A 38-year-old physician developed polyuria and hypodipsia four days after the onset of an upper respiratory tract infection. Subsequent investigation showed a concentration defect with dehydration that partially corrected with vasopressin injection (Pitressin) administration compatible with partial central diabetes insipidus (DI). Skull roentgenograms, EEG, and lumbar puncture were normal. The polyuria and hypodipsia slowly resolved without treatment. Normal urinary concentration ability was achieved by the 48th day, but a residual elevation in serum osmolarity persisted for one year. Review of the literature failed to show previous documentation of transient DI with elevated serum osmolarity from an acute, febrile illness. The mechanism is speculative, but may be related to a subclinical encephalitis. The true frequency of this syndrome and its relationship to the frequent observation of transient polydipsia and polyuria in "benign" febrile illness remains to be determined.
(Arch Intern Med 137:1479-1481, 1977)