FLORENCE N. HUTCHISON, M.D.; EDITH A. PEREZ, M.D.; DAVID R. GANDARA, M.D.; H. JEFFREY LAWRENCE, M.D.; GEORGE A. KAYSEN, M.D., Ph.D.
HUTCHISON FN, PEREZ EA, GANDARA DR, LAWRENCE HJ, KAYSEN GA. Renal Salt Wasting in Patients Treated with Cisplatin. Ann Intern Med. 1988;108:21-25. doi: 10.7326/0003-4819-108-1-21
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Published: Ann Intern Med. 1988;108(1):21-25.
Although cisplatin nephrotoxicity is well documented, renal sodium wasting has rarely been reported. Seven of seventy patients treated with cisplatin over 18 months developed salt-wasting nephropathy and orthostatic hypotension. All patients presented 2 to 4 months after starting cisplatin with severe orthostatic hypotension (mean orthostatic change in blood pressure, -37 ± 8 mm Hg) without preceding extrarenal volume loss or diuretic use. Urinary sodium concentration was 85 to 145 mmol/L, fractional excretion of sodium was 1.0% to 8.0%, and urinary osmolar concentration was 340 to 619 mmol/kg, while orthostatic hypotension was present. Six patients were hyponatremic (116 to 137 mmol/L). Serum creatinine and urea levels were elevated in five patients but fell after rehydration. Vasopressin averaged 5.4 pg/mL (2.1 to 12.7 pg/mL) (n=5) and was suppressed with hydration (mean, 2.5 pg/mL, 1.5 to 4.3 pg/mL). Plasma renin activity was undetectable in two patients and low in three patients, and aldosterone was low in six patients despite clinical volume depletion. Cisplatin may produce renal salt wasting causing symptomatic orthostatic hypotension and hyponatremia associated with abnormalities of the renin-aldosterone system.
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Print ISSN: 0003-4819 | Online ISSN: 1539-3704
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