Cisplatinum-induced renal salt wasting.

We report two patients who developed high urinary excretion of sodium chloride after receiving cisplatinum. One patient became symptomatically hyponatremic during intravenous administration of hypotonic fluid. The second patient developed orthostatic hypotension. Urine sodium and chloride concentrations exceeded 130 mmol/liter despite hyponatremia or volume depletion. There was no evidence of adrenal cortical impairment and no improvement with fludrocortisone. We propose that cisplatinum may inhibit solute transport by the thick ascending limb of Henle, causing clinically significant, previously unreported toxicity in patients receiving chronic cisplatinum antitumor therapy.

Duke Scholars

Author Joanne Kurtzberg Pediatrics, Transplant and Cellular Therapy