Central diabetes insipidus (DI) is the clinical syndrome resulting from the deficiency of arginine vasopressin, also called antidiuretic hormone (ADH). Antidiuretic hormone is produced by large neurons that originate in the supraoptic and paraventricular nuclei of the hypothalamus and project through the pituitary stalk to terminate on capillary plexuses scattered throughout the pars nervosa (posterior lobe) of the pituitary gland.
Central diabetes insipidus is a well-known disorder in both dogs and cats, but is an uncommon diagnosis in both species. True estimates of prevalence are not available, largely because the condition is frequently misdiagnosed due to failure to identify other causes of polyuria and polydipsia. The condition can occur at any age, and there is no apparent breed or sex predisposition Common missed differentials include hyperadrenocortism, occult pyelonephritis or renal disease, and hyperthyroidism.
There are many recognized causes of DI in dogs and cats.
In most dogs and cats with DI, an underlying cause cannot be identified. Although these are generally termed idiopathic in dogs and cats, most of these “idiopathic” cases are found to have a genetic basis in humans. Genetic mutations in the signal peptide and hormone-specific neurophysin (the carrier proteins vasopressin) have been demonstrated to cause impaired posttranslational modification, transport or secretion of arginine vasopressin. No such mutations have yet been identified in dogs or cats.
Neoplasia is the most common identified cause in dogs, of which chromophobe adenoma, chromophobe adenocarcinomas and craniopharyngioma appear most common.
Trauma-induced DI is a relatively common cause in cats; it has been rarely reported in dogs. Trauma-induced DI may be transient or permanent, presumably related to the degree of damage to the hypothalamic nuclei or site of transection of the pituitary stalk. The development of transient or permanent DI has been reported as a complication of hypophysectomy in dogs, primarily performed for the treatment of pituitary-dependent hyperadrenocorticism.
Finally, inflammation or infection of the hypothalamus or the posterior pituitary can also cause to reduced secretion of vasopressin leading to DI.