Marshall University Joan C. Edwards School of Medicine Huntington, WV
Adolfo A.. Torres, BS1, Omar Almetwali, MBBCh2, Amro Altarawneh, MD2, Tejas Joshi, MD2, Yasmeen Obeidat, MD2, Wesam Frandah, MD2 1Joan C. Edwards School of Medicine, Marshall University, Hurricane, WV; 2Marshall University Joan C. Edwards School of Medicine, Huntington, WV 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 male 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 MELD-Na 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.
Disclosures: Adolfo Torres indicated no relevant financial relationships. Omar Almetwali indicated no relevant financial relationships. Amro Altarawneh indicated no relevant financial relationships. Tejas Joshi: Salix, Gilead, Echosens – Advisor or Review Panel Member, Consultant, Grant/Research Support. Yasmeen Obeidat indicated no relevant financial relationships. Wesam Frandah: Boston Scientific – Advisor or Review Panel Member, Consultant. Merritt – Consultant. Olympus corporation of America – Consultant.
Adolfo A.. Torres, BS1, Omar Almetwali, MBBCh2, Amro Altarawneh, MD2, Tejas Joshi, MD2, Yasmeen Obeidat, MD2, Wesam Frandah, MD2. P1789 - Trenbolone Enanthate-Induced Hepatorenal Dysfunction Requiring Simultaneous Liver and Kidney Transplant: A Case Report, ACG 2025 Annual Scientific Meeting Abstracts. Phoenix, AZ: American College of Gastroenterology.