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Diabetes insipidus affects about three out of 100,000 persons. This disorder is caused by a deficiency or ineffectiveness of vasopressin (ADH). It can be transient or chronic diabetes insipidus. Diabetes insipidus is characterized by excretion of excessive quantities of dilute urine and excessive thirst due to a compromised ability to conserve free water. Diabetes insipidus is easily distinguished from other causes of polyuria by the absence of a solute load (particularly glucose) and an abnormally low.

Two types of diabetes insipidus are recognized: neurogenic (central) and nephrogenic (peripheral) (Table 4). Many underlying conditions can produce diabetes insipidus (Table 5). The most common form is neurogenic diabetes insipidus and is classified as either idiopathic or secondary to an intracranial event. Causes of diabetes insipidus in adults include idiopathic (25 percent), benign brain tumors (20 percent), blunt head trauma (17 percent), neurosurgery (9 percent), metastatic cancer (8 percent), and ischemic or toxic brain injury (6 percent). In contrast, only 8 percent of diabetes insipidus in children is idiopathic. The most common causes of childhood cases are tumors, neurosurgery, trauma, and meningitis. Idiopathic diabetes insipidus is invariably permanent.

Classification of Diabetes Insipidus

Cause Type

Decreased arginine vasopressin Neurogenic

(AVP) secretion Cranial




Decreased AVP effect Nephrogenic


Excessive water intake Primary polydipsia

Increased AVP metabolism Gestational

Causes of Diabetes Insipidus

Neurogenic causes



Neoplastic: craniopharyngioma, lymphoma, meningioma, metastatic carcinoma, other brain tumor

Head trauma


Ischemia: shock, cardiac arrest, Sheehan's syndrome (postpartum pituitary necrosis), aneurysm, sickle cell crisis


Sarcoidosis, histiocytosis

Infectious: tuberculosis, encephalitis, meningitis



Nephrogenic causes



Drug-induced: lithium, demeclocycline (Declornycin), methoxyflurane (Penthrane)

Metabolic: hypokalemia, hypercalciuria, usually with hypercalcemia Renal disease: polycystic kidney disease, obstructive uropathy, chronic pyelonephritis, sickle cell nephropathy, sarcoidosis, chronic renal failure, multiple myeloma, Sjogren's disease, analgesic nephropathy

and nephrogenic forms. A mild form of dehydration is induced in a controlled fashion, with hourly monitoring of urine osmolality and specific gravity and serum sodium and osmolality. Adequate dehydration is documented by a weight loss of 1.3 to 2.25 kg (3.0 to 5.0 lb) in adults or two successive urine osmolality values that differ by less than 30 mOsm per kg in children, indicating that a maximum concentration steady state has been

The key to diagnosing diabetes insipidus and distinguishing between neuro-genie and nephrogenic forms lies not in the absolute test results, but in the ADH level and the association between urine and serum osmolality in response to

A closely monitored trial of desmopressin (DDAVP) also may be used to diagnose diabetes insipidus. The patient has neurogenic diabetes insipidus if a standard treatment with DDAVP (2 to 4 meg subcutaneously every 12 hours

If a patient is diagnosed with neurogenic diabetes insipidus, the underlying cause must be determined. In patients who are otherwise asymptomatic, MRI of the head is used to detect possible hypo-thalamic tumors. MRI is thought to be

Treatment. Patients with neurogenic diabetes insipidus are treated with intranasal DDAVP (Stimate). DDAVP, a synthetic analog of vasopressin without pressor or uterine effects, is the formulation of ADH that is best tolerated,