Diabetes Insipidus
History. A client presents her 6-month-old female Boston terrier with the complaint of excessive water consumption and urination.
Clinical Examination. The physical examination reveals no abnormalities.
The dog is alert and active. A urinalysis is normal, and the urine specific gravity is 1.002 (osmolality, 152 mθsm∕kg H2O). The serum chemistry profile and a complete blood cell count (CBC) are normal.You admit the dog to your clinic for a modified water deprivation test. The urine fails to become concentrated despite a 5% loss of body weight. You administer vasopressin (ADH), and the urine specific gravity is 1.029 (osmolality, 852 mθsm∕kg H2O) 1 hour later.
Comment. The dog has central diabetes insipidus (DI), which is a deficiency of antidiuretic hormone (ADH). The urine is diluted by the thick ascending limb of Henles loop and the distal convoluted tubule. Solute-free water absorption in the collecting duct depends on the action of ADH. In the absence of ADH, excessive volumes of water are excreted, and the dog drinks voraciously to prevent dehydration.
Other causes of excretion of dilute urine (urine osmolality much lower than serum osmolality) are psychogenic polydipsia, Fiyperadrenocorticism, glucocorticoid therapy, hypercalcemia, hypokalemia, and nephrogenic Dl. Most of these can be detected from a thorough history, physical examination, CBC, and serum chemistry profile. When only psychogenic polydipsia, central DI, and nephrogenic DI remain in the differential diagnosis, the diagnosis usually can be made using the modified water deprivation test. Animals with psychogenic polydipsia can secrete ADH and have normal kidneys; therefore they concentrate their urine after water deprivation. Dogs with DI can concentrate their urine minimally or not at all after water deprivation. If the problem is insufficient ADH release (central DI), the urine concentration increases in response to exogenous ADH. If the kidney is unresponsive to ADH (nephrogenic DI), the urine concentration does not increase further in response to additional ADH.
Treatment. Treatment of central DI includes free access to water and daily administration of a vasopressin analogue, such as desmopressin (DDAVP), by parenteral or intranasal route.