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)