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Diabetes insipidus (DI) results from insufficient AVP production by the hypothalamus or from impaired AVP action in the kidney. AVP deficiency is characterized by production of large amounts of dilute urine. In central DI, insufficient AVP is released in response to physiologic stimuli. Causes include acquired (head trauma; neoplastic or inflammatory conditions affecting the hypothalamus/posterior pituitary), congenital, and genetic disorders, but almost half of cases are idiopathic. In gestational DI, increased metabolism of plasma AVP by an aminopeptidase (vasopressinase) produced by the placenta leads to a relative deficiency of AVP during pregnancy. Primary polydipsia results in secondary insufficiency of AVP due to physiologic inhibition of AVP secretion by excessive fluid intake. Nephrogenic DI is caused by AVP resistance at the level of the kidney; it can be genetic or acquired from drug exposure (lithium, demeclocycline, amphotericin B), metabolic conditions (hypercalcemia, hypokalemia), or renal damage.