Abstract
Diabetes insipidus, a syndrome characterized by polyuria, polydipsia and excretion of urine of low specific gravity, may result from a deficiency of the neurohypophyseal antidiuretic hormone.1 Since this hormone is presumed to control the "facultative" reabsorption of water in the distal tubule of the kidney the specific physiologic "defect" in diabetes insipidus is usually attributed to a decrease or absence of renal reabsorption of water in this portion of the nephron.2 As a consequence of this physiologic abnormality, the untreated patient with diabetes insipidus may suffer from dehydration resulting from loss of water in excess of intake, unless he is . . .