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Physiology · Renal and acid–base: magnesium and calcium handling in the thick ascending limb
Sample itemA patient on long-term high-dose furosemide has increased urinary magnesium and calcium excretion. Which mechanism explains this?
Original practice item, not a recalled exam question. Nothing here is recorded.
The answer and the reasoning
B. Loss of the lumen-positive potential that drives paracellular divalent cation reabsorption
Potassium recycling through ROMK in the thick ascending limb makes the lumen positive relative to the interstitium, and this potential drives paracellular reabsorption of calcium and magnesium. Blocking NKCC2 with a loop diuretic abolishes the potential, so both ions are lost in the urine.
Option by option
A. Inhibition of PTH secretion by the diuretic
PTH secretion is not inhibited by loop diuretics.
B. Loss of the lumen-positive potential that drives paracellular divalent cation reabsorption (correct)
Correct. The lumen-positive potential that drives paracellular reabsorption is lost.
C. Increased reabsorption of sodium in the proximal tubule
Loop diuretics do not increase proximal sodium reabsorption.
D. Direct inhibition of calcium channels in the distal tubule
Loop diuretics act on the thick ascending limb, and thiazides, not loop diuretics, act on the distal tubule calcium handling.
Source note: Original NextPrep sample item — pending expert review. This item is original practice material awaiting independent expert review, so confirm important facts in a standard textbook.
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