Central diabetes insipidus | |
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Other names | Arginine vasopressin deficiency; pituitary diabetes insipidus; neurohypophyseal diabetes insipidus; cranial diabetes insipidus; neurogenic diabetes insipidus |
Specialty | Endocrinology ![]() |
Symptoms | Polyuria, nocturia, and polydipsia. |
Central diabetes insipidus, recently renamed arginine vasopressin deficiency (AVP-D),[1] is a form of diabetes insipidus that is due to a lack of vasopressin (ADH) production in the brain. Vasopressin acts to increase the volume of blood (intravascularly), and decrease the volume of urine produced. Therefore, a lack of it causes increased urine production and volume depletion.
It is also known as neurohypophyseal diabetes insipidus,[2][3] referring to the posterior pituitary (neurohypophysis), which is supplied by the hypothalamus in the brain. This condition has only polyuria in common with diabetes. Although not mutually exclusive, with most typical cases, the name diabetes insipidus is misleading.[4]
Untreated patients with central diabetes insipidus often experience polyuria, nocturia, and polydipsia due to the initial increase in serum sodium and osmolality. Central diabetes insipidus can be caused by various congenital or acquired lesions, and when the cause is unknown, it is classified as idiopathic.
The water deprivation test (WDT) is a commonly used test for diabetes insipidus, a two-step process involving parenteral desmopressin administration after an initial 8-hour water fast. It differentiates primary polydipsia from diabetes insipidus and central diabetes insipidus from nephrogenic diabetes insipidus. Diabetes insipidus is trated by restoring free water deficit, replacing the missing hormone, and addressing the underlying ailment. Desmopressin, an arginine vasopressin analog, is used to treat central diabetes insipidus.