Abstract: PUB010
Filtration Fiasco: A Case of Tenofovir-Alafenamide False Creatinine Elevation
Session Information
Category: Acute Kidney Injury
- 101 AKI: Epidemiology, Risk Factors, and Prevention
Authors
- Johnson, Jeshanah, University of Cincinnati, Cincinnati, Ohio, United States
- Nysather, Jacob A., University of Cincinnati, Cincinnati, Ohio, United States
Introduction
Human Immunodeficiency Virus (HIV) is a viral infection most transmitted by sexual contact and injection drug use. The development of anti-retroviral therapy has positively impacted life expectancy and reduced the progression of disease.1 HIV treatment is composed of an integrase inhibitor and reverse transcriptase inhibitor.2 Commonly used Biktarvy includes Tenofovir alafenamide (TAF), a reverse transcriptase inhibitor. This case explores the effect of TAF on the interpretation and monitoring of renal function.
Case Description
We report a case of a 50-year-old male with TAF false serum creatinine (SCr) elevation. He was diagnosed with HIV on a screening test (HIV-1 viral load 10,100 copies/mL) and started on Biktarvy. Pre-therapy SCr was 1.3 mg/dL and rose to a peak of 2.3 mg/dL six months later. Evaluation for acute kidney injury was unrevealing and other historical tenofovir nephrotoxicity including proximal tubulopathy and Fanconi Syndrome were ruled out. No signs of chronic kidney disease associated abnormalities were seen. A Cystatin-C (CysC) of 1.04 mg/L (SCr 1.77 mg/dL) showing a discordance. A 24-hr creatinine clearance of 46 and 24-hr urea nitrogen of 25 for a mean GFR of 35 (3 liters of volume), aligning with SCr estimation. A Tc-99m nuclear GFR scan showing a GFR 113 mL/min/1.73sq.m aligning with the CysC eGFR. The patient’s SCr stabilized around 1.7 mg/dL. Of note, the patient remained TAF throughout evaluation and remains on treatment given disease control (HIV-1 viral load <20 copies/mL).
Discussion
TAF therapy has largely replaced previously used tenofovir disoproxil fumarate (TDF) which is associated with proximal tubular toxicity at the mitochondria. In this case, the presumed cause of SCr and CysC discordance is inhibition of creatinine secretion by unclear mechanism (e.g. trimethoprim). A small elevation in SCr of 0.1mg/dL was noted on initial clinical trials.3 Our case demonstrates the need for individualized evaluation of SCr changes in those taking TAF due to the potential clinical impact on management of HIV.