2011
DOI: 10.1155/2011/354908
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Tenofovir Nephrotoxicity: 2011 Update

Abstract: Tenofovir is an acyclic nucleotide analogue reverse-transcriptase inhibitor structurally similar to the nephrotoxic drugs adefovir and cidofovir. Tenofovir is widely used to treat HIV infection and approved for treatment of hepatitis B virus. Despite initial cell culture and clinical trials results supporting the renal safety of tenofovir, its clinical use is associated with a low, albeit significant, risk of kidney injury. Proximal tubular cell secretion of tenofovir explains the accumulation of the drug in t… Show more

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Cited by 203 publications
(282 citation statements)
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References 75 publications
(120 reference statements)
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“…Adverse events of tenofovir treatment was reported in clinical studies as nausea; headache; nasopharyngitis; fatigue; abdominal and back pain; increase of ALT, AST, serum amylase, serum creatinine, and serum creatine kinase (34,35).…”
Section: Discussionmentioning
confidence: 99%
“…Adverse events of tenofovir treatment was reported in clinical studies as nausea; headache; nasopharyngitis; fatigue; abdominal and back pain; increase of ALT, AST, serum amylase, serum creatinine, and serum creatine kinase (34,35).…”
Section: Discussionmentioning
confidence: 99%
“…Paediatric data on TDF renal toxicity are also controversial, showing conflicting results from no renal dysfunction to increased rates of proteinuria and hypophosphataemia 124. Extrapolating from adult studies showing that renal dysfunction is associated with increased TDF plasma levels and PI use 125, dosing accuracy and meticulous attention to monitoring for renal dysfunction in children, especially in those who are on concomitant PIs, are of particular importance.…”
Section: Drug Toxicities and Interactionsmentioning
confidence: 99%
“…Proximal tubular dysfunction causes a partial or complete Fanconi syndrome with metabolic acidosis and increased phosphate loss, both of which contribute to bone demineralisation. Tenofovir also reduces calcitriol synthesis in proximal tubular mitochondria, contributing to bone demineralisation [41]. BMD decline begins after 12-24 weeks and has been noted after up to 144 weeks on therapy.…”
Section: Discussionmentioning
confidence: 99%