Diabetes insipidus (DI) is an uncommon condition that occurs when the kidneys are unable to conserve water as they perform their function of filtering blood. The amount of water conserved is controlled by antidiuretic hormone (ADH, also called vasopressin).

ADH is a hormone produced in a region of the brain called the hypothalamus. It is then stored and released from the pituitary gland, a small gland at the base of the brain.

DI caused by a lack of ADH is called central diabetes insipidus. When DI is caused by failure of the kidneys to respond to ADH, the condition is called nephrogenic diabetes insipidus. The major symptoms of diabetes insipidus are excessive urination and extreme thirst. The sensation of thirst stimulates patients to drink large amounts of water to compensate for water lost in the urine.

Central diabetes insipidus is caused by damage to the hypothalamus or pituitary gland as a result of surgery, infection, tumor, or head injury. Although rare, central DI is more common than nephrogenic DI.

Nephrogenic DI involves a defect in the parts of the kidneys that reabsorb water back into the bloodstream. It occurs less often than central DI. Nephrogenic DI may occur as an inherited disorder in which male children receive the abnormal gene that causes the disease on the X chromosome from their mothers.

Nephrogenic DI may also be caused by diseases of the kidney (for example, polycystic kidney disease) and the effects of certain drugs (for example, lithium, amphotericin B, demeclocycline).

If thirst mechanisms are normal and adequate fluids are consumed, there are no significant effects on body fluid or salt balance. If inadequate fluids are consumed, the large amount of water lost in the urine may cause dehydration and high sodium levels in the blood.