Fanconi syndrome cidofovir

Vittecoq D, Dumitrescu L, Beaufils H, and Deray G. 1997. Fanconi syndrome associated with cidofovir therapy.Anf/m/crobAgents Cbemotber 41 1846. 

Experience from clinical trials suggest that twenty five percent or more of patients receiving intravenous doses of cidofovir of 3 mg/kg or more develop ARF, often associated with a Fanconi syndrome with tubular proteinuria and evidence of proximal tubular dysfunction with glucosuria, hypophosphatemia, and urinary bicarbonate wasting, with evidence of proximal... 

Gastrointestinal complaints (eg, nausea, diarrhea, vomiting, flatulence) are the most common adverse effects but rarely require discontinuation of therapy. Other potential adverse effects include headache and asthenia. Tenofbvir-associated proximal renal tubulopathy causes excessive renal phosphate and calcium losses and 1-hydroxylation defects of vitamin D, and preclinical studies in several animal species have demonstrated bone toxicity (eg, osteomalacia). Monitoring of bone mineral density should be considered with long-term use in those with risk factors for or with known osteoporosis, as well as in children. Reduction of renal function over time, as well as cases of acute renal failure and Fanconi s syndrome, have been reported in patients receiving tenofovir alone or in combination with emtricitabine. For this reason, tenofovir should be used with caution in patients at risk for renal dysfunction. Tenofovir may compete with other drugs that are actively secreted by the kidneys, such as cidofovir, acyclovir, and ganciclovir. 

Nephrotoxicity is the principal dose-limiting side effect of intravenous cidofovir. Proximal tubular dysfunction includes proteinuria, azotemia, glycosuria, metabolic acidosis and, uncommonly, Fanconi s syndrome. Concomitant oral probenecid and saline prehydration reduce the risk of renal toxicity. 

---