[Severe hypernatremia in acquired disorder of thirst and vasopressin regulation]

Three patients with severe adipsic hypernatremia (greater than 171 mmol/l) are presented. In two of them, hypernatremia occurred after the operation of a ruptured aneurysm of the A. communicans anterior, in one patient the cause of the disease remained obscure. Despite high plasma osmolality, all patients had low or undetectable plasma vasopressin levels, even throughout hypertonic saline infusion. Urine concentrating ability was partially maintained, suggesting activation of alternative extra- and intrarenal concentrating mechanisms or increased renal sensitivity to low vasopressin concentration. Nonosmolar stimulation (insulin-induced hypoglycemia) did increase vasopressin concentration only subnormally in the two patients tested. This finding might be due to an extended and complex dysfunction of the anterior hypothalamus rather than to a circumscribed defect of the osmoreceptor/thirst center or the supraoptic nuclei.