A patient on carbamazepine for epilepsy develops hyponatremia with serum sodium of 126 mEq/L. What is the mechanism underlying this adverse effect?
- A Carbamazepine inhibits renal sodium-potassium-ATPase causing sodium wasting
- B Carbamazepine stimulates V2 vasopressin receptors in renal collecting duct, enhancing aquaporin-2 insertion and water reabsorption ✓
- C Carbamazepine blocks aldosterone receptors in distal tubule
- D Carbamazepine upregulates SIADH via hypothalamic osmoreceptor stimulation
Explanation
Carbamazepine-induced hyponatremia results from an antidiuretic hormone (ADH)-like action: it directly stimulates V2 vasopressin receptors (or enhances renal tubular sensitivity to ADH) in the collecting duct, leading to aquaporin-2 upregulation and excessive water reabsorption. This dilutional hyponatremia is a form of drug-induced SIADH. Management includes fluid restriction; demeclocycline or vasopressin receptor antagonists (tolvaptan) can be considered in refractory cases. Oxcarbazepine carries an even higher risk (up to 25-30%) of hyponatremia.
Reference: KD Tripathi, Essentials of Medical Pharmacology, 8th ed.
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