Clinical meaning
Diabetes insipidus (DI) is a disorder of water balance characterised by the excretion of abnormally large volumes of dilute urine (polyuria) and compensatory excessive thirst (polydipsia). It results from either deficient antidiuretic hormone (ADH, also called vasopressin) production or impaired renal response to ADH. Despite the name, it is entirely unrelated to diabetes mellitus - the shared word 'diabetes' simply refers to excessive urine production.
Normal water balance relies on ADH secreted by the posterior pituitary gland. When plasma osmolality rises above approximately 280 mOsm/kg (or blood volume decreases), osmoreceptors in the hypothalamus stimulate ADH release. ADH acts on V2 receptors in the renal collecting duct, activating aquaporin-2 water channels that allow water reabsorption from the tubular fluid back into the hypertonic medullary interstitium. This concentrates the urine and returns plasma osmolality toward normal. Without ADH or its renal action, the collecting duct remains impermeable to water, and large volumes of dilute urine are excreted.
Central (neurogenic) diabetes insipidus results from insufficient ADH production or secretion by the hypothalamic-posterior pituitary axis. Causes include pituitary surgery (especially transsphenoidal surgery for pituitary adenoma - the most common iatrogenic cause), traumatic brain injury, brain tumours (craniopharyngioma, metastases), infiltrative diseases (sarcoidosis, histiocytosis), autoimmune hypophysitis, and infections (meningitis, encephalitis). Approximately 25-30% of cases are idiopathic (presumed autoimmune).
Post-surgical DI following transsphenoidal pituitary surgery has a characteristic triphasic pattern: initial DI (days 1-5, from surgical trauma causing transient ADH deficiency), followed by inappropriate ADH release (days 5-10, from dying posterior pituitary neurons releasing stored ADH), then permanent DI if sufficient neurons were destroyed. Many post-surgical cases are transient.