Confirm AKI + exclude mimics
- Look for infection, bleeding, true hypovolemia and nephrotoxins
- Exclude obstruction, abdominal hypertension and structural renal injury
- Urine sodium/FENa alone do not reliably distinguish HRS
Exclude reversible/structural causes, treat precipitating infection or volume loss, then use albumin plus an appropriate vasoconstrictor while monitoring respiratory safety and transplant candidacy.
Cirrhosis + progressive AKI: exclude reversible/structural causes before labeling HRS-AKI
HRS-AKI is a diagnosis made after active exclusion and correction of competing causes; response to therapy must be reassessed continuously.
In cirrhosis with ascites and AKI, rapidly evaluate infection, GI/other bleeding, true hypovolemia, nephrotoxins, obstruction, abdominal hypertension and structural kidney injury. Urine sodium/FENa are often low in cirrhosis and cannot reliably distinguish HRS from other AKI.
Treat the precipitant, stop nephrotoxins and optimize effective circulating volume. In an appropriate HRS-AKI phenotype, use albumin with a vasoconstrictor: terlipressin where appropriate/available, or norepinephrine as an effective ICU alternative. Midodrine plus octreotide is generally less effective when these options are available.
Before and during terlipressin, assess oxygenation and volume status. Avoid or stop/escalate review in clinically important hypoxemia or evolving respiratory failure, and avoid excessive albumin/volume loading; terlipressin-associated respiratory failure risk is greatest in advanced illness and volume overload.
Current ADQI/ICA HRS-AKI diagnostic and management consensus.
AASLD ascites/HRS management guidance.
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