Liver and Bile

Hepatology. 2024;79(5):1048–64

Premkumar M, Kajal K, Reddy KR, Izzy M, Kulkarni AV, Duseja AK, Sihag KB, Divyaveer S, Gupta A, Taneja S, De A, Verma N, Rathi S, Bhujade H, Chaluvashetty SB, Roy A, Kumar V, Siddhartha V, Singh V, Bahl A

Evaluation of terlipressin-related patient outcomes in hepatorenal syndrome-acute kidney injury using point-of-care echocardiography


Background and aims: Treatment of hepatorenal syndrome-acute kidney injury (HRS-AKI), with terlipressin and albumin, provides survival benefits, but may be associated with cardiopulmonary complications. The authors analyzed the predictors of terlipressin response and mortality using point-of-care echocardiography (POC-Echo) and cardiac and renal biomarkers. Approach: Between December 2021 and January 2023, patients with HRS-AKI were assessed with POC-Echo and lung ultrasound within 6 hours of admission, at the time of starting terlipressin (48 h), and at 72 hours. Volume expansion was done with 20% albumin, followed by terlipressin infusion. Clinical data, POC-Echo data, and serum biomarkers were prospectively collected. Cirrhotic cardiomyopathy (CCM) was defined per 2020 criteria.
Results: 140 patients were enrolled (84% men, 59% alcohol-associated disease, mean MELD-Na 25 ± standard deviation [SD] 5.6). A median daily dose of infused terlipressin was 4.3 mg/day (interquartile range, 3.9–4.6); mean duration 6.4 ± SD 1.9 days; the complete response was in 62% and partial response in 11%. Overall mortality was 14% and 16% at 30 and 90 days, respectively. Cut-offs for prediction of terlipressin non-response were cardiac variables (ratio of early mitral inflow velocity and mitral annular early diastolic tissue doppler velocity > 12.5 [indicating increased left filling pressures, C-statistic: 0.774], tissue doppler mitral velocity < 7 cm/s [indicating impaired relaxation; C-statistic: 0.791], > 20.5% reduction in cardiac index at 72 hours [C-statistic: 0.885]; p < 0.001) and pretreatment biomarkers (cystatin C > 2.2 mg/l, C-statistic: 0.640 and N-terminal brain natriuretic peptide > 350 pg/ml, C-statistic: 0.655; p < 0.050). About 6% of all patients with HRS-AKI and 26% of patients with CCM had pulmonary edema. The presence of CCM (adjusted hazard ratio [aHR] = 1.9; 95% confidence interval [CI]: 1.8–4.5, p = 0.009) and terlipressin non-response (aHR = 5.2; 95% CI: 2.2–12.2, p < 0.001) were predictors of mortality independent of age, sex, obesity, diabetes mellitus, etiology, and baseline creatinine.

Conclusions: Cirrhotic cardiomyopathy (CCM) and reduction in cardiac index, reliably predict terlipressin non-response. CCM is independently associated with poor survival in hepatorenal syndrome-acute kidney injury.

M. Premkumar, Department of Hepatology, Postgraduate Institute of Medical Education and Research, Chandigarh, India, E-Mail: drmadhumitap@gmail.com

DOI: 10.1097/hep.0000000000000691

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