A patient with chronic metabolic alkalosis (from villous adenoma causing K+ and Cl- loss) shows persistent alkalemia despite volume repletion. Which renal mechanism perpetuates metabolic alkalosis in this scenario?
- A Decreased bicarbonate reabsorption in the proximal tubule
- B Hypokalemia causing intracellular H+ shift and paradoxical aciduria maintaining HCO3 excess ✓
- C Increased urinary bicarbonate excretion correcting the alkalosis
- D Reduced aldosterone secretion decreasing distal H+ secretion
Explanation
In hypokalemia-induced metabolic alkalosis, intracellular K+ depletion causes H+ to shift into cells in exchange for K+ to maintain electroneutrality. This intracellular acidosis in renal tubular cells stimulates H+ secretion and HCO3 reabsorption — creating 'paradoxical aciduria' (acid urine despite systemic alkalosis). The kidney thus perpetuates alkalosis by continuing to reabsorb bicarbonate. Volume depletion also increases proximal HCO3 reabsorption. Options A and C are opposite to what occurs; option D incorrectly involves aldosterone when the primary driver here is hypokalemia.
Reference: Guyton & Hall, Textbook of Medical Physiology, 14th ed.
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