A patient with SIADH has serum Na+ 118 mEq/L and urine osmolality 580 mOsm/kg. The mechanism by which ADH excess causes hyponatremia in SIADH despite the kidney's ability to excrete free water normally is:
- A ADH directly inhibits renal Na+ reabsorption causing natriuresis
- B ADH stimulates thirst leading to polydipsia that overwhelms the kidneys
- C Excess ADH causes water retention beyond what the kidney can excrete; continued water intake exceeds the maximally concentrated urine output capacity, diluting serum Na+ ✓
- D ADH increases renal plasma flow reducing the ability to concentrate tubular fluid
Explanation
In SIADH, ADH is secreted inappropriately (regardless of osmolality/volume). The collecting duct becomes maximally permeable to water (AQP2 inserted apically), and the kidney excretes maximally concentrated urine. However, if water intake (oral + IV) exceeds the volume of maximally concentrated urine that can be produced per day, positive water balance accumulates, diluting serum sodium. The kidney can excrete ~0.6–1 L of maximally concentrated urine (urine osmolality ~1200 mOsm/kg), so if input exceeds this, net water retention occurs. Hyponatremia develops because retained water distributes equally across all body water compartments, diluting Na+. ADH's effect on Na+ transport is minimal; the primary issue is water excess.
Reference: Guyton & Hall, Textbook of Medical Physiology, 14th ed.
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