for decades as long as enough water is consumed to offset the urinary losses. However, there is a continuous risk of dehydration and loss of potassium that may lead to hypokalemia. Cause The several forms of diabetes insipidus are: Central Central (or Neurogenic) DI has many possible causes. According to the literature, the principal causes of central DI and their oft-cited approximate frequencies are as follows: Idiopathic – 30% Malignant or benign tumors of the brain or pituitary – 25% Cranial surgery – 20% Head trauma – 16% Nephrogenic Nephrogenic diabetes insipidus is due to the inability of the kidney to respond normally to vasopressin. Dipsogenic Dipsogenic DI or primary polydipsia results from excessive intake of fluids as opposed to deficiency of arginine vasopressin. It may be due to a defect or damage to the thirst mechanism, located in the hypothalamus, or due to mental illness. Treatment with desmopressin may lead to water intoxication. Gestational Gestational DI occurs only during pregnancy and the postpartum period. During pregnancy, women produce vasopressinase in the placenta, which breaks down antidiuretic hormone (ADH). Gestational DI is thought to occur with excessive production and/or impaired clearance of vasopressinase. Most cases of gestational DI can be treated with desmopressin (DDAVP), but not vasopressin. In rare cases, however, an abnormality in the thirst mechanism causes gestational DI, and desmopressin should not be used. Diabetes insipidus is also associated with some serious diseases of pregnancy, including pre-eclampsia, HELLP syndrome and acute fatty liver of pregnancy. These cause DI by impairing hepatic clearance of circulating vasopressinase. Pathophysiology Electrolyte and volume homeostasis is a complex mechanism that balances the body's requirements for blood pressure and the main electrolytes sodium and potassium. In general, electrolyte regulation precedes volume regulation. When the volume is severely depleted, however, the body will retain water at the expense of deranging electrolyte levels. The regulation of urine production occurs in the hypothalamus, which produces ADH in the supraoptic and paraventricular nuclei. After synthesis, the hormone is transported in neurosecretory granules down the axon of the hypothalamic neuron to the posterior lobe of the pituitary gland, where it is stored for later release. In addition, the hypothalamus regulates the sensation of thirst in the ventromedial nucleus by sensing increases in serum osmolarity and relaying this information to the cortex. Neurogenic/central DI results from a lack of ADH; occasionally it can present with decreased thirst as regulation of