ABSTRACT
The investigation of choice in DI is the water deprivation test. In this test, the patient has their urine and plasma osmolarity measured at hourly intervals while being deprived of fluid. The patient’s weight is also measured, and the test is stopped if the patient loses over 3% of their body weight. In normal individuals, fluid restriction causes the plasma osmolarity to rise, which in turn stimulates ADH secretion and water reabsorption. In DI, the patient continues to produce large volumes of dilute urine despite being dehydrated. Patients who do not concentrate their urine during the test are given a dose of desmopressin, which is a synthetic ADH analogue. If the diabetes insipidus is due to a lack of ADH secretion, i.e. cranial DI, the desmopressin causes the kidney to reabsorb water and concentrate the urine. If the patient has nephrogenic DI, their kidneys cannot respond to the desmopressin, and therefore the patient continues to produce large volumes of dilute urine. Thus, cranial DI can be treated with desmopressin, whereas nephrogenic DI cannot. In nephrogenic DI, the urine output can be slowed by using thiazide diuretics and non-steroidal anti-inflammatory drugs, although the most important treatment is good fluid management.
