Diabetes insipidus overview
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]
Overview
Diabetes insipidus (DI) is a syndrome characterized by the excretion of abnormally large volumes of dilute urine. It can be caused by any of 4 fundamentally different defects that must be distinguished for safe and effective management. They are: (1) pituitary DI also called neurogenic or central DI, due to inadequate production and secretion of antidiuretic hormone, arginine-vasopressin (AVP); (2) gestational DI due to degradation of arginine vasopressin by an enzyme made in placenta; (3) primary polydipsia, due to suppression of arginine vasopressin secretion by excessive fluid intake; and (4) nephrogenic DI due to renal insensitivity to the antidiuretic effect of AVP. Patients with DI typically present with excessive day and nighttime urination, excessive drinking of fluids in order to compensate for the lost fluids in urine which may lead to electrolyte imbalances such as hypo- or hypernatremia. The causes of Diabetes insipidus are unique to the type of the diabetes insipidus caused, and the treatment should be targeted at understanding the underlying cause of the disease.
Historical Perspective
Classification
Diabetes insipidus is a disease in which large volumes of dilute urine (polyuria) are excreted due to vasopressin (AVP) deficiency [central diabetes insipidus (CDI)], AVP resistance [nephrogenic diabetes insipidus (NDI)], or excessive water intake (primary polydipsia). Polyuria is characterized by a urine volume in excess of 2 l/m2/24 h or approximately 150 ml/kg/24 h at birth, 100–110 ml/kg/24 h until the age of 2 years and 40–50 ml/kg/24 h in the older child and adult.