Abstract: SA-PO0539
Tenofovir-Associated Progressive Kidney Failure Reversed After Transition from Bictegravir/Emtricitabine/Tenofovir Alafenamide to Long-Acting Cabotegravir/Rilpivirine
Session Information
- CKD: Clinical - Therapies, CKM Health, Special Populations, and More
October 24, 2026 | Location: Exhibit Hall A, Convention Center
Abstract Time: 10:00 AM - 12:00 PM
Category: CKD (Non-Dialysis)
- 2202 CKD (Non-Dialysis): Clinical, Outcomes, and Trials
Authors
- Rodriguez, Yoan Ernesto, UF Health Jacksonville, Jacksonville, Florida, United States
- Couto Barbosa, Elias I., UF Health Jacksonville, Jacksonville, Florida, United States
- Heilig, Charles W., UF Health Jacksonville, Jacksonville, Florida, United States
- Jaikaransingh, Vishal, UF Health Jacksonville, Jacksonville, Florida, United States
Introduction
Tenofovir-containing antiretroviral therapy may cause acute kidney injury, proximal tubular dysfunction, and chronic kidney disease (CKD). Although tenofovir alafenamide (TAF) is considered less nephrotoxic than tenofovir disoproxil fumarate, clinically significant renal dysfunction may still occur. We report a case of progressive CKD associated with bictegravir/emtricitabine/tenofovir alafenamide (Biktarvy) that improved after transitioning to cabotegravir/rilpivirine (Cabenuva).
Case Description
A 74-year-old man with HIV, hypertension, diabetes mellitus, and CKD was referred to nephrology for worsening renal function while receiving Biktarvy. Baseline serum creatinine was 1.3–1.4 mg/dL in 2023 and progressively increased to 1.63 mg/dL by October 2024. Evaluation for alternative causes of CKD, including autoimmune and paraprotein studies, was unrevealing. Urinalysis showed minimal proteinuria with bland sediment, and the patient denied NSAID use. Nephrology raised concern for chronic tenofovir-associated nephrotoxicity.
By June 2025, creatinine increased to 1.91 mg/dL with eGFR 36 mL/min. Infectious Disease documentation acknowledged concern that Biktarvy was contributing to renal dysfunction, and therapy was transitioned to Cabenuva on July 25, 2025. Following discontinuation of tenofovir, renal function improved. Creatinine decreased to 1.39 mg/dL with eGFR 53 mL/min by October 2025 and to 1.29 mg/dL with eGFR 58 mL/min by January 2026. HIV remained well controlled with persistently undetectable viral load and stable CD4 counts.
Discussion
Tenofovir nephrotoxicity is believed to result from proximal tubular mitochondrial injury causing oxidative stress, tubular dysfunction, and tubulointerstitial fibrosis. The temporal association between tenofovir discontinuation and renal recovery, together with exclusion of alternative etiologies, supports tenofovir-associated nephrotoxicity in this patient. Although TAF-containing regimens are generally considered safer than tenofovir disoproxil fumarate, this case demonstrates that clinically significant renal dysfunction may still occur in high-risk patients. Early recognition and transition to alternative antiretroviral therapy may allow recovery of kidney function while maintaining virologic suppression.