In a patient with syndrome of inappropriate ADH secretion (SIADH), serum Na+ is 118 mEq/L, serum osmolality is 245 mOsm/kg, urine osmolality is 600 mOsm/kg, and urine Na+ is 65 mEq/L. Why is the urine Na+ elevated despite hyponatraemia?
- A ADH directly stimulates the Na+-K+-2Cl cotransporter (NKCC2) in the thick ascending limb, increasing urinary Na+ loss
- B Low serum osmolality inhibits proximal tubular Na+ reabsorption, wasting Na+ in urine
- C Volume expansion from water retention suppresses aldosterone and increases ANP, causing natriuresis that lowers serum sodium further ✓
- D Inappropriate ADH causes amiloride-sensitive Na+ channels in the collecting duct to malfunction, leaking Na+ into urine
Explanation
In SIADH, excessive ADH causes water retention and dilutional hyponatraemia. The water retention expands the extracellular (and plasma) volume. This volume expansion has two consequences that produce urinary sodium loss: (1) atrial stretch causes ANP and BNP release, which inhibit tubular sodium reabsorption and promote natriuresis; and (2) volume expansion suppresses RAAS, lowering aldosterone, thereby reducing distal tubular sodium reabsorption. This natriuresis worsens the hyponatraemia further. The elevated urinary Na+ (>40 mEq/L) in the context of hyponatraemia and dilute serum (but concentrated urine) is a key diagnostic criterion for SIADH. Options B–D describe incorrect mechanisms.
Reference: Guyton & Hall, Textbook of Medical Physiology, 14th ed.
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