A 30-year-old woman with polyuria and polydipsia has a serum sodium of 148 mEq/L. After water deprivation for 8 hours, urine osmolality is 200 mOsm/kg. After desmopressin administration, urine osmolality rises to 650 mOsm/kg. The diagnosis and mechanism are:

• A Nephrogenic diabetes insipidus; ADH present but V2 receptor or AQP2 mutation prevents concentration
• B Central diabetes insipidus; lack of ADH but intact V2 receptor-aquaporin 2 response in collecting duct ✓
• C Primary polydipsia; medullary washout of concentration gradient from excess water intake
• D Partial nephrogenic DI; partial response of collecting duct to supraphysiologic ADH levels

Explanation

The pattern — failure to concentrate urine with water deprivation but brisk response to exogenous desmopressin (dDAVP) — is diagnostic of central (neurogenic) diabetes insipidus. In CDI, the posterior pituitary fails to secrete adequate ADH, so collecting duct V2 receptors are unstimulated and AQP2 channels remain in intracellular vesicles. Desmopressin activates V2 receptors, triggers cAMP-PKA signaling, and causes AQP2 insertion into the apical membrane, restoring water reabsorption. In nephrogenic DI, desmopressin would produce no or minimal response.

Reference: Guyton & Hall, Textbook of Medical Physiology, 14th ed.

High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP

Written and medically reviewed by the StethoPrep medical team.