A 60-year-old woman on long-term furosemide has persistent hypokalaemia (serum K+ 3.0 mmol/L) despite aggressive oral potassium replacement, with continued urinary potassium losses. Serum magnesium is 1.2 mg/dL (low). Her potassium deficit cannot be corrected until magnesium is replaced because hypomagnesaemia:
- A Increases activity of the Na+/K+-ATPase in principal cells, driving potassium into the lumen
- B Stimulates aldosterone secretion independently of the renin-angiotensin axis
- C Removes the normal intracellular block on ROMK channels in the distal nephron, increasing renal potassium secretion ✓
- D Reduces sodium reabsorption through ENaC, increasing luminal flow rate and potassium washout
Correct answer: C. Removes the normal intracellular block on ROMK channels in the distal nephron, increasing renal potassium secretion
Explanation
Intracellular magnesium normally occludes the pore of the ROMK channel from the cytosolic side. When magnesium is depleted, this block is lifted, potassium exits cells into the lumen more freely, and renal potassium wasting persists regardless of how much potassium is given. Aldosterone and ENaC activity are unaffected by magnesium, and Na+/K+-ATPase activity is actually reduced in magnesium depletion, which kills option A.
Reference: Ganong's Review of Medical Physiology, 26th ed.
High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP
Written and medically reviewed by the StethoPrep medical team.