DIABETES insipidus, a clinical syndrome characterized by the passage of large volumes of dilute urine and the presence of an inordinate thirst, was properly defined one hundred and sixty-two years ago (1). Recently acquired knowledge of the pathogenesis of diabetes insipidus in experimental animals, and the development of a variety of test procedures designed to induce a release of antidiuretic hormone from the pars nervosa of the pituitary, now permit a more precise evaluation of the patient with diabetes insipidus than was heretofore possible. Despite these additions to our knowledge of this syndrome, the differential diagnosis in a patient with polyuria and polydipsia may sometimes be difficult. Improperly conducted test procedures not infrequently contribute to a diagnostic dilemma, and occasionally there are dangerous sequelae from injudicious use of vasopressin (Pitressin) preparations in patients with “suspected” diabetes insipidus. Some experiences in the diagnosis and treatment of patients with diabetes insipidus form the basis of this communication. However, before discussion of the clinical syndrome, it is pertinent to review briefly some of the experimental data concerning 1) the antidiuretic hormone, and 2) the induction of diabetes insipidus in animals.