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.
- Stop diuretics and nephrotoxic medicines initially, assess volume carefully, and replace documented losses without reflexively flooding a patient with tense ascites.
- Diagnostic paracentesis is time-critical in decompensation because SBP may cause AKI without striking abdominal symptoms or fever.
- Terlipressin with albumin is specialist therapy and a bridge to recovery or transplantation, not definitive correction of advanced cirrhosis.
- The MHRA advises avoiding terlipressin in advanced renal dysfunction or ACLF grade 3 unless benefits outweigh risks and mandates respiratory monitoring.
- Renal replacement therapy follows standard emergency indications but should be planned with transplant candidacy, prognosis and the person's goals in view.
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.
Fever may be absent; new encephalopathy, hypotension, abdominal tenderness, hypothermia or unexplained decompensation can indicate infection or SBP and should trigger cultures and ascitic sampling.
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.
- Measure urine output, electrolytes and creatinine serially, seek early hepatology advice and involve nephrology for active sediment, persistent severe AKI or renal-replacement questions.
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.Albumin is not harmless volume. Pulmonary oedema and respiratory failure can occur, especially with excess exposure; monitor oxygenation, examination, fluid balance and weight, and reduce or stop if overload develops.
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.Avoid or use only when benefit clearly outweighs risk in ACLF grade 3, very advanced renal dysfunction, hypoxia or significant ischaemic disease. Monitor for respiratory failure, sepsis, hyponatraemia and cardiac, mesenteric or peripheral ischaemia.