Abstract
The antidturetic properties of hydrochlorothiazide were studied in 4 subjects with congenital vasopressin-resistant diabetes insipidus. Evidence is presented which suggests that the antidiuresls results from mild sodium depletion and is not due to a unique property of the thiazlde derivatives. A mechanism is discussed whereby reduction in body sodium may lead to intrarenal alterations resulting in a reduced volume of urine of higher osmolallty. Data are presented which suggest that the natrluretic effect of hydrochlorothlazlde may be overcome by the endogenous release of aldosterone and by diminishing the delivery of filtrate to the distal sites where this agent is active. It is concluded that when employed in conjunction with supplemental potassium and a restricted dietary intake of sodium, hydro-chlorothlazlde is of value in reducing the urine output of patients with vasopressin-resistant diabetes insipidus.