Recognition of Partial Defects in Antidiuretic Hormone Secretion

TLDR

Prolonged dehydration can deplete limited ADH stores in some patients, converting partial deficiency into severe deficiency. The test involves water deprivation until urine osmolality plateaus, then comparing that value to plasma osmolality after ADH injection. Patients with normal ADH or primary polydipsia had high urine osmolality that did not rise after ADH, whereas severe ADH deficiency patients had low urine osmolality that increased >50% after ADH, and partial deficiency was identified by urine osmolality exceeding plasma after deprivation and a 9–67% rise after ADH.

Abstract

A dehydration procedure has been used to identify patients with partial antidiuretic hormone (ADH) deficiency. The test consists of water deprivation until the osmolality of hourly voided urines reaches a plateau and then relating the urine osmolality at which this occurs to the osmolality recorded after subsequent injection of ADH. In patients with normal neurohypophysial function and patients with primary polydipsia, urine osmolality at the end of such a period of deprivation was much greater than plasma osmolality and did not increase more than 5% after the injection of 5 units of aqueous vasopressin. In patients with severe ADH deficiency urine osmolality before ADH was much less than plasma osmolality; after ADH injection, however, it was increased by more than 50%. Thirteen patients in whom urine osmolality was greater than plasma osmolality after water deprivation and was further increased by 9% to 67% after ADH injection were considered to have partial ADH deficiency. Some patients with ADH deficiency apparently exhausted their limited neurohypophysial ADH stores during prolonged dehydration, with resultant change from partial to severe hormone deficiency.