Abstract: FR-PO0625
Entecavir-Associated Fanconi Syndrome in a Liver Transplant Recipient
Session Information
- Fluid, Electrolyte, and Acid-Base Disorders: Clinical - 2
November 07, 2025 | Location: Exhibit Hall, Convention Center
Abstract Time: 10:00 AM - 12:00 PM
Category: Fluid, Electrolytes, and Acid-Base Disorders
- 1102 Fluid, Electrolyte, and Acid-Base Disorders: Clinical
Authors
- Paul, Koushik, University of Minnesota Twin Cities, Minneapolis, Minnesota, United States
- Allam, Krishna C, University of Minnesota Twin Cities, Minneapolis, Minnesota, United States
- Murray, Sean, University of Minnesota Twin Cities, Minneapolis, Minnesota, United States
- Karam, Sabine, University of Minnesota Twin Cities, Minneapolis, Minnesota, United States
Introduction
Fanconi syndrome is characterized by generalized proximal tubular dysfunction resulting in urinary losses of glucose, phosphate, uric acid, bicarbonate, and amino acids. While nucleos(t)ide analogs such as adefovir and tenofovir are well-established culprits, especially in HIV or HBV populations, Entecavir is rarely implicated. Only a single published case to date has reported acquired Fanconi syndrome within 1–2 years of Entecavir initiation. We present a case of Fanconi syndrome associated with long-term Entecavir therapy in a liver transplant recipient.
Case Description
A 60-year-old male with HBV-related cirrhosis status-post liver transplantation, chronic antibody-mediated rejection (on Tacrolimus and Prednisone), type 2 diabetes mellitus, and chronic kidney disease (baseline Creatinine (Cr) 1.4–1.6 mg/dL) presented with recurrent falls and altered mental status. Notable medications included Entecavir started 5 years prior , Voriconazole (for phaeohyphomycosis), and Atovaquone/Sulfadiazine (for disseminated toxoplasmosis). Initial laboratory workup revealed: elevated Cr (1.56 mg/dL, eGFR 51 mL/min/1.73m2), low phosphorus level (Phos) (2.1, (2.5 - 4.5 mg/dL )), hyperchloremic non-anion gap metabolic acidosis (Chloride 109 (98-107 mmol/L) , CO2 19 (22-29 mmol/L) and normal uric acid level (5.8 mg/dL). The potassium level was 4.5 mEq/L (3.4-5.3 mmol/L) and there was glucosuria (>1,000 mg/dL) with concurrent hyperglycemia (243 mg/dL). Nephrology was consulted and the patient was found to have elevated fractional excretion (Fe) of phos (FePhos 54% (< 20%)), and uric acid (FeUrate 16.4% (4-11%).
Discussion
Occurrence of hallmark features—including phosphaturia, uricosuria, and hyperchloremic metabolic acidosis—suggests a potential class effect of nucleos(t)ide analogs in susceptible individuals. Thus, clinicians should maintain a high index of suspicion for Fanconi syndrome in patients receiving long-term nucleos(t)ide analog therapy—even when using agents like Entecavir that are considered to have a lower nephrotoxic profile.