A patient with profuse vomiting develops metabolic alkalosis. Which renal mechanism PARADOXICALLY perpetuates alkalosis by excreting acid urine?
- A Volume depletion activates the RAAS, promoting Na+ and HCO3- reabsorption and H+ secretion in the distal nephron ('contraction alkalosis' maintained by secondary hyperaldosteronism) ✓
- B Elevated serum HCO3- increases filtered load, directly inhibiting collecting duct H+/K+-ATPase
- C Hypokalaemia activates carbonic anhydrase in the proximal tubule, increasing H+ secretion
- D Chloride loss causes metabolic alkalosis which is self-limiting due to renal bicarbonate wasting
Correct answer: A. Volume depletion activates the RAAS, promoting Na+ and HCO3- reabsorption and H+ secretion in the distal nephron ('contraction alkalosis' maintained by secondary hyperaldosteronism)
Explanation
Vomiting causes HCl loss (raising HCO3−) and volume contraction with hypokalemia. Volume depletion activates the RAAS; aldosterone promotes ENaC-mediated Na+ reabsorption in the collecting duct, creating an electronegative lumen that drives H+ and K+ secretion, generating 'paradoxical aciduria.' This perpetuates the alkalosis despite elevated serum HCO3−. Chloride-responsive metabolic alkalosis (urinary Cl− < 10 mEq/L) is corrected by saline replenishment, which suppresses RAAS.
Reference: Harper's Illustrated Biochemistry, 32nd ed.
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