Author information

¹Toronto Centre for Liver Disease, University Health Network, Toronto, Ontario, Canada.

²Division of Nephrology, Department of Medicine, Massachusetts General Hospital, Boston, Massachusetts, USA.

³Division of Gastroenterology, Department of Medicine, University of California-San Francisco, San Francisco, California, USA.

⁴Baylor University Medical Center, Dallas, Texas, USA.

⁵Liver Center, Division of Gastroenterology, Department of Medicine, Massachusetts General Hospital, Boston, Massachusetts, USA.

⁶Department of Internal Medicine, University of Michigan Health, Ann Arbor, Michigan, USA.

⁷Division of Gastroenterology and Transplant Hepatology, Mayo Clinic, Rochester, Minnesota, USA.

⁸Section of Gastroenterology and Hepatology, Department of Medicine, Baylor College of Medicine, Houston, Texas, USA.

⁹Division of Gastroenterology and Hepatology, Indiana University School of Medicine, Indianapolis, Indiana, USA.

¹⁰Department of Transplantation, Mayo Clinic, Jacksonville, Florida, USA.

¹¹Department of Surgery, Massachusetts General Hospital, Boston, Massachusetts, USA.

¹²Division of Nephrology, Medical College of Wisconsin, Milwaukee, Wisconsin, USA.

¹³Section of Nephrology, Department of Internal Medicine, Yale University, New Haven, Connecticut, USA.

¹⁴CT and VA Connecticut Healthcare, West Haven, Connecticut, USA.

¹⁵Michael E. DeBakey Veterans Affairs Medical Center, Houston, Texas, USA.

Abstract

Background & aims: The development of acute kidney injury (AKI) in the setting of alcohol-associated hepatitis (AH) portends a poor prognosis. Whether the presence of AH itself drives worse outcomes in patients with cirrhosis and AKI is unknown.

Methods: Retrospective cohort study of 11 hospital networks of consecutive adult patients admitted in 2019 with cirrhosis and AKI. AKI phenotypes, clinical course, and outcomes were compared between AH and non-AH groups.

Results: A total of 2062 patients were included, of which 303 (15%) had AH, as defined by National Institute on Alcohol Abuse and Alcoholism (NIAAA) criteria. Patients with AH, compared to those without, were younger and had higher Model for End-stage Liver Disease-Sodium (MELD-Na) scores on admission. AKI phenotypes significantly differed between groups (p < 0.001) with acute tubular necrosis occurring more frequently in patients with AH. Patients with AH reached more severe peak AKI stage, required more renal replacement therapy, and had higher 90-day cumulative incidence of death (45% [95% CI: 39%-51%] vs. 38% [95% CI: 35%-40%], p = 0.026). Using no AH as reference, the unadjusted sHR for 90-day mortality was higher for AH (sHR: 1.24 [95% CI: 1.03-1.50], p = 0.024), but was not significant when adjusting for MELD-Na, age and sex. However, in patients with hepatorenal syndrome, AH was an independent predictor of 90-day mortality (sHR: 1.82 [95% CI: 1.16-2.86], p = 0.009).

Conclusions: Hospitalised patients with cirrhosis and AKI presenting with AH had higher 90-day mortality than those without AH, but this may have been driven by higher MELD-Na rather than AH itself. However, in patients with hepatorenal syndrome, AH was an independent predictor of mortality.