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Causes of deficiency may be:
Causes of deficiency may be:
:'''Central''': failure to synthesise or release of ADH
:'''Central''': Central DI is characterized by decreased secretion of antidiuretic hormone (ADH)—also known as arginine vasopressin (AVP)—which gives rise to polyuria and polydipsia by diminishing the patient’s ability to concentrate urine.
:'''Nephrogenic''': failure of the [[:Category:Nephron|nephrons]] to respond to ADH present in the kidney
Diminished or absent ADH can be the result of a defect in 1 or more sites involving the hypothalamic osmoreceptors, the supraoptic or paraventricular nuclei, or the supraopticohypophyseal tract.
:'''Nephrogenic''': failure of the [[:Category:Nephron|nephrons]] to respond to ADH present in the kidney.Is characterized by a decrease in the ability to concentrate urine due to a resistance to ADH action in the kidney. Nephrogenic DI can be observed in chronic renal insufficiency, lithium toxicity, hypercalcemia, hypokalemia, and tubulointerstitial disease, rarely, diabetes insipidus may be hereditary.
'''Psychogenic diabetes insipidus (psychogenic polydipsia)''' : It results from a neurological disorder of thirst control or as a result of some behavioral problem that triggers excessive water intake. In either case, the abnormally large volume of excreted urine in animals with psychogenic polydipsia is caused by excessive water intake (polydipsia), rather than by some primary problem with kidney, pituitary or hypothalamic function.
== Clinical Signs ==
== Clinical Signs ==