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Diuretic-Induced Hyponatremia

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Supported in part by grants AM12639, FR05356, 5-SO1-RR-05356, and 5-RO1-HE12796, U.S. Public Health Service, Washington, D.C.; grant RR-43, General Clinical Research Centers Program of the Division of Research Resources, National Institutes of Health, Bethesda, Md.; Sandoz Pharmaceuticals, Hanover, N.J.; and from the Professional Staff Association of the Los Angeles County-USC Medical Center, Los Angeles, Calif.

▸Requests for reprints should be addressed to Marshal P. Fichman, M.D., University of Southern California School of Medicine, 2025 Zonal Ave., Los Angeles, Calif. 90033

Los Angeles, California

Ann Intern Med. 1971;75(6):853-863. doi:10.7326/0003-4819-75-6-853
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Severe hyponatremia (serum Na, 91 to 120 mEq/liter) secondary to the use of diuretics was observed in 25 nonedematous patients with clinically normal hydration and creatinine clearances; it was distinguishable from other hyponatremic syndromes by the presence of hypokalemia and alkalosis, the return of serum Na to normal and unimpaired excretion of a water load of 20 ml/kg body weight 3 to 10 days after withdrawing diuretics, and the recurrence of hyponatremia within 2 to 12 days of readministering the drugs. Bioassay of plasma samples in ethanol-anesthetized rats showed elevated (1 to 15 µunits/ml) antidiuretic hormone (ADH) activity in 10 of 10 patients with diuretic-induced hyponatremia, 20 of 23 patients with inappropriate-ADH syndrome, but in none of 10 patients with hypopituitarism. Simultaneous isotope dilution studies in 10 diuretic-induced hyponatremic patients showed a marked decrease in measured exchangeable potassium in relation to a 75%-predicted mean but only a borderline decrease in mean exchangeable sodium. Increasing potassium intake improved hyponatremia. Hyponatremia apparently results from potassium depletion, which exaggerates the volume receptor release of vasopressin that is the response to minimal diuretic-induced sodium loss.





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