Hypernatremia Due to Hypodipsia and Elevated Threshold for Vasopressin Release

Abstract

A woman previously operated for craniopharyngioma has chronic hypernatremia without polyuria or polydipsia. The hypernatremia appears to be due both to derangement of the thirst mechanism and to an elevation of the osmotic threshold for antidiuretic-hormone secretion. Long-term administration of hydrochlorothiazide has kept the serum sodium within normal limits, primarily by limiting renal free water clearance. Chlorpropamide and tolbutamide also proved to be strikingly effective in correcting the hypernatremia, by markedly increasing urinary osmolality. It is speculated that the sulfonylureas increase the concentration of cyclic adenosine monophosphate in the renal medulla as well as in the pancreatic beta cells, and that this accounts for their effects on urinary concentration and insulin secretion.