Abstract: SA-PO0309
Risk of AKI Is Significantly Increased in Patients with Acute Alcoholic Hepatitis and Serum Bile Acids >150 umol/L
Session Information
- AKI: Epidemiology and Risk Factors
October 24, 2026 | Location: Exhibit Hall A, Convention Center
Abstract Time: 10:00 AM - 12:00 PM
Category: Acute Kidney Injury
- 101 AKI: Epidemiology, Risk Factors, and Prevention
Author
- Stange, Jan, University of Rostock, Rostock, MV, Germany
Background
Subjects with decompensated steatotic liver disease are at risk to develop secondary organ failures. Hypoperfusion, inflammation, increased susceptibility to infections and direct cytotoxicity of albumin bound toxins, such as bile acids, towards renal cellular structures can induce kidney injury. The aim of this research was to investigate an association between total serum bile acid concentration at baseline and development of secondary akute kidney injury (AKI).
Methods
Bile Acids of control subjects (total n=73; samples available n=28) of a prospective RCT (VTI 308- NCT02612428) including Subjects with acute alcoholic hepatitis (Exclusion criteria were intractable bleeding, sepsis, shock and creatinine>1.3 mg/dl) were measured
at baseline and bile acid levels were analyzed with respect to development of AKI, defined by an increase of creatinine by more than 0,3 mg/dl within 48 hours despite standard of care.
Results
Out of 28 subjects, 24 subjects had a total bile acid concentration of >100 umol/l (normal value<8 umol/l) and 18 had a total bile acid concentration of >150 umol/l). In latter group, the fraction developing increase of creatinine was significantly higher (15 out of 18) than the fraction where creatinine increase could be avoided by SOC (3 out of 18).
Conclusion
Subjects with therapy resistant intrahepatic cholestasis reaching total bile acid concentrations>150 umol/l are at significant risk to develop Acute Kidney Injury. Which concentration will evolve into an appropriate threshold for interventional measures to intervene (e.g. by detoxification) deserves further prospective interventional clinical studies.
Acknowledgment
The authors are grateful to Mrs. Weiss Reinig for measuring total bile salts in the sample and the entire VTI 208 Study Group.
Funding
- Government Support – Non-U.S.