Abstract
A patient demonstrating acute symptomatic hyponatremia following the administration of therapeutic doses of chlorothiazide is presented, with appropriate balance data. It is suggested that this hyponatremia was initiated by both a renal and extrarenal effect and then maintained via the mediation of a receptor system sensitive to minute changes in extracellular fluid volume. The effector site of this system was renal and associated with the release of antidiuretic hormone and water conservation despite marked serum hypotonicity. That hyponatremia is not attributable to a direct effect of chlorothiazide on the renal tubule is stressed. A new mechanism for chlorothiazide-induced hyponatremia, independent of manifest renal losses of sodium and water, is described in detail.
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