BPG is committed to discovery and dissemination of knowledge
Minireviews
©The Author(s) 2025.
World J Nephrol. Dec 25, 2025; 14(4): 110414
Published online Dec 25, 2025. doi: 10.5527/wjn.v14.i4.110414
Table 1 Characteristic features of acute kidney injury in acute fatty liver of pregnancy
Feature
Description
IncidenceOccurs in 60%-70% of AFLP cases (vs < 15% in HELLP)
Clinical severityOften moderate to severe; RRT required in < 5%
Initial presentationAKI may be an early or presenting feature
Liver function testsAST/ALT: Moderately elevated (< 300 IU/L)- Bilirubin: Markedly elevated. GGT: Usually normal (↑ in viral hepatitis)
DifferentiationAFLP: Microvesicular steatosis → cholestasis → ↑ bilirubin > transaminases. HELLP/Hepatitis: Hepatocellular necrosis → ↑. AST/ALT > bilirubin- 20% of AFLP cases may overlap with HELLP- May show features of TMA
Metabolic disturbancesHyperuricemia: Markedly raised (hepatic + renal causes). Acidosis: Mixed lactic and anion gap acidosis
UrinalysisMild-moderate proteinuria in about 70%; hematuria uncommon
AKI type/urine outputNon-oliguric AKI: Common in mild/prerenal cases- Oliguric AKI (about 20%): Often from ATN or hepatorenal-like physiology. Rare postpartum cases present abruptly with oliguria and MODS
Recovery patternTypically rapid after delivery with supportive care. Most recover in 1-3 weeks. Delayed in MODS
Liver vs kidney recoveryLiver: Transaminases drop rapidly post-delivery; bilirubin and synthesis markers recover slowly. Kidney: Gradual, linear recovery
Post-recovery issuesRare delayed/biphasic recovery. Risk of second hits (sepsis, DIC, volume depletion). Temporary RRT may be needed. Usually reversible (renal cortical necrosis very rare)
Renal histopathologyCommonly ATN without glomerular/immune complex involvement; tubular fatty acid deposition reported


Write to the Help Desk