Abstract
The cause of diabetes insipidus is either impaired vasopressin secretion (central diabetes insipidus) or lack of its function (nephrogenic diabetes insipidus). In patients with polyuria it is crucial to rule-out osmotic diuresis and kidney disease.
The dehydration test is necessary for differential diagnosis between diabetes insipidus and primary polydipsia. Desmopressin has been the drug of choice for central diabetes insipidus for many years.
Only sublingual form is available today, when less than 1 % of administered dose is absorbed. Sufficient compensation is usually achieved by the dose of 120 μg twice a day, sometimes higher and/or more frequent doses are needed.
Should hyponatraemia appear during treatment the desmopressin dose is decreased; complete withdrawal is dangerous as natraemia rises too quickly and the patient is in danger of pontine myelinolysis. Patients with impaired thirst sensation represent the major problem.
In nephrogenic diabetes insipidus the diuresis can be decreased by salt restriction with thiazide diuretics and nonsteroide anti-inflammatory drugs. Some specific types of nephrogenic diabetes insipidus caused by V2 receptor mutations respond to treatment with soluble non-peptide agonists.