Central diabetes insipidus results from deficiency of ADH production. Which of the following would be the expected finding in a patient with this condition?

Explanation

## Central Diabetes Insipidus: Pathophysiology and Findings ### Definition **Key Point:** Central diabetes insipidus (CDI) is caused by insufficient ADH secretion from the posterior pituitary, resulting in inability to concentrate urine despite high plasma osmolality. ### Expected Laboratory and Clinical Findings | Parameter | Normal | Central DI | | --- | --- | --- | | Plasma osmolality | 280–295 mOsm/kg | **↑ (>295 mOsm/kg)** | | Urine osmolality | 50–1200 mOsm/kg (variable) | **↓ (<200 mOsm/kg, often <100)** | | Urine output | 1–2 L/day | **↑ (5–20 L/day) — polyuria** | | ADH level | ↑ when plasma osmolality ↑ | **↓ (inappropriately low)** | | Response to exogenous ADH | N/A | **Urine osmolality ↑ dramatically** | ### Pathophysiology 1. **ADH deficiency** → collecting duct remains impermeable to water 2. **Water loss in urine** → plasma osmolality rises 3. **Osmoreceptor stimulation** → thirst mechanism activated 4. **Polyuria + polydipsia** → clinical presentation 5. **Exogenous ADH administration** → restores aquaporin-2 insertion → urine osmolality normalizes ### Diagnostic Algorithm ```mermaid flowchart TD A[Polyuria + High plasma osmolality]:::outcome --> B{Urine osmolality?}:::decision B -->|Low| C[ADH deficiency vs nephrogenic DI]:::decision C -->|Give desmopressin|D[Urine osmolality ↑?]:::decision D -->|Yes|E[Central DI]:::outcome D -->|No|F[Nephrogenic DI]:::outcome B -->|High|G[Primary polydipsia]:::outcome ``` **High-Yield:** The **desmopressin (synthetic ADH) challenge test** is the gold standard to differentiate central from nephrogenic DI. Central DI responds; nephrogenic does not. **Clinical Pearl:** Patients with CDI present with severe polydipsia (thirst) and polyuria. If access to water is restricted, severe hypernatremia and dehydration develop rapidly. [cite:Harrison 21e Ch 297; Costanzo 6e Ch 4]