfredini
R; Fabbian F.
Authors Full Name
De Giorgi, A; Storari, A; Forcellini, S; Manfredini, F; Lamberti, N; Todeschini, P; La Manna, G;
Manfredini, R; Fabbian, F.
Institution
De Giorgi, A. Department of Medical Sciences, School of Medicine, University of Ferrara, Italy.
degiorgialfredo@libero.it.
Adult
Aged
Body Mass Index
Cardiovascular Diseases/di [Diagnosis]
Cardiovascular Diseases/et [Etiology]
Cardiovascular Diseases/mo [Mortality]
Cause of Death
Female
Graft Rejection/di [Diagnosis]
Graft Rejection/mo [Mortality]
Humans
Male
Metabolic Syndrome/pa [Pathology]
Middle Aged
Obesity/co [Complications]
Risk Factors
Survival Analysis
Abstract
Page 129
OBJECTIVE: Kidney transplant recipients (KTRs) are bound to develop cardiovascular disease (CVD),
and obesity represents a well-known risk factor for CVD. It has been reported that the metabolic syndrome
(MetS) is a frequent finding in KTRs, and MetS could develop even if body mass index (BMI) is only
mildly increased. We compared the impact of BMI and MetS on the development of major clinical events
(MCEs) in a cohort of 107 KTRs during a follow-up of 63 +/- 31 months.
PATIENTS AND METHODS: Clinical characteristics were recorded at the time of enrollment and
patients were classified on the basis of MCEs development. In a Cox model, MCEs were the dependent
variable while age, sex, history of CVD, glomerular filtration rate, length of dialysis pre-transplantation,
BMI classes and diagnosis of MetS were independent variables. Patients were classified into 3 groups:
normal (BMI < 25 kg/m2), overweight (BMI of 25 to 30 kg/m2) and obese (BMI > 30 kg/m2).
RESULTS: During follow-up, 55 MCEs were recorded: 16 patients died (15%), 19 (18%) had major
cardiovascular events (CVEs), and 20 (19%) started dialysis due to graft failure. KTRs who had MCEs (n =
42) were older, had a lower renal function, longer dialysis vintage pre-transplantation, higher prevalence of
history of CVD and higher BMI than those without MCEs. Cox regression analysis showed that length of
dialysis pre-transplantation, renal function, previous CVD, and BMI classes (overweight and obesity) were
related to MCEs.
CONCLUSIONS: BMI, but not MetS, predicted MCEs in KTRs as well as non-traditional CVD risk
factors such as length of dialysis pre-transplantation and graft function. Thus, a simple evaluation during
clinic visits could identify KTRs at high risk for MCEs.
Publication Type
Journal Article.
Year of Publication
2017

<99>
Unique Identifier
28967791
Title
Adipose tissue DNA methylome changes in development of new-onset diabetes after kidney
transplantation.
Source
Epigenomics. 9(11):1423-1435, 2017 11.
VI 1
Record Owner
Status
MEDLINE
Authors
Baheti S; Singh P; Zhang Y; Evans J; Jensen MD; Somers VK; Kocher JA; Sun Z; Chakkera HA.
Authors Full Name
Baheti, Saurabh; Singh, Prachi; Zhang, Yun; Evans, Jared; Jensen, Michael D; Somers, Virend K; Kocher,
Jean-Pierre A; Sun, Zhifu; Chakkera, Harini A.
Institution
Baheti, Saurabh. Division of Biomedical Statistics & Informatics, Mayo Clinic, Rochester, MN, USA.
Singh, Prachi. Department of Cardiovascular Medicine, Mayo Clinic, Rochester, MN, USA.
Zhang, Yun. Division of Biomedical Statistics & Informatics, Mayo Clinic, Rochester, MN, USA.
Page 130
Zhang, Yun. Department of Biostatistics & Computational Biology, University of Rochester, Rochester,
NY, USA.
Evans, Jared. Division of Biomedical Statistics & Informatics, Mayo Clinic, Rochester, MN, USA.
Jensen, Michael D. Division of Endocrinology, Mayo Clinic, Rochester, MN, USA.
Somers, Virend K. Department of Cardiovascular Medicine, Mayo Clinic, Rochester, MN, USA.
Kocher, Jean-Pierre A. Division of Biomedical Statistics & Informatics, Mayo Clinic, Rochester, MN,
USA.
Sun, Zhifu. Division of Biomedical Statistics & Informatics, Mayo Clinic, Rochester, MN, USA.
Chakkera, Harini A. Divisions of Nephrology & Hypertension, Mayo Clinic, Arizona, AZ, USA.
*Adipose Tissue/me [Metabolism]
Adult
Aged
*DNA Methylation
*Diabetes Mellitus/ge [Genetics]
Diabetes Mellitus/me [Metabolism]
Female
Genome, Human
Humans
Male
Middle Aged
Keyword Heading
*DNA methylation
*RRBS
*adipose tissue
*new-onset diabetes after transplant
Abstract
AIM: New-onset diabetes after kidney transplant (NODAT) adversely impacts kidney allograft and
patient survival. Epigenetic alterations in adipose tissue like DNA methylation may play a contributory
role.
METHODS: Adipose tissue DNA of the patients with NODAT and their age, sex and BMI matched
controls (nine each) were sequenced by reduced representation bisulfite sequencing. Differentially
methylated CpGs (DMCs) and differentially methylated regions (DMRs) were studied.
RESULTS: Adipose tissue from the patients had reduced DNA methylation in intergenic and intronic
regions. DMCs were found to be more hypomethylated in repeat regions and hypermethylated in CGIs and
promoter region. About 900 DMRs were found and their associated genes were significantly enriched in 32
pathways, the top ones of which were associated with insulin resistance and inflammation. Some DMR or
DMC genes have known T2DM associations.
CONCLUSION: Changes in DNA methylation in adipose tissue may be suggestive of future NODAT.
Publication Type
Year of Publication
2017

Page 131
<100>
Unique Identifier
28920721
Title
[Changes in carbohydrate metabolism after kidney transplantation and their effects on cardiovascular
risk]. [Hungarian]
Original Title
Vesetranszplantacio utani szenhidratanyagcsere-valtozasok es annak hatasai a cardiovascularis rizikora.
Source
Orvosi Hetilap. 158(38):1512-1516, 2017 Sep.
VI 1
Record Owner
Status
MEDLINE
Authors
Borda B; Szederkenyi E; Hodi Z; Ottlakan A; Szabo V; Lazar G.
Authors Full Name
Borda, Bernadett; Szederkenyi, Edit; Hodi, Zoltan; Ottlakan, Aurel; Szabo, Viktor; Lazar, Gyorgy.
Institution
Borda, Bernadett. Sebeszeti Klinika, Szegedi Tudomanyegyetem, Altalanos Orvostudomanyi Kar Szeged,
Semmelweis u. 8., 6720.
Szederkenyi, Edit. Sebeszeti Klinika, Szegedi Tudomanyegyetem, Altalanos Orvostudomanyi Kar
Szeged, Semmelweis u. 8., 6720.
Hodi, Zoltan. Sebeszeti Klinika, Szegedi Tudomanyegyetem, Altalanos Orvostudomanyi Kar Szeged,
Ottlakan, Aurel. Sebeszeti Klinika, Szegedi Tudomanyegyetem, Altalanos Orvostudomanyi Kar Szeged,
Szabo, Viktor. Csaladorvosi Intezet es Rendelo, Szegedi Tudomanyegyetem, Altalanos Orvostudomanyi
Kar Szeged.
Lazar, Gyorgy. Sebeszeti Klinika, Szegedi Tudomanyegyetem, Altalanos Orvostudomanyi Kar Szeged,
Adult
Biomarkers/me [Metabolism]
Blood Glucose
*Cardiovascular Diseases/me [Metabolism]
*Diabetes Mellitus, Type 2/me [Metabolism]
Female
Humans
Hypoglycemic Agents/tu [Therapeutic Use]
Insulin Resistance
Kidney Failure, Chronic/me [Metabolism]
Male
Middle Aged
Keyword Heading
cardiovascular risk factors
cardiovascularis riziko
new onset diabetes mellitus
vesetranszplantacio
ujonnan kialakult diabetes mellitus
Abstract
Page 132
INTRODUCTION: Cardiovascular disease is the major cause of deaths after transplantation, with diabetes
mellitus being the main risk factor in development.
AIM: The aim of our study was to assess the prevalence of new onset diabetes mellitus in connection
with the cardiovascular risk predicted by the HEART Score.
METHOD: 44 patients were involved in our study; after overview of baseline data, OGTT was
performed, followed by patient classification into the following groups: normal, impaired fasting
glucose/impaired glucose tolerance, and new onset diabetes mellitus. Insulin resistance and kidney function
were also assessed.
RESULTS: Concerning baseline data, cold ischemic time (p = 0.016), body weight (p = 0.035), BMI (p =
0.025), and HbA1C (p = 0.0024) proved to be significantly different between normal and diabetic patients.
Significant difference was found based on HOMA IR between the two groups 1.69+/-0.51 vs 6.46+/-1.42;
p = 0.0017). Based on the HEART Score, patients with new onset diabetes mellitus were put into Group 3,
which also reflects the risk which diabetes carries for the development of cardiovascular diseases.
CONCLUSION: Cardiovascular risk can be decreased with increased allograft survival by early
diagnosis and management of diabetes. Orv Hetil. 2017; 158(38): 1512-1516.
0 (Biomarkers). 0 (Blood Glucose). 0 (Hypoglycemic Agents).
Publication Type
Journal Article.
Year of Publication
2017

Page 133

Medline 1 - 100

Uploaded by

Document Information

Copyright

Available Formats

Share this document

Share or Embed Document

Sharing Options

Did you find this document useful?

Is this content inappropriate?

Copyright:

Available Formats

Medline 1 - 100

Uploaded by

Copyright:

Available Formats

Base de datos: Buscar en Ovid Medline

Link to the Ovid Full Text or citation:

Link to the Ovid Full Text or citation:

Link to the Ovid Full Text or citation:

CASE PRESENTATION: A 45-year-old Caucasian male affected by autosomal polycystic kidney

Link to the Ovid Full Text or citation:

Link to the Ovid Full Text or citation:

Link to the Ovid Full Text or citation:

Link to the Ovid Full Text or citation:

Link to the Ovid Full Text or citation:

Link to the Ovid Full Text or citation:

Link to the Ovid Full Text or citation:

METHODS: We performed a single-center retrospective study of 123 nondiabetic patients receiving a

Link to the Ovid Full Text or citation:

Link to the Ovid Full Text or citation:

Link to the Ovid Full Text or citation:

Link to the Ovid Full Text or citation:

Link to the Ovid Full Text or citation:

Link to the Ovid Full Text or citation:

Link to the Ovid Full Text or citation:

Link to the Ovid Full Text or citation:

Link to the Ovid Full Text or citation:

Link to the Ovid Full Text or citation:

Link to the Ovid Full Text or citation:

Link to the Ovid Full Text or citation:

Link to the Ovid Full Text or citation:

Link to the Ovid Full Text or citation:

Link to the Ovid Full Text or citation:

Link to the Ovid Full Text or citation:

Link to the Ovid Full Text or citation:

Link to the Ovid Full Text or citation:

Link to the Ovid Full Text or citation:

Link to the Ovid Full Text or citation:

Link to the Ovid Full Text or citation:

Link to the Ovid Full Text or citation:

Link to the Ovid Full Text or citation:

Link to the Ovid Full Text or citation:

Link to the Ovid Full Text or citation:

Link to the Ovid Full Text or citation:

Link to the Ovid Full Text or citation:

Link to the Ovid Full Text or citation:

Link to the Ovid Full Text or citation:

Link to the Ovid Full Text or citation:

Link to the Ovid Full Text or citation:

Link to the Ovid Full Text or citation:

Link to the Ovid Full Text or citation:

Link to the Ovid Full Text or citation:

RESULTS: Renal transplantation resulted in an increase in eGFR of 38.6+/-18.9 mL/min/1.73 m2 as

Link to the Ovid Full Text or citation:

MATERIAL/METHODS: Fifteen non-diabetic kidney transplant recipients, receiving CyA-based

CONCLUSIONS: Tissue insulin sensitivity estimated by hyperinsulinemic, euglycaemic clamp technique

Link to the Ovid Full Text or citation:

Link to the Ovid Full Text or citation:

Link to the Ovid Full Text or citation:

Link to the Ovid Full Text or citation:

RESEARCH DESIGN AND METHODS: A total of 21 patients taking tacrolimus as primary

Link to the Ovid Full Text or citation:

Link to the Ovid Full Text or citation:

CONCLUSIONS: The OGTT-derived ISI(TX) may be a useful estimate of IS in Caucasian renal

Link to the Ovid Full Text or citation:

Link to the Ovid Full Text or citation:

Link to the Ovid Full Text or citation:

Link to the Ovid Full Text or citation:

Link to the Ovid Full Text or citation: