Steroid therapy is linked to lower incidence of acute kidney injury in patients with severe alcohol-associated hepatitis

Authors

Laura Buttler, Department of Gastroenterology, Hepatology, Infectious Diseases and Endocrinology, Hannover Medical School, Carl-Neuberg-Str.1, 30625, Hannover, Germany. buttler.laura@mh-hannover.de.
Jan Stange, Center for Extracorporeal Organ Support (CEOS), Department of Nephrology, Biomedical Research Center, University of Rostock, Rostock, Germany.
Nikolaos Pyrsopoulos, Liver Disease in New Jersey, NYU Grossman School of Medicine, NYU Langone Transplant Institute, New York, USA.
Tarek Hassanein, Southern California Research Center, Coronado, CA, USA.
Heiner Wedemeyer, Department of Gastroenterology, Hepatology, Infectious Diseases and Endocrinology, Hannover Medical School, Carl-Neuberg-Str.1, 30625, Hannover, Germany.
Benjamin Maasoumy, Department of Gastroenterology, Hepatology, Infectious Diseases and Endocrinology, Hannover Medical School, Carl-Neuberg-Str.1, 30625, Hannover, Germany.
Markus Busch, Department of Gastroenterology, Hepatology, Infectious Diseases and Endocrinology, Hannover Medical School, Carl-Neuberg-Str.1, 30625, Hannover, Germany.
VTL-308 study group
David J. Kramer, Advocate Health - MidwestFollow

Recommended Citation

Buttler L, Stange J, Pyrsopoulos N, et al. Steroid therapy is linked to lower incidence of acute kidney injury in patients with severe alcohol-associated hepatitis. Sci Rep. 2025;15(1):43271. Published 2025 Dec 8. doi:10.1038/s41598-025-29912-4

Affiliations

Aurora St. Luke's Medical Center

Abstract

Acute kidney injury (AKI) is a common complication in patients with severe alcohol-associated hepatitis (sAH), yet its risk factors and outcomes remain incompletely defined. Corticosteroids are the only established therapy for sAH, but their impact on renal outcomes is unknown. A post-hoc analysis of the prospective multicenter VTL-308 trial including 151 patients with sAH was conducted to evaluate the incidence and predictors of AKI, the association of corticosteroid therapy with AKI risk, and factors associated with AKI reversal during 90 days of follow-up. AKI was independently associated with significantly higher 90-day mortality (subdistribution hazard ratio (sHR) = 8.74; p < 0.001). In multivariate competing risk analysis, higher bilirubin levels (sHR = 1.06; p = 0.003) were linked to increased AKI risk, while corticosteroids were associated with an ameliorated AKI risk (sHR = 0.47; p = 0.01). Time-censored analyses confirmed the protective association of corticosteroids (HR = 0.25; p = 0.001). Once AKI occurred, corticosteroids did not promote renal recovery (HR = 1.15; p = 0.74). Elevated bilirubin levels were linked to a lower probability of AKI reversal. In conclusion, AKI is a devastating complication in sAH. Corticosteroid therapy is independently associated with a significantly lower risk of AKI development but does not influence recovery once AKI has occurred. Future prospective trials are required to provide further validation of these findings.

Type

Article

PubMed ID

41354748