Hepatorenal syndrome–AKI in cirrhosis persisting after vasoconstrictor therapy: what to do next

Clinical Scenario

This protocol applies to hepatorenal syndrome–acute kidney injury (HRS-AKI) in patients with cirrhosis and ascites — specifically when rapidly developing AKI (serum creatinine rise of ≥0.3 mg/dl within two days, or ≥50% from baseline, and/or urinary output ≤0.5 ml/kg over ≥6 h, with no other evident cause such as shock or nephrotoxins) has not responded to first-line vasoconstrictor treatment.

Previous Treatment Line — Escalation Trigger

The prior regimen — norepinephrine with albumin to increase mean arterial pressure, or octreotide combined with midodrine plus albumin as alternatives to terlipressin — did not achieve the required goal: improvement in serum creatinine (HRS reversal). Failure to reach this target is the trigger for escalation to this protocol.

Protocol Direction (Partial)

The full protocol defines the definitive approach for HRS in this setting — one that targets the underlying hepatic condition rather than its haemodynamic consequences alone. The complete structured regimen is available below.

Instant Access to Structured Evidence-Based Regimens

References

DOI: 10.1016/j.jceh.2022.03.002

HRS-AKI is a rapidly developing AKI defined as an increase in serum creatine by ≥ 0.3 mg/dl within two days or ≥50% from baseline value and/or decrease in urinary output ≤0.5 ml/kg in ≥6 h in patients with cirrhosis and ascites with no other evident cause for acute renal injury such as shock or nephrotoxins.

Liver transplantation is the definitive therapy for HRS.

View source ↗