Diabetes Insipidus

– A transient or permanent disturbance of water metabolism that results in excretion of excessive quantities of very dilute urine. It may be pituitary (central), renal (nephrogenic), or intake regulated (primary) in nature.

Causes and Incidence

Central diabetes insipidus (DI) is the result of a lack of antidiuretic hormone (ADH), which can be caused by brain injury from head trauma, neurosurgery, irradiation of the pituitary, hypothalamic tumors, or infiltrative metastatic diseases. More than half of diagnosed cases are idiopathic. Nephrogenic DI results when the body is unable to respond normally to ADH. The condition is inherited as an X-linked recessive disorder or acquired in association with disorders such as renal disease, sickle cell disease, fibrosarcoma, granuloma, polynephritis, metabolic disease, polycystic disease, or pregnancy or with toxic agents that reduce glomerular filtration. Primary DI results from excessive water intake caused by psychogenic disorders (e.g., schizophrenia) or dipsogenic disorders (e.g., multiple sclerosis, meningitis, encephalitis, neurosarcoidosis, or tuberculosis).

Disease Process

Central DI begins when some form of brain injury reduces the amount of ADH. This leads to a decrease in the hydroosmotic permeability of the distal collecting tubes in the kidney, allowing the dilute urine formed in the proximal nephrons to be excreted unchanged. The result is a slight dehydration effect, an increase in plasma osmolality, and stimulation of the thirst mechanism. The individual drinks more, and as a result input and output are balanced and osmotic pressure in the body stabilizes at an above-normal level. In nephrogenic DI the kidneys are rendered ADH resistant and hydroosmotic permeability is reduced, with the same end result as in central DI. Primary polydipsia is caused by excessive water intake, either because of a severe cognitive dysfunction or because the thirst regulator has been disrupted by disease or trauma. Plasma osmolality is reduced, which causes a decrease in the production of ADH and dilutes the urine, and excretion rises to meet intake. As intake and output are balanced, plasma osmolality stabilizes at below-normal levels.


The most common presenting signs and symptoms are unquenchable thirst, polydipsia, frequency of urination, polyuria, nocturia, dry skin, slight dehydration, and constipation.

Potential Complications

A prolonged increase in urine volume and flow can lead to hydroureter and hydronephrosis. An individual who has no thirst mechanism may experience severe dehydration and circulatory collapse.

Diagnostic Tests

Fluid deprivation test
Central and nephrogenic DI: urine osmolality remains low Primary DI: osmolality increases.

Vasopressin administration after fluid deprivation
Central DI: osmolality rises Nephrogenic and primary DI: osmolality is unchanged.


None unless related to underlying disease.

Central DI: synthetic vasopressin or chlorpropamide to increase urine osmolality.

Nephrogenic DI: thiazide diuretics to reduce urine volume.

Identification and treatment of any underlying organic cause for DI; reduction of sodium and caffeine in diet for central DI and nephrogenic DI; monitoring for hypoglycemia if chlorpropamide is prescribed; information about long-term hormone replacement therapy.