Open AccessTenofovir alafenamide nephrotoxicity in an HIV-positive patient
Author(s) -
Tessa K. Novick,
Michael Choi,
Avi Z. Rosenberg,
Blaithin A. McMahon,
Derek M. Fine,
Mohamed G. Atta
Publication year - 2017
Publication title -
medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.59
H-Index - 148
eISSN - 1536-5964
pISSN - 0025-7974
DOI - 10.1097/md.0000000000008046
Subject(s) - tenofovir alafenamide , nephrotoxicity , medicine , prodrug , mitochondrial toxicity , tenofovir , cobicistat , fanconi syndrome , mitochondrion , rilpivirine , pharmacology , reverse transcriptase inhibitor , kidney , elvitegravir , urology , human immunodeficiency virus (hiv) , virology , antiretroviral therapy , viral load , biology , biochemistry
Rationale: Tenofovir alafenamide (TAF) is novel prodrug of Tenofovir, a nucleotide reverse transcriptase inhibitor. TAF is less nephrotoxic than its predecessor prodrug, tenofovir disoproxil fumarate (TDF). Tenofovir causes mitochondrial dysfunction and tubular injury when there is elevated accumulation in proximal tubule cells. TAF's unique pharmacokinetic profile enables provision of lower required doses for antiviral efficacy. Lower concentrations reach renal tubules minimizing intracellular accumulation and mitochondrial damage. TAF has not been associated with the histologic markers of tenofovir-associated nephrotoxicity that are seen with TDF, such as dysmorphic mitochondria in proximal tubule cells. Here, we report a patient with dysmorphic mitochondria on kidney biopsy after initiating therapy with TAF. Lessons: This case suggests that at risk individuals may experience tubular mitochondrial injury from lower concentrations of tenofovir with TAF.