In patients who present with polyuria and polydipsia, the initial differential diagnosis is between primary polydipsia and diabetes insipidus, of course, this is after diabetes mellitus has been excluded. The test used to diagnose diabetes insipidus is the dehydration test, which should be conducted under close supervision. First, a baseline body weight is measured and samples of both urine and serum are collected for osmolality determinations. Then total fluid restriction is begun at 0700 hours. Hourly serial measurements of body weight and urine osmolality are collected until the urine osmolality stabilizes (hourly increase for urine osmolality less than 30 mOsm/kg for 3 hours). At this point, blood is drawn for determination of the plasma osmolality, a value greater than 288 mOsm/kg assures adequate dehydration. Next, aqueous vasopressin (5 units) is administered subcutaneously and then the urine and plasma osmolality are measured one hour later.
Interpretation:
Patients with diabetes insipidus manifest hyposthenuria (urine osmolality less than 150 mOsm/L) despite ongoing polyuria, plasma hypertonicity and loss of body weight. Neurogenic diabetes insipidus and type II nephrogenic disease are diagnosed in patients whose urine osmolality rises greater than 150 mOsm/kg after vasopressin is given. Patients with type I nephrogenic diabetes insipidus lack any response to the administration of exogenous vasopressin. The dehydration test should be conducted with the patient under close observation. The test should be discontinued if the patients weight loss exceeds 3% of their baseline value.
Treatment of diabetes insipidus requires correction of any underlying disorder (brain tumors, neurologic infections, infiltrative diseases, hypercalcemia or hypokalemia). Emergency treatment of neurogenic diabetes insipidus entails the administration of subcutaneous vasopressin in oil (Pitressin Tannate) every 12 hours to maintain urine volume at approximately three liters per day. Chronic treatment of neurogenic diabetes insipidus is accomplished with the administration of short acting lypressin or long acting desmopressin (DDAVP). Partial defects in ADH deficiency may be corrected with chlorpropamide or clofibrate, which increase ADH release and the renal response to ADH, respectively.