INTRODUCTION — The major symptoms of central insipidus (DI) are polyuria, nocturia, and polydipsia due to
the concentrating defect. Treatment of this disorder is primarily aimed at decreasing the urine output, usually by increasing
the activity of antidiuretic hormone (ADH, also called arginine vasopressin or AVP).
Replacement of previous and ongoing fluid losses is also important. Most patients with central DI have a normal or only
mildly elevated plasma sodium concentration because concurrent stimulation of thirst minimizes the degree of net water
loss. However, hypernatremia can occur if thirst is impaired or the patient has no access to water [1]. Correction of the
hypernatremia requires repair of this free water deficit.