Furosemide is a loop diuretic. The electrolyte abnormality most likely with chronic high-dose furosemide therapy, and its mechanism, is:

• A Hyperkalemia due to distal tubule potassium retention from ENaC blockade
• B Hypernatremia due to free water excretion exceeding sodium excretion
• C Hypermagnesemia due to magnesium reabsorption in the proximal tubule
• D Hypokalemia, because increased sodium delivery to the distal nephron (collecting duct) activates aldosterone-stimulated Na+/K+ exchange, causing K+ wasting ✓

Explanation

Furosemide blocks NKCC2 in the thick ascending limb, dramatically increasing sodium delivery to the distal convoluted tubule and collecting duct; aldosterone-sensitive principal cells respond to the increased luminal Na+ by upregulating ENaC (Na+ entry) and ROMK (K+ secretion), causing hypokaliuria — rather, kaliuresis — and hypokalemia. Concurrent hypomagnesemia and metabolic alkalosis (from H+ secretion) are also expected. Hypokalemia is the most clinically important chronic complication requiring potassium supplementation or potassium-sparing diuretic co-administration.

Reference: KD Tripathi, Essentials of Medical Pharmacology, 8th ed.

High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP

Written and medically reviewed by the StethoPrep medical team.