AKI in pregnancy can occur early, late, or post-pregnancy due to various causes. The most common cause is preeclampsia. HELLP syndrome, a severe form of preeclampsia, can cause AKI in 3-15% of cases. TTP and HUS may also precipitate AKI. Late pregnancy complications like AFLP, abruptio placenta, and amniotic fluid embolism can result in cortical necrosis and AKI. Prompt delivery is usually indicated for severe preeclampsia and AFLP. Management involves supportive care, dialysis, and addressing the underlying etiology. Outcomes depend on the severity and etiology of AKI, with cortical necrosis carrying the

1. AKI in PREGNANCY
Dr AJISH JOHN
Consultant Nephrologist
Caritas Hospital Kottayam

2. • Pregnancy - lower baseline S Creatinine
• S Creatinine > 1mg/dL ---s/o AKI
• AKI requiring RRT about 1 in 20,000
pregnancies

3. AETIOLOGY
EARLY PREGNANCY (<20 wks)
• Prerenal due to hyperemesis gravidarum
• Ruptured ectopic pregnancy
• Septic abortion
• Infections – pyelonephritis, sepsis

4. LATE PREGNANCY(>20 wks)
• Severe Preeclampsia
• HELLP syndrome
• Acute fatty liver of pregnancy
• TTP & HUS
• Abruptio placenta, PPH, prolonged IUD, amniotic
fluid embolism, chorioamnionitis – ATN/Cortical
necrosis

5. POSTPARTUM
• Severe Preeclampsia
• HUS
• Nephrotoxic drugs
• PPH
• Sepsis

6. • Acute Pyelonephritis
• Urinary tract obstruction
• Most common cause of AKI - Preeclampsia

7. • HELLP syndrome
• TTP
• HUS
• AFLP
• Cortical Necrosis

8. HELLP Syndrome
• Severe form of Preeclampsia
• Hemolysis + elevated liver enzymes + low
platelet count
• 15-20% may not have preceding
HTN/proteinuria

9. • 10-20% of patients with severe PE/E
• 3rd trimester
• Right upper quadrant abdominal pain &
tenderness
• AKI occur in 3-15%
• Other complications – DIC, liver
hematoma, abruptio placenta, pulmonary
oedema

10. Lab diagnostic Criteria :-
• Microangiopathic hemolytic anemia
• PLC ≤ 1 lakh
• S.Bilirubin ≥ 1.2 mg/dL
• AST ≥ 70

11. Management :-
• Initial stabilisation + Decision of
termination of Pregnancy
• Prompt termination if –
≥ 34 wks of gestation
Nonreassuring foetal status
Maternal complications

12. • Antihypertensives
• IV MgSO4
• Platelet transfusion
• Role of Dexamethasone

13. TTP
• Usually in 2nd or 3rd trimester when ADAMTS 13
level is low.
• Pregnancy can precipitate relapse in patients with
history of TTP.
• Can induce onset or relapse of ADAMTS-13
deficiency related TTP.

14. • Delivery – not beneficial
• Plasma exchange
• Dialysis & Supportive treatment of AKI

15. HUS
• Near term or postpartum
• Usually 1st episode - familial or sporadic
• Relapse also can occur
• Mutations in CFH(20%) & CFI(15%)

16. • Nonimmune hemolytic anemia, severe
thrombocytopenia, severe renal
involvement
• PE/HELLP syndrome may or not be
associated – may be difficult to distinguish

17. • Delivery – not beneficial
• Plasma exchange
• Dialysis & Supportive treatment of AKI
• Eculizumab

18. • Prognosis – poor
• Maternal mortality – 20-45%
• Fetal mortality – 80%
• CKD – 45%

19. AFLP
• Rare, about 1 in 20,000 pregnancies
• Mortality – 18%
• 3rd trimester or near term
• Nausea, vomiting, abdominal pain,
anorexia, jaundice

20. • HEPATIC FAILURE – severe
transaminitis, hyperBR, elevated ALP &
GGT, hypoglycemia, raised PT/INR &
S.NH3.
• RENAL FAILURE
• May cause Pancreatitis
• Rule out Viral Hepatitis, Cholestasis of
pregnancy

21. • Inherited defect in mitochondrial beta-
oxidation of fatty acid
• Heterozygous deficiency of LCHAD (long
chain 3 hyroxyacyl CoA dehydrogenase)
• Accumulation of long & medium chain
fatty acids produced by foetus or placenta
 hepatotoxicity

22. • Prompt termination of pregnancy
• Supportive treatment of hepatic failure
• Remits postpartum with no residual hepatic
or renal impairment
• Avoid subsequent pregnancy due to high
recurrence.

23. Pregnancy AKI + TMA
• Preeclampsia/HELLP Syndrome
• TTP/HUS
• ALFP
• SLE with APLAS
• Sepsis with DIC

24. PARAMETER PE/HELLP TTP HUS AFLP
ONSET 2nd & 3RD Tt 2nd & 3RD Tt Postpartum Near term
CLINICAL FEATURES Hypertension
& proteinuria
neurological Renal failure Nausea, vomiting,
liver failure
THROMBOCYTOPENIA ++ +++ +++ -/+
FEVER - + - -
HEMOLYSIS + +++ +++ ±
COAGULOPATHY ± - - ++
HYPOGLYCEMIA - - - ++

25. PARAMETER PE/HELLP TTP HUS AFLP
HYPERTENSION ++ - - -
PROTEINURIA ++ - - -
LIVER DISEASE + - - +
↑BILIRUBIN + + + + + +
↑AST + + - - + +
AMMONIA Normal Normal Normal High
DELIVERY Recovery No effect No effect Recovery
MANAGEMENT Supportive PLEX PLEX Supportive

26. Lupus flare (vs PE) –
• low C3,C4
• Active urinary sediments
• Normal uric acid & liver enzymes
• Elevated antids DNA titer

27. CORTICAL NECROSIS
• Abruptio placenta, placenta previa,
prolonged IUD, amniotic fluid embolism,
septic abortion, severe eclampsia
• Initiating event – DIC, severe renal
ischemia

28. • Severe endothelial injury, impaired local
Nitric oxide release, accelerated thrombosis
& fibrin deposition

29. • Triad of anuria, gross hematuria, flank pain
• Xray Abdomen – renal cortical calcification
after 4-5 wks
• CECT – absent opacification of renal cortex,
enhancement of subcapsule & medulla
without excretion of contrast
• Renal Biopsy – glomerular & tubular
necrosis with Ghost like cells

30. • Prognosis – depends on extent of necrosis.
• Patchy – partial recovery, may became
dialysis independent
• Gross – dialysis dependant, Transplantation

31. Thank You