This protocol addresses Portal hypertension presenting as hepatorenal syndrome–acute kidney injury (HRS-AKI) in patients with cirrhosis and ascites — a rapidly developing, life-threatening renal complication requiring prompt, structured intervention.
HRS-AKI is defined as rapidly developing AKI with an increase in serum creatinine by ≥0.3 mg/dL within two days, or ≥50% from baseline, and/or a decrease in urinary output ≤0.5 ml/kg over ≥6 h — occurring in a patient with cirrhosis and ascites with no other evident cause such as shock or nephrotoxins.
The preferred approach combines vasoconstrictor-based pharmacotherapy with albumin as an essential adjunct, initiated early. Earlier initiation — before creatinine rises further — is the strongest positive predictor of response. The complete regimen, including agent selection and monitoring guidance, is available in the full protocol.
HRS reversal, defined as reduction in serum creatinine to below 1.5 mg/dL.
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.
Terlipressin is the most investigated drug for HRS and is the preferred first-line treatment for HRS-AKI.
Vasoconstrictors and albumin are the primary pharmacological agents for the treatment of HRS.
Vasoactive peptides for HRS should be initiated early as the most significant positive predictor of response to therapy is lower baseline creatinine.
Multiple clinical trials and meta-analyses have demonstrated the efficacy of terlipressin and albumin in HRS reversal (reduction in serum creatinine to < 1.5 mg/dL).
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