After a motor vehicle accident, a 24-year-old man develops polyuria of 8 L/day and polydipsia. During a supervised water deprivation test, urine osmolality rises only to 180 mOsm/kg after 6 hours. Desmopressin is given subcutaneously and urine osmolality subsequently rises above 600 mOsm/kg. What is the underlying lesion?

• A Mutation in the vasopressin V2 receptor gene impairing renal response
• B Hypercalcemia-induced impairment of the countercurrent concentrating gradient
• C Primary polydipsia suppressing ADH release chronically
• D Loss of antidiuretic hormone secretion from destruction of the hypothalamo-neurohypophyseal tract ✓

Explanation

Failure to concentrate urine during water deprivation followed by a brisk rise in osmolality after desmopressin defines central (neurogenic) diabetes insipidus: the kidney and its receptors are intact, so exogenous ADH works. Trauma to the skull base can sever the supraopticohypophyseal tract and cause permanent ADH deficiency. In nephrogenic DI (option A) or hypercalcemic concentrating defects (option B), desmopressin would produce no rise in urine osmolality. Primary polydipsia concentrates normally once water intake stops.

Reference: Harrison's Principles of Internal Medicine, 21st ed.

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