S5485 Trenbolone Enanthate-Induced Hepatorenal Dysfunction Requiring Simultaneous Liver and Kidney Transplant: A Case Report

Introduction: Trenbolone Enanthate, a potent anabolic-androgenic steroid (AAS) not approved for human use, has gained popularity in the fitness community. Although hepatotoxicity from AAS is recognized, trenbolone-associated severe liver injury and secondary renal failure requiring multiorgan transplantation is rarely reported. This case illustrates the clinical complexity and life-threatening complications of trenbolone-induced drug-induced liver injury (DILI) and bile cast nephropathy. Case Description/Methods: A 40-year-old man with a history of treated hepatitis C presented with jaundice, dark urine, light-colored stools, and early satiety. He reported a recent 7-week course of trenbolone enanthate, along with creatine monohydrate, whey protein, and “liver detox” supplements. Despite no recent alcohol intake or infection, labs revealed severe transaminasemia, hyperbilirubinemia, and progressive renal impairment. Imaging showed hepatosplenomegaly and portal hypertension. Liver biopsy revealed marked cholestasis, sinusoidal dilatation, and cholangitis-like changes, consistent with mixed hepatocellular and cholestatic injury. Concurrent renal dysfunction was attributed to bile cast nephropathy, a rare complication of severe cholestasis. His Model for End-Stage Liver Disease-Sodium score peaked at 40. Due to rapid decompensation, he underwent simultaneous liver-kidney transplantation. Post-transplant, the patient demonstrated marked improvement in hepatic and renal function under standard immunosuppression. Discussion: This case exemplifies a rare but serious complication of anabolic steroid use: dual organ failure requiring transplantation. Histologic findings of bland cholestasis, cholangitis-like changes, and bile cast nephropathy reflect the multifactorial injury induced by Trenbolone, potentially involving impaired bile salt export, oxidative stress, and disrupted hepatocyte transporter activity. The absence of alternative etiologies, combined with the histologic pattern and timing of exposure, supported causality. Given the growing accessibility of non-regulated AAS, clinicians should consider this diagnosis in young patients with acute liver injury, even without overt substance abuse history. Early diagnosis, multidisciplinary management, and cessation of the offending agent are critical to prevent irreversible organ damage. This case adds to the limited literature on injectable AAS toxicity and underscores the need for public education and tighter regulation.