HDCN Article Review/Hyperlink

Navarro JF, Quereda C, Gallego H, et al

Nephrogenic diabetes insipidus and renal tubular acidosis secondary to foscarnet therapy

Am J Kidney Dis (Mar) 27:431-434 1996

Navarro et al describe a 27-year old man with HIV treated for cytomegalovirus retinitis with foscarnet. After two weeks of foscarnet induction therapy, 180 mg/kg/day, and nearly six months of foscarnet maintenance, 90 mg/kg/day, the patient complained of increased thirst and polyuria. Hypernatremia and a normal anion gap metabolic acidosis were present. The patient's urine was dilute and had a pH of 6.7. Water deprivation failed to result in increased urine osmolality. Sixteen grams of sodium bicarbonate were given over 48 hours. The serum bicarbonate normalized, but the urine pH increased only slightly. Seventeen days after foscarnet was discontinued, serum and urine values returned to normal.

Comment: Therapy with foscarnet for cytomegalovirus infection in immunosuppressed patients may cause acute tubular necrosis, hypocalcemia, hypokalemia and nephrogenic diabetes insipidus. More than half of the patients treated with foscarnet may develop renal impairment. These authors report the fist case of foscarnet-induced distal renal tubular acidosis. Although foscarnet inhibits sodium-phosphate cotransport in the tubule, its effect on the collecting duct is unknown, as are the mechanisms of foscarnet-induced diabetes insipidus and renal tubular acidosis. (George R. Aronoff, M.D., University of Louisville)