Diabetes insipidus

Diabetes insipidus is a water-balance disorder marked by excessive production of dilute urine and intense thirst. It results from insufficient vasopressin activity or kidneys that do not respond properly to vasopressin.

Vasopressin: A hormone that helps the kidneys conserve water by increasing water reabsorption. Too little vasopressin causes the central form of this disorder.
Central diabetes insipidus: Diabetes insipidus caused by deficient production or release of vasopressin. It is the form caused by inadequate hormone supply.
Water deprivation test: A supervised test that assesses whether urine concentrates during fluid restriction and after vasopressin administration. It helps separate diabetes insipidus from excessive drinking and distinguish its major forms.
Diabetes mellitus: A group of disorders characterized by elevated blood glucose due to problems with insulin secretion or action. Despite the shared word, it involves glucose regulation rather than vasopressin and water balance.
Collecting duct: The final kidney tubule segment where water reabsorption is regulated before urine leaves the kidney. Impaired water reabsorption here produces unusually dilute urine.
Nephrogenic diabetes insipidus: Diabetes insipidus caused by kidney resistance to vasopressin. It is the form in which hormone is present but kidney response is impaired.
Desmopressin: A synthetic vasopressin analogue used to treat vasopressin deficiency and some other conditions. It replaces missing hormone activity in central diabetes insipidus.
Syndrome of inappropriate antidiuretic hormone secretion: A disorder in which excessive vasopressin activity causes water retention and low blood sodium. It produces the opposite water-balance pattern: retained water rather than excessive dilute urine.
Aquaporin 2: A water-channel protein inserted into collecting-duct cells in response to vasopressin. Vasopressin-resistant disease can disrupt this channel’s function or placement.
Gestational diabetes insipidus: Diabetes insipidus arising during pregnancy, usually because placental enzymes increase vasopressin breakdown. Pregnancy can produce a distinct, often temporary vasopressin-deficiency form.

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