Tenofovir-Related Nephrotoxicity: Case Report and Review of the Literature

Christopher W. James, Pharm.D.; Mary C. Steinhaus, A.N.P.; Susan Szabo, M.D.; Robert M. Dressler, M.D.


Pharmacotherapy. 2004;24(3) 

In This Article

Case Report

A 54-year-old man who came to the outpatient clinic was diagnosed with new-onset renal insufficiency. He had been diagnosed with HIV infection 12 years earlier. His medical history was also significant for hypertension, which had been well controlled with lisinopril 10 mg/day for over 2.5 years. His HIV infection was well controlled with a drug regimen consisting of lopinavir-ritonavir, nevirapine, stavudine, and lamivudine, all of which were started a little over 2 years before his clinic visit.

Approximately 7 months before his clinic visit, the patient developed peripheral neuropathy. At that time, the patient's CD4+ count was 402 cells/mm3 and his HIV RNA was less than 50 copies/ml. Stavudine was discontinued and tenofovir 300 mg/day was begun; the other antiretroviral agents were continued. The patient's renal function was within normal limits, with blood urea nitrogen (BUN) and serum creatinine levels of 18 and 1.2 mg/dl, respectively. Urinalysis 2 months later was also within normal limits.

At the patient's clinic visit, 7 months after the start of tenofovir therapy, his BUN level had increased to 40 mg/dl (normal range 8-22 mg/dl) and serum creatinine level to 3.0 mg/dl (0.8-1.3 mg/dl). Urinalysis revealed protein 2+, glucose 1 g/dl, and hyaline and granular casts. Serum carbon dioxide had decreased to 20 mEq/L (24-32 mEq/L). The patient's HIV infection remained well controlled, with a CD4+ count of 536 cells/mm3 and HIV RNA less than 50 copies/ml. Lisinopril was discontinued, but 1 week later, BUN and serum creatinine levels were 35 and 2.7 mg/dl, respectively.

A month after the patient's clinic visit, urinalysis still revealed protein 2+, glucose 1 g/dl, and hyaline and granular casts. Further laboratory analysis showed a serum glucose level of 71 mg/dl (normal range 70-120), uric acid 2.0 mg/dl (3.8-8.0), and phosphorus 2.0 mg/dl (2.5-4.5). We suspected that tenofovir was contributing to the patient's renal insufficiency, leading to renal losses of phosphate, glucose, uric acid, and protein. Thus, drug-induced Fanconi's syndrome was considered, and tenofovir was discontinued. Antiretroviral therapy was modified with the restart of stavudine; the other agents were continued.

The patient's BUN and serum creatinine levels began to improve 1 week after tenofovir was stopped, and continued to return to normal along with other laboratory parameters. At 12 weeks, laboratory values demonstrated a BUN level of 23 mg/dl, serum creatinine 1.6 mg/dl, phosphorus 2.8 mg/dl, uric acid 3.7 mg/dl, carbon dioxide 28 mEq/L, and glucose 79 mg/dl; urinalysis was negative for protein and glucose. After modification of antiretroviral therapy, the patient's viral load remained undetectable (< 50 copies/ml) and his CD4+ count was stable at 272 cells/mm3.


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