In a patient with central diabetes insipidus, which of the following findings would be expected in response to a water deprivation test followed by exogenous ADH administration?

Explanation

## Water Deprivation Test in Central Diabetes Insipidus **Key Point:** Central diabetes insipidus (CDI) results from **deficient ADH production or release** by the posterior pituitary. The kidneys retain normal ability to respond to ADH. Therefore, exogenous ADH administration restores normal water reabsorption and increases urine osmolality. ### Pathophysiology of Central DI | Feature | Central DI | Nephrogenic DI | |---------|-----------|----------------| | **ADH Level** | Low/absent | Normal or elevated | | **Kidney Response to ADH** | Normal (intact V2 receptors & AQP2) | Absent (defective receptor/channel) | | **Urine Osmolality (baseline)** | < 300 mOsm/kg | < 300 mOsm/kg | | **After Water Deprivation** | Minimal increase (ADH still low) | No increase (kidneys cannot respond) | | **After Exogenous ADH** | **Increases significantly** | Remains low (kidneys unresponsive) | **High-Yield:** The **water deprivation test + ADH challenge** is the gold standard diagnostic algorithm: 1. **Phase 1 (Water deprivation):** If urine osmolality rises to > 600 mOsm/kg → primary polydipsia (normal response). If remains < 300 → proceed to Phase 2. 2. **Phase 2 (Exogenous ADH):** - **Urine osmolality rises** → Central DI (kidneys respond to exogenous ADH) - **Urine osmolality unchanged** → Nephrogenic DI (kidneys cannot respond) ### Clinical Correlation **Clinical Pearl:** Patients with central DI present with: - Polyuria (urine output 5–20 L/day) - Polydipsia (intense thirst) - Hypernatremia (if water intake is restricted) - Normal kidney function on baseline labs Treatment: Desmopressin (synthetic ADH analog) — effective in central DI, ineffective in nephrogenic DI. **Mnemonic:** **CDIADH** — **C**entral DI responds to **ADH** (exogenous); **N**ephrogenic DI does **N**ot.