Synopsis
Detect acute kidney injury early in cirrhosis, reverse common causes, diagnose HRS-AKI carefully, and use vasoconstrictor therapy without causing respiratory or ischaemic harm.
- Small creatinine rises matter in cirrhosis because low muscle mass can conceal major loss of glomerular filtration behind a deceptively modest value.
- Common causes include hypovolaemia, sepsis or SBP, haemorrhage, over-diuresis, nephrotoxins, acute tubular injury and urinary obstruction.
- HRS-AKI describes functional renal failure in advanced liver disease after alternative explanations and lack of response to appropriate initial management are established.
Key red flags
A rising creatinine compared with a recent baseline is more informative than whether it remains inside the laboratory reference interval. Verify timing and check urine output promptly.
Investigation priorities
Confirm AKI, stage its evolution and judge response to initial measures.
Management branches
Creatinine has risen from baseline or urine output has fallen in a person with cirrhosis.
- Confirm the trend, perform ABCDE assessment, review blood pressure and losses, send blood and urine studies, obtain cultures and arrange prompt ascitic sampling when ascites is present.
- Withhold diuretics, NSAIDs and other plausible nephrotoxins, treat haemorrhage or sepsis using the appropriate emergency pathway, and replace documented volume loss with repeated clinical reassessment.
Key medicines
Human albumin solutionGive only under the decompensated-cirrhosis or transplant-centre protocol, with indication-specific dosing based on weight, clinical context and response; reassess before every further administration.
TerlipressinInitiate and titrate only through the current specialist HRS-AKI protocol; dosing and continuation depend on creatinine response, adverse effects and whether bolus or continuous infusion is selected.