Renal Failure

ISSN: 0886-022X (Print) 1525-6049 (Online) Journal homepage: https://www.tandfonline.com/loi/irnf20

Serum CRP Levels in Pre-Dialysis Patients

Effat Razeghi, Sayeh Parkhideh, Farrokhlagha Ahmadi & Patricia Khashayar

To cite this article: Effat Razeghi, Sayeh Parkhideh, Farrokhlagha Ahmadi & Patricia Khashayar
(2008) Serum CRP Levels in Pre-Dialysis Patients, Renal Failure, 30:2, 193-198, DOI:
10.1080/08860220701810539

To link to this article: https://doi.org/10.1080/08860220701810539

Published online: 07 Jul 2009.

Submit your article to this journal

Article views: 656

View related articles

Citing articles: 10 View citing articles

Full Terms & Conditions of access and use can be found at

https://www.tandfonline.com/action/journalInformation?journalCode=irnf20
Renal Failure, 30:193–198, 2008
Copyright © Informa Healthcare USA, Inc.
ISSN: 0886-022X print / 1525-6049 online
DOI: 10.1080/08860220701810539

CLINICAL STUDY
LRNF

Serum CRP Levels in Pre-Dialysis Patients

Effat Razeghi and Sayeh Parkhideh

CRP in Patients with Chronic Renal Failure

Internal Medicine Diseases Department (Nephrology), Sina Hospital, Medical Sciences, University of Tehran, Tehran, Iran

Farrokhlagha Ahmadi
Internal Medicine Diseases Department (Nephrology), Imam Khomeini Hospital, Medical Sciences,
University of Tehran, Tehran, Iran

Patricia Khashayar
Research and Development Center, Sina Hospital, Medical Sciences, University of Tehran, Tehran, Iran

Background. An elevated serum C-reactive protein (CRP)
is strongly associated with morbidity and mortality in dialysis
patients. However, the significance of high CRP levels in
pre-dialysis patients has not been studied extensively. The aim of
this study was to determine the prevalence of elevated serum
CRP in pre-dialysis patients and to analyze its correlation with
renal function and other inflammatory and nutritional factors.
Methods. In a cross-sectional study, 100 pre-dialysis patients
who had been visited in two outpatient nephrology clinics from
2005 until 2006 and had the serum creatinine ≥ 1.5 mg/dL for at
least three months were studied. Demographic characteristics,
medications, GFR, hemoglobin, as well as inflammatory and
nutritional parameters (CRP, Albumin, Fibrinogen, Transferin,
Ferritin, TG, Chol, LDL, and HDL) were measured and com-
pared between the patients in regard to the CRP level. Results.
The mean of serum CRP level was 5.7 ± 5.1mg/L; elevated level
were reported in 17 patients (17%). Serum CRP levels was signif-
icantly correlated with GFR, albumin, fibrinogen, transferring, and
ferritin. Conclusion. Similar to the dialysis population, we
found that serum CRP was elevated in pre-dialysis patients. In
addition, a positive correlation between serum CRP levels and
several inflammatory factors was found. CRP serum level was
also negatively correlated with GFR, the indicator of renal function.
Keywords dialysis, C-reactive protein, GFR, serum albumin
Address correspondence to Patricia Khashayar, MD, Sina
Hospital, Hasan Abad Sq., Imam Khomeini St., P.O. Box 11367-
46911, Tehran, Iran; Tel./Fax: +98-21-66716546; E-mail:
patricia.kh@gmail.com
INTRODUCTION
Despite the remarkable advances in the field of
dialysis within the last 20 years, the mortality rate in
patients with end stage renal disease (ESRD) is quite high.
Cardiovascular diseases, with a mortality rate of 9%, are
the major cause of death in this group; this rate is 10–20
times higher than the normal population even after age,
gender, race, and diabetes mellitus adjustments. Such a
high rate indicates the presence of an accelerated athero-
genesis process.[1,2]
In addition to traditional risk factors of arthrosclero-
sis, uremia and dialysis-related factors may also release
the pre-inflammatory cytokines and disturb the endothe-
lial performance. It may also produce an acute or
chronic systemic inflammatory response (increase in the
C-reactive protein [CRP] level and other proathrotrombic
factors), consequently accelerating the arthrosclerosis
process. Therefore, inflammation has a major role in
arthrosclerosis in ESRD patients.[3,4]
C-reactive protein has the most important role in
the inflammatory response and is the most common
index for diagnosing inflammation. [5,6] An elevated
serum CRP is reported in 20–65% of ESRD patients
(pre-dialysis and those under hemodialysis and perito-
neal dialysis). This increase in serum CRP and other
acute-phase proteins are caused by underlying factors
that lead to acute phase responses and the activation of
the inflammatory cascade.[7,8] However, a reduction in
renal clearance of pre-inflammatory cytokines in addi-
tion to diseases and their accompanying complications,
like cardiac failure and advanced glycation end product
(AGEs) accumulation, as well as dialysis-related

193
194 E. Razeghi et al.

factors can cause inflammation and increase the serum
CRP levels in ESRD patients.[1,9,10]
Several studies have proved the relationship between
an elevated serum CRP levels and renal function (GFR
reduction), arthrosclerosis, malnutrition, low serum
albumin, anemia, low hemoglobin resistant to erythropoi-
etin, and frequent hospitalizations, as well as general mor-
bidity and mortality due to cardiovascular diseases in
patients undergoing hemodialysis or peritoneal dialy-
sis.[11,12] Few studies have been carried out to study the
correlation between the inflammation and the serum CRP
levels in pre-dialysis patients (patients with decreased
GFR who do not require dialysis or kidney transplant) and
its relationship with renal function.
The population of pre-dialysis patients consists of a
higher number of patients compared to dialysis group; as
they are different from each other in various aspects, the
potential inflammation-causing factors in pre-dialysis
patients may be different from those of dialysis patients.
Moreover, because the renal function of pre-dialysis
patients has been observed in various stages, their inflam-
matory conditions may also be different. Thus, in the
present study, the serum CRP levels and its correlation
with renal function and other inflammatory and nutritional
factors were studied in patients with chronic renal failure
referred to two outpatient nephrology clinics.
• The CRP negative group: patients with CRP <10 mg/L
• The CRP positive group: patients with serum CRP
≥10 mg/L
The data were analyzed using SPSS 10 software. Mann-
Whitney U (variables without normal distribution) and T-test
(variables with normal distribution) were used to compare
the quantitative variables between the above-mentioned
groups; chi-square test was also used for comparing qualita-
tive variables. Linear regression was used to study the corre-
lation between the two quantitative variables; amounts with
p < 0.05 were considered statistically significant.
RESULTS
One hundred pre-dialysis patients with chronic renal fail-
ure were studied; 55 of which were male. The mean age of
the patients was 55.8 ± 13.32, years, ranging between 21 and
70 years. Hypertension (65%), diabetes (33%), and unknown
etiology (23%) were the most common causes of CRF in our
cases. Table 1 outlines the underlying diseases for renal fail-
ure in these cases.
The demographic data and laboratory findings are
described in Table 2. Table 3 demonstrates the laboratory
findings in the two groups. There was no significant

MATERIALS AND METHODS Table 1

The underlying disease for renal failure in these cases
Pre-dialysis patients with a creatinine levels higher than
1.5 mg/dL for at least three months referred to two general CI 95%
Renal disease Number of
hospitals in Tehran, Iran, in 2005 were enrolled in this study. etiology patients Lower Upper
They were all older than 70 years old. Those with a positive
history of MI and CCU admission (for more than three days) DM 8 2.68 13.32
within a year prior to this study; those with a positive history HTN 40 30.39 49.61
of infectious diseases within a six-month period; those in the DM&HTN 25 16.51 33.49
active phase of vasculitis, malignancy, or amyloidosis; and GN 2 0 4.75
those administrating nitrates were excluded from the study. PKD 1 0 2.96
Idiopathic 23 14.75 31.25
The study was conducted according to the Helsinki
TB 1 0 2.96
principles. Informed consent was taken from all patients.
The nephrologists examined the patients thoroughly, and Underlying factors
Heart disease 22 13.88 30.12
demographic data, past medical history (cardiovascular
diseases), and administered medications were recorded. Drugs used
Laboratory findings, including albumin, creatinine, BUN, ASA 18 10.47 25.53
Statins 14 7.19 20.81
CRP, CBC-Diff, lipid profile, ferritin, transferrin, and
ACE Inhibitors 41 31.36 50.64
fibrinogen, were also recorded; all samples were sent to
Vitamin E 29 20.1 37.9
Tehran Noor Pathobiological Laboratory. GFR was calcu-
lated in each patient using Cockcroft-Gault formula. Serum Sex
Male 55 45.24 64.76
albumin and CRP were measured using Bromocrosol Green
Female 45 35.24 54.76
and photometry, respectively.
According to their CRP serum levels, patients were Abbreviations: GN = glomerulonephritis, PKD = polycystic
divided into two groups: kidney disease
 CRP in Patients with Chronic Renal Failure 195

Table 2
The demographic data and laboratory findings of the enrolled patients

Variables Mean Median Standard deviation Minimum Maximum

Age 55.76 60 13.32 21 70

GFR (mL/min) 32.04 28.85 16.34 5 74.7
Albumin (gr/dL) 4.25 4.3 0.65 2.1 5.4
Fibrinogen (mg/dL) 360.05 341 148.60 72 770
Transferin (mg/dL) 262.46 270 94.51 70 700
Triglycerides (mg/dL) 180.53 160 97.95 60 521
Cholesterol (mg/dL) 194.66 188.5 52.42 76 348
HDL (mg/dL) 50.91 45.5 25.20 16 188
LDL (mg/dL) 92.52 89 40.06 15 227
Hemoglobin (g/dL) 11.96 12 2.39 5.4 18.1
Ferritin (ng/mL) 238.95 133 278.33 17 2000
CRP (mg/L) 5.77 4.5 5.16 0.5 37

Table 3
The laboratory findings in the two groups (in regard with CRP levels)

CRP 10 < mg/L CRP ≥10 mg/L CI 95% of mean

difference
N = 83 N = 17
Mean
Variables Mean SD Mean SD p difference Lower Upper

Age 55.36 13.42 57.71 13.00 0.511 −2.34 −9.40 4.71

GFR (mL/min) 33.61 16.33 24.32 14.48 0.032 9.29 0.82 17.77
Albumin (gr/dL) 4.30 0.62 4.00 0.75 0.082 0.30 −0.04 0.64
Fibrinogen (mg/dL) 345.61 134.63 430.53 193.32 0.100 −84.91 −161.96 −7.87
Transferin (mg/dL) 271.88 95.41 216.47 76.85 0.027 55.41 6.47 104.35
Triglycerides (mg/dL) 184.76 102.02 159.88 74.03 0.343 24.88 −26.90 76.65
Cholesterol (mg/dL) 198.20 51.62 177.35 54.43 0.136 20.85 −6.67 48.37
HDL (mg/dL) 52.19 26.77 44.65 14.42 0.263 7.55 −5.75 20.84
LDL (mg/dL) 93.41 38.68 88.18 47.30 0.626 5.23 −16.01 26.48

difference between the demographic data of the two

groups. The mean serum CRP level of the patients was
5.8 ± 5.1 mg/L (0.5–37). Seventeen patients were diag-
nosed to be CRP positive. The findings of the present Table 4
study revealed no statistically meaningful difference The correlation between different laboratory
between the amounts of triglyceride, cholesterol, LDL, findings and CRP level
and HDL levels in either group (p > 0.05).
Table 4 shows the correlation between different labo- Variables Pearson CC p
ratory findings and CRP levels. The mean GFR in the Age 0.18 0.074
CRP-negative group was significantly lower than that in GFR (mL/min) −0.26 0.010
the CRP-positive group (<10 mg/L) (24.3 ± 14.4 mL/min Albumin (gr/dL) −0.20 0.046
vs. 33.6 ± 16.3 mL/min, p = 0.03); serum CRP level was Fibrinogen (mg/dL) 0.27 0.007
significantly correlated with GFR (r = −0.256, p = 0.01). Transferin (mg/dL) −0.31 0.002
Serum transferrin was the other factor reported to be sig- Triglycerides (mg/dL) −0.09 0.373
nificantly different between the two groups; it was Cholesterol (mg/dL) −0.20 0.045
reported to be adversely related with the serum CRP level HDL (mg/dL) −0.04 0.714
(r = −0.3, p = 0.002). It should be noted that ferritin and LDL (mg/dL) −0.05 0.601
fibrinogen were positively correlated with CRP (r = 0.3 Hemoglobin (g/dL) −0.16 0.115
Ferritin (ng/mL) 0.35 0.000
and 0.2, respectively).
196 E. Razeghi et al.
This study shows the difference between the mean
serum hemoglobin of the CRP-positive (≥10 mg/L) and
the CRP-negative (<10 mg/L) groups were not statistically
significant (11.2 ± 2.5 mg/L vs. 12.1 ± 2.3 mg/L, p = 0.2),
and the serum CRP level and hemoglobin level of patients
were not correlated (r = −0.16, p = 0.115).
The prevalence of a CRP-positive (≥10mg/L) result in
patients using ASA (11.1% vs. 18.3%, p = 0.4), statins
(14.3% vs. 17.4%, p = 0.7), ACEI (14.6% vs. 18.6%,
p = 0.6), or vitamin E (13.8 vs. 18.3%, p = 0.5) was lower
than the patients who did not use the said medications.
DISCUSSION
Activated acute phase response is shown to be preva-
lent in dialysis patients[13]; however, few researches have
studied the increase of serum CRP in pre-dialysis patients.
Various rates of increase have been shown in these stud-
ies. Panichi et al.[14] reported the increased serum CRP
(>5 mg/L) in 42% of the patients (mean creatinine clear-
ance of 36.3 ± 23.1 mL/min). Stenvinkel et al.[15] stated
that 32% of their patients (mean creatinine clearance of
7 ± 1 mL/min) to have an elevated serum CRP level (≥10 mg/
L). In another study, this rate (CRP > 6 mg/L) reached 35%
(mean creatinine clearance of 14 ± 4 mL/min).[16] The
frequency of serum CRP levels reported in the present study
was lower than the previous ones. Several reasons may
explain such discrepancy. The serum CRP was quantitatively
measured using the nephelometry method in previous studies;
thus, various figures were considered as the normal value. In
the present study, the amounts less than 10 mg/L were con-
sidered as normal; this justifies the lower frequency of
patients with elevated serum CRP levels. On the other hand,
the target population of the previous studies included patients
with a lower GFR levels and a more progressive chronic renal
failure, as compared with ours. It is noteworthy that the inci-
dence of elevated serum CRP level in Asian patients is lower
than American and Europeans.[17] The very concept indicates
that causes other than dialysis-related factors such as differ-
ences in lifestyle and nutritional habits justify the increased
serum CRP in Asian patients.[18,19]
The underlying mechanism of activated acute phase
response in pre-dialysis patients is not clearly specified.
In our study, the mean GFR in the CRP-positive group
was significantly lower than the CRP-negative group.
This indicates that any decrease in CRP clearance may
activate the acute phase response. Indeed, the inflam-
matory process and the elevated serum CRP levels in
patients with chronic renal failure reduce GFR.[1,7] Ates
and Panichi[14,20] also found a negative correlation
between the serum CRP and GRF levels; however, the
said correlation was not found in other studies.[16]
The acute phase response is set by several pre-inflam-
matory cytokines (IL-6, TNF-α, INF-β, INF-γ, IL-1).[21]
Any reduction in renal clearance of the cytokines is the
other possible cause of elevated serum CRP levels in pre-
dialysis patients. The positive correlation between creati-
nine clearance, cytokines, and their soluble receivers is
proved in various stages of renal failure.[14,22]
Creatinine clearance is introduced as an independent
factor influencing the serum CRP level of pre-dialysis
patients[20]; however, the abnormal distribution of CRP
levels in these patients, like the present study, indicates
renal dysfunction is not solely responsible for inflamma-
tory responses. As a result, other factors, including infec-
tions of teeth and gum as well as Chlamydia pneumonia,
often accompanied with renal failure may activate the
acute phase response.
Moreover, some medications administered in CRF
patients may also affect the acute phase response. Recent
studies have shown that the use of ACE inhibitors in ESRD
patients to be accompanied with significant reduction in
serum CRP levels.[23] It is also stated that taking aspirin is
correlated with serum CRP level in patients with cardiac
angina.[24] Recent studies have reported that statins have
significant anti-inflammatory effects and reduce the serum
CRP level in patients with or without renal dysfunction.[25]
Using vitamin E is also shown to be accompanied with
reduction in CRP and IL-6 levels[26]; high doses of vitamin
E decrease cardiovascular and myocardial infarction-
related mortalities.[27] On the contrary, CRP levels were not
reported to be different in our patients who used aspirin,
ACE inhibitors, statins, or vitamin E. This may be due to
the limitations of the present study: having no control
groups and not making follow-ups, on the one hand, and
enrolling patients who used different doses of the
mentioned medications, on the other, may be the reasons.
Albumin and transferrin are among the negative acute
phase proteins, the synthesis of which reduces during the
inflammation. On the contrary, ferrtin and fibrinogen are
positive acute phase proteins.[16] In our study, a statistical
negative correlation was found between the serum CRP
levels and the patients’ negative acute phase proteins,
while positive acute phase proteins were positively corre-
lated with CRP levels. This was similar to the findings of
other studies[14,16,20]; however, the negative correlation
between serum CRP and serum transferrin was only
reported in the study of Ates et al.[20]
Contrary to Ortega’s study,[16] Ates et al.[20] reported
a highly positive correlation between serum CRP and
ferritin. Stenvinkel et al.[15] reported the correlation
between serum CRP and fibrinogen levels in 109 pre-
dialysis patients. In the present study, the serum CRP level
was also highly correlated with fibrinogen and ferritin levels.
Similar to other studies, our study revealed no statistically
 CRP in Patients with Chronic Renal Failure
meaningful difference between the amounts of trigly-
ceride, cholesterol, LDL, and HDL in either of the
groups.[15,16,20]
Anemia is an independent risk factor for cardiovascu-
lar diseases and general mortality in patients with chronic
renal failure.[28] The activated acute phase response in
dialysis patients results in anemia and resistance to eryth-
ropoietin; this may be through several potential mecha-
nisms, including suppressing erythropoiesis in the bone
marrow, reducing the secretion of erythropoietin, GI
bleeding, and disorders in iron metabolism.[29] A significant
negative correlation between serum CRP and hemoglobin
levels of pre-dialysis patients was reported in the studies
of Ortega[16] and Ates.[20] However, in the present
study, the serum CRP and hemoglobin levels were not
correlated. It is possible that a more acute inflammation is
required for any remarkable decrease in serum hemoglobin
occurrence.
Similar to dialysis patients, the prevalence of elevated
serum CRP seems to be high in pre-dialysis patients.
Reducing inflammation plus routine measurement of CRP
in these patients may improve the nutritional and cardio-
vascular condition and consequently slow down the renal
failure process and extend the patients’ lifespan.
REFERENCES
1. Stenvinkel P, Alvestrand A. Inflammation in end-stage renal
disease: Sources, consequences, and therapy. Semin Dial.
2002;15(5):329–337.
2. Nube M. The acute phase response in chronic hemodialysis
patients: A marker of cardiovascular disease? Nephrol Dial
Transplant. 2002;17:19–23.
3. Rattazzi M, et al. New markers of accelerated atherosclerosis
in end stage renal disease. J Nephrol. 2003;16:11–20.
4. Kaysen GA, Eiserich JP. Characteristics and effects of
inflammation in end-stage renal disease. Semin Dial.
2003;16(6):438–446.
5. Verhave JC, et al. The association between atherosclerotic
risk factors and renal function in the general population. Kid-
ney Int. 2005;67:1967–1973.
6. Park JS, Kim SB. C-reactive protein as a cardiovascular risk
factor and its therapeutic implications in end-stage renal dis-
ease patients. Nephrology. 2003;8:S40–S44.
7. Vidt DG. Inflammation in renal disease. Am J Cardiol.
2006;97(2A):20A–27A.
8. Wanner C, Metzger T.C-reactive protein a marker for all-
cause and cardiovascular mortality in hemodialysis patients.
Nephrol Dial Transplant. 2002;17:29–32.
9. Lacson Jr E, Levin NW. C-reactive protein and end-stage
renal disease. Semin Dial. 2004;17(6):438–448.
10. Lacson Jr E, et al. What are the causes and consequences of
the chronic inflammatory state in chronic dialysis patients?
Semin Dial. 2000;13(3):164–166.
197
11. Busch M, et al. Potential cardiovascular risk factors in
chronic kidney disease: AGEs, total homocysteine and
metabolites, and the C-reactive protein. Kidney Int. 2004;
66:338–347.
12. Stenvinkel P. Inflammation in end-stage renal disease: The
hidden enemy. Nephrology. 2006;11:36–41.
13. Zoccali C, Benedetto FA, Mallamaci F, Tripepi G, Fermo I,
Foca A, Paroni R, Malatino LS. Inflammation is associated
with carotid atherosclerosis in dialysis patients. J Hypertens.
2000;18:1207–1213.
14. Panichi V, Migliori M, De Pietro S, Taccola D, Bianchi AM,
Norpoth M, Metelli MR, Giovannini L, Tetta C, Palla R.C
reactive protein in patients with chronic renal diseases. Ren
Fail. 2001;23(3–4):551–562.
15. Stenvinkel P, et al. Strong association between malnutrition,
inflammation, and atherosclerosis in chronic renal failure.
Kidney Int. 1999;55:1899–1911.
16. Ortega O, Gallar P, Munoz M, Rodriguez I, Carreno A, Ortiz
M, Molina A, Oliet A, Lozano L, Vigil A. Significance of
high C-reactive protein levels in pre-dialysis patients. Neph-
ron Dial Transplant. 2002;17:1105–1109.
17. Nascimento MM, Pecoits-Filho R, Lindholm B, Riella MC,
Stenvinkel P. Inflammation, malnutrition and atherosclerosis
in end stage renal disease: A global perspective. Blood Purif.
2002;20:454–458.
18. Wong JS, Port FK, Hulbert-Shearon TE, et al. Survival
advantage in Asian American end-stage renal disease
patients. Kidney Int. 1999;55:2515–2523.
19. Stenvinkel P, Lindholm B, Heimbürger O. Novel
approaches in an integrated therapy of inflammatory-associ-
ated wasting in end stage renal disease. Semin Dial. 2004;17:
505–515.
20. Ates K, Yilmaz O, Kutlay S, Ates A, Nergizoglu G, Erturk S.
Serum C-reactive protein level is associated with renal function
and it affects echocardiographic cardiovascular disease in pre-
dialysis patients. Nephron Clin Pract. 2005;101(4):c190–c197.
21. Gabay C, Kushner I. Acute-phase proteins and other systemic
responses to inflammation. N Engl J Med. 1999; 340:448–454.
22. Pecoits-Filho R, Heimbürger O, Barany P, Suliman M,
Fehrman-Ekholm I, Lindholm B, Stenvinkel P. Associations
between circulating inflammatory markers and residual renal
function in CRF patients. Am J Kidney Dis. 2003;41:1212–1218.
23. Stenvinkel P, Andersson A, Wang T, Lindholm B, Bergström J,
Palmblad J, Heimbürger O, Cederholm T. Do ACE-inhibitors
suppress tumor necrosis factor-α production in advanced
chronic renal failure? J Intern Med. 1999; 246:503–507.
24. Ridker PM, Cushman M, Stampfer MJ, Russell PT, Hennek-
ens CH. Inflammation, aspirin and the risk of cardiovascular
disease in apparently healthy men. N Engl J Med. 1999;
336:973–979.
25. Chang JW, Yang WS, Min WK, Lee SK, Park JS, Kim SB.
Effects of simulation on high-sensitivity C-reactive protein
and serum albumin in hemodialysis patients. Am J Kidney
Dis. 2002;39:1213–1217.
26. Devaraj S, Jialal I. Alpha tocopherol supplementation
decreases serum C-reactive protein and monocyte interleu-
kin-6 levels in normal volunteers and type-2 diabetic
patients. Free Radic Biol Med. 2000;29:790–792.
198 E. Razeghi et al.

27. Boaz M, Smetana S, Weinstein T, Matas Z, Gafter U, Iaina A,
Knecht A, Weissgarten Y, Brunner D, Fainaru M, Green MS.
Secondary prevention with antioxidants of cardiovascular
disease in endstage renal disease (SPACE): Randomised pla-
cebo-controlled trial. Lancet. 2000;356:1213–1218.
28. Locatelli F, Cante F, Marcelli D. The impact of haematocrit
levels and erythropoetin treatment on overall and cardiovas-
cular mortality and morbidity: The experience of the Lom-
bardy Dialysis Registry. Nephrol Dial Transplant. 1998;
13:1642–1644.
29. Stenvinkel P, Barany P. Anaemia, rHuEPO resistance, and
cardiovascular disease in end stage renal failure: Links to
inflammation and oxidative stress. Nephrol Dial Transplant.
2002;17(Suppl. 5):32–37.