What is Diabetes Inspidus?
DI is a disorder characterized by a deficiency in vasopressin-mediated electrolyte-free water reabsorption. DI can denote a defect either in pituitary vasopressin secretion (neurogenic or central DI) or vasopressin action (nephrogenic DI). It manifests as polyuria—defined as more than 3 L of daily urine output. The urine is dilute due to excessive urinary electrolyte-free water loss. In most patients, an intact thirst perception and ready access to electrolyte-free water prevent a rise in the serum sodium concentration. However, hypernatremia will ensue if free water access is limited. Note that polyuria with polydipsia are also characteristic of primary polydipsia, but the polyuria is secondary, not primary; serum sodium concentration is normal or low, and water restriction does not lead to hypernatremia.
Neurogenic DI can result from a number of etiologies including trauma, granulomatous disease, tumors, infection, or aneurysm affecting the hypothalamus or pituitary. Nephrogenic DI can be either congenital or acquired, the latter being associated with intrinsic kidney disease, hypercalcemia, hypokalemia, and drugs including lithium and demeclocycline. Unlike nephrogenic DI, patients with the neurogenic form will exhibit a robust response to administration of a vasopressin agonist by producing concentrated urine.