Furosemide acts by inhibiting the Na-K-2Cl cotransporter (NKCC2) in the thick ascending limb of the loop of Henle. Which electrolyte abnormality is a direct consequence of this inhibition that is not seen with thiazide diuretics?
- A Hypernatraemia from excessive sodium retention in the distal tubule
- B Hypocalcaemia due to increased urinary calcium excretion (calciuria) ✓
- C Hypermagnesaemia from reduced magnesium filtration
- D Hyperkalaemia from blockade of potassium secretion in collecting duct
Explanation
NKCC2 inhibition by furosemide blocks calcium reabsorption in the thick ascending limb (which normally occurs by the lumen-positive electrical gradient generated by NKCC2). This causes increased urinary calcium excretion (hypercalciuria), leading to hypocalcaemia with prolonged use — the reason furosemide is used to treat hypercalcaemia of malignancy. In contrast, thiazide diuretics increase calcium reabsorption in the distal convoluted tubule, causing hypercalcaemia. Both loop and thiazide diuretics cause hypokalaemia (not hyperkalaemia), and hyponatraemia (not hypernatraemia).
Reference: KD Tripathi, Essentials of Medical Pharmacology, 8th ed.
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