CASE DISCUSSION

Presenter: Dr. Wondale (R2)

Moderator: Dr. Getachew (MD, Internist,
Nephrologist)
 Outline
• Case presentation
• Investigations
• Differentials
• AKI in pregnancy overview
• Dialysis in pregnancy
 History
• Identification
– Name: M.K Age: 28 sex: F MRN: 825225
• C/C
– Referred from Debre Markos referral hospital
• HPI
– this is 28 years old para ll (01alive, 01 END) mother who
gave birth at Debre Markos and referred from this hospital
– Complains decreased urine amount of 1 day duration
 Cont…
– She was told to have raised BP 2 wks back at DM hospital
– She has blurring of vision and epigastric pain
– She has generalized body swelling started from the leg
– She delivered at this hospital after induction and the
outcome was END
– She has excessive vaginal bleeding after delivery
– She has no cough, SOB, abnormal body movement, loss of
consciousness, diarrhea, vomiting
• She was admitted for 2 days at Debre Markos referral
hospital , transfused with 03 units of whole blood, 500ml of
NS and Lasix 40 mg IV given
• She referred with the diagnosis of AKI +
thrombocytopenia+ sever anemia+ 1st post partal day
• She has no personal history of DM, HTN, asthma and
cardiac illnes
 Physical Examination
• GA: ASL
• V/S: BP:130/80 PR:108 RR: 22 T˚: 36.7 0c
• HEENT: Pink conjunctiva and NIS
• LGS: No LAD, No breast Tenderness
• CHEST: clear and resonant
• CVS: S1 and S2 well heard, No gallop and murmur
• ABD: well contracted 20 week sized uterus,
no abdominal tenderness, no sign of fluid collection
• GUS: No active vaginal bleeding
• MSS: no edema
• CNS: COTPP GCS: 15/15
 V/S
Date Time B/P PR RR T0 Spo2
1/12/12 12PM 130/80 105 24 36.7 96
8AM 120/80 98 22 35.9 98
2 8AM 122/76 88 22 35.9 97
6PM 130/60 84 23 36.8 97
3 11PM 120/84 91 24 36.7 98
4 2:3O DLT 140/80 91 24 95
6;00DLT 115 39 38.4 91
3PM 120/80 97 38 38.7 95
6PM 110/70 95 36 94
5 9AM 140/80 85 22 35.9 98
6PM 130/80 93 24 36 97
6 9AM 120/80 85 22 36 95
3PM 130/70 93 24 36.7 97
 Investigation
CBC DATE __/12/12
Referral 1 1 2 3 4

WBC (K _____ 14.7 15.9 12.3 11.8 15.6

cells)
NEUT % ----------- 75.3 76.6 86.2 84

Hgb(g/dl) _____ 5.1 4.8 6.2 6.1 8.4

HCT % 18 15.7 13.8 17.1 24

MCV ---------- 84.4 87.7 84.2 85.7

Plt (k cells) 27 47 37 45 44 88
OFT DATE __/12/12
Referral 1 2 3 4
ALT _______ 226 156 132 35
AST _______ 277 137 88 45
ALP 281 _______ _______ 387
BUN _______ 77 _______ 105 112
Creatinine 2.62 2.8 3.65 4.24 5.67
K _______ 3.95 _______ _______ 5.5
Na _______ 128.3 _______ _______
Cl _______ 104.2 _______ _______
OTHERS IX
• BG&RH =O+
• U/A; ALB=+2, Blood =+3, WBC= 3-5 RBC=many,
granular cast =1-2 (4/12/12)
• B/F= No H/p
 Differential Diagnosis
• ????????
AKI IN PREGNACY

INTRODUCTION
AKI is the abrupt loss of kidney function
resulting in
 Retention of urea and other nitrogenous waste products
 Dys-regulation of extracellular volume and electrolytes.
Can be caused by any of the disorders leading
to AKI in the general population
DEFINITION
 AKI is defined by the abrupt loss of kidney function
 No agreed definition of AKI in pregnancy, but
 Investigate women with a serum creatinine of 90 µmol/l (>1 mg/dl) or
 greater or an increase within 48 hours of 44 µmol/l (0.5 mg/dl) above
baseline
 GFR increases ~50 %, resulting in a lower baseline serum
Cr
 Normal serum Cr levels (eg, 0.7 to 0.9 ) may represent
increases from baseline
EPIDEMIOLOGY
Is uncommon in the developed world
The true incidence is difficult to estimate
Higher in countries where ANC is less available and
where illegal abortions are performed.
India and Africa report incidence as high as 10 to 20 %
Egypt reported AKI requiring dialysis of only 0.6 % of
5600 deliveries
ETIOLOGIES
 AKI early <20 wks  AKI later in pregnancy
 Prerenal disease due to HEG  Severe preeclampsia
 ATN resulting from a septic  Severe preeclampsia with
abortion HELLP syndrome
 AKI associated with either  TTP- HUS
 Viral (eg, influenza) or  Acute fatty liver of
 Bacterial infection and /sepsis pregnancy
 ATN or acute cortical
necrosis associated with
hemorrhage
acute Pyelonephritis, urinary tract obstruction (less commenly),
NSAIDs
 Preeclampsia with or without HELLP
 The most common cause of AKI during pregnancy
 Preeclampsia refers to
 The new onset of hypertension and
 Proteinuria or other signs of systemic disease
 Usually after 20 weeks of gestation
 Preeclampsia complicates 3 to 5 % of all pregnancies
 GFR decreases on average by only 30 to 40 %
 AKI requiring RRT is uncommon except in pts with
 Very severe preeclampsia and
 When there is accompanying hemorrhage and ischemic ATN
 AKI is more common when PE is accompanied by features of
the HELLP
 AKI occurs in 3 to 15 percent
 The renal & extra renal abnormalities begin to resolve within
2-3 days postpartum
 Complete recovery of GFR occurs within 8 wks postpartum
 Moderately increased albuminuria may persist
 PE may be at ↑ risk of developing ESRD later in life, but the
absolute risk is small
 Thrombotic thrombocytopenic purpura or hemolytic
uremic syndrome
 Presence of microthrombi of fibrin &/or platelets in multiple organ
systems, particularly kidney & brain
 Presenting features include
 Thrombocytopenia & microangiopathic hemolytic anemia without another
apparent cause and,
 In many patients, neurologic and/or renal abnormalities
 Pregnancy may trigger either TTP or HUS
 TTP- caused by acquired or constitutional deficiency of activity of
ADAMTS13
 A Von Willebrand factor-processing protein
 Pregnancy induce the onset or relapse of ADAMTS13 deficiency
 HUS is caused by mutations in genes that encode complement-
regulatory proteins
 Pregnancy is a well-recognized trigger for episodes of HUS in
patients with these mutations
 TTP associated with ADAMTS13 deficiency occurs predominantly
in the 2nd and 3rd trimesters
 HUS more commonly occurs in the postpartum period
 AKI may occur in either TTP or HUS, (more common with HUS)
 If thrombocytopenia & hemolysis resolve but AKI persists biopsy
• Plasma exchange is an important component of treatment
of AKI due to either pregnancy-associated TTP or HUS
• If AKI fails to improve after three to five treatments with
plasma exchanges, treatment with eculizumab
• Considerations for RRT are similar to nonpregnant
adults with AKI
• BP control is important and may enhance endothelial cell
recovery
 Acute fatty liver of pregnancy
 Rare complication of Px that is associated with AKI in up to 60 %
of cases
 Pts present in the 3rd TM with clinical signs
 Consistent with preeclampsia (hypertension, thrombocytopenia)
 but also have
 Hypoglycemia, hypofibrinogenemia,
 LFT abnormalities with hyperbilirubinemia, and a
 Prolonged PTT in the absence of abruptio placentae
 Therapy consists of rx of DIC & immediate delivery of fetus
 Lab abnormalities begin to improve within 1-2 days after delivery
 Renal cortical necrosis
• Important cause of AKI associated with catastrophic obstetric
emergencies
– Placental abruption with massive hemorrhage or amniotic fluid embolism
• Quite rare in developed countries, however, and is responsible for only
1 - 2 % of all cases of AKI
• problem in parts of world where obstetric hemorrhage occurs remote
from a hospital
• Potential complication of postpartum hemorrhage
• Both primary DIC and severe renal ischemia likely cause cortical
necrosis
• Abrupt onset of oliguria or anuria following an obstetric catastrophe
• Oliguria or anuria is frequently accompanied by gross hematuria,
flank pain, and hypotension
• The triad of oliguria/anuria, gross hematuria, and flank pain is
unusual in the other causes
• Dx can usually be established by U/S or CT
• No specific therapy has been shown to be effective
• Many pts require dialysis, but 20 to 40 % have partial recovery with
a Cr clearance that stabilizes b/n 15 and 50 mL/min
 Acute pyelonephritis
• May develop at any time is more likely to occur after
20 weeks
• Diagnosis is generally made by clinical features,
urinalysis, and urine culture
• Renal function generally improves after treatment
with antibiotics
 Urinary tract obstruction
 Relaxation of ureteral smooth muscle and pressure on the
ureters by the gravid uterus
 Result in mild to moderate dilatation of the collecting systems
 This functional hydronephrosis, which tends to be more
prominent on the right
 is not usually associated with renal dysfunction
 Occasionally, obstruction of the ureters by the uterus is
sufficient to cause renal failure
 AKI resolves with relief of obstruction
 Postpartum AKI associated with nonsteroidal
anti-inflammatory drugs
• NSAIDs are routinely used for postpartum analgesia,
particularly after C/s
• uncommon, among such patients who receive
NSAIDs
• AKI may develop if there are predisposing conditions
such as volume depletion or preeclampsia
 DIAGNOSTIC APPROACH AND DDx
• Increased serum Cr above the pt’s usual baseline
• 1st exclude causes of AKI that are unrelated to px
• Careful review of the medical history and prior
laboratory values is important
• All medications should be carefully reviewed
• Hx may also suggest causes of prerenal AKI
or ATN /acute cortical necrosis
Obtain the following tests:
 Dipstick urinalysis and microscopic analysis of sediment
 24-hour urine collection or by protein-to-cr ratio
 Urine culture
 Hgb & Plt count with peripheral blood smear to evaluate for
microangiopathic hemolysis and thrombocytopenia
 Total, direct, and indirect bilirubin concentration; haptoglobin; and
LDH to evaluate for hemolysis
 AST and/or ALT
 Renal ultrasound
• In patients with urinary findings consistent with
glomerulonephritis
• C3, C4, ANA, ANCA, etc
 TREATMENT
• Treatment is targeted to the specific cause of AKI
• The treatment of AKI is supportive.
• Dialysis should be initiated based on the usual criteria
– For pts in the nonobstetric setting & particularly if oliguria
is present
 DIALYSIS IN PREGNANCY
 Improvement in the outcome of px requiring dialysis during
Px over the past 2 decades
 Most receiving ASA & calcium as preeclampsia prophylaxis
 Development of preeclampsia was the major issue
 Dialysis prescription was ↑ from baseline in all women
 Px on dialysis now have one-half to two-thirds chance of
fetal survival
 80% chance of prematurity
 Initiating Dialysis for Progressive Chronic
Kidney Disease
• Generally recommended to commence dialysis at
– eGFR below 20 ml/min or
– BUN 50 mg/dl (serum urea >17 mmol/l) and
– aim for predialysis blood urea below 15 mmol/l (BUN 45 mg/dl)
• likelihood of successful pregnancy
– dialysis initiated during Px greater than continuation of maintenance
Women Already Needing Regular Dialysis
• Childbearing age on dialysis have 1 in 20 chance of conceiving
• Need to be counseled about adequate contraception
 Dialysis Regimens in Pregnancy
 Daily hemodialysis may be necessary
 More intensive dialysis improves phosphate control
 There is no need to switch from PD to hemodialysis
 Other management necessary for a successful pregnancy
 Control of maternal BP, generally to 110 - 140/80 - 90 mm Hg
 Active management of anemia with iron and ESA
 Target hemoglobin value should be 10 to 11 g/dl
 Detection and early treatment of sepsis
 Fetal monitoring include at least U/S scans every 2 - 4 wks
 CURRENT DX & MG’T
P1; 7th post partal day • Ceftriaxone
P2: SPE • Metronidazole
P3: partial HELLP syndrome • Plasil
P4: sever Anemia 2◦ to blood loss • Cimetidine
P5: AKI 20 to ?ATN + Endometritis

Over all assessment: Improving

THANK YOU!
 Reference
• Uptodate 2018

• Comprehensive Clinical Nephrology 6th EDITION