A patient with chronic respiratory alkalosis from prolonged mechanical hyperventilation develops a serum HCO3- of 16 mEq/L. This represents which renal compensatory mechanism at the molecular level?
- A Decreased H+ secretion via NHE3 in the proximal tubule, reducing HCO3- reclamation
- B Increased Cl-/HCO3- exchange (pendrin) in type B intercalated cells of the collecting duct ✓
- C Upregulation of carbonic anhydrase IV in the thick ascending limb
- D Decreased aldosterone stimulating H+ retention in type A intercalated cells
Correct answer: B. Increased Cl-/HCO3- exchange (pendrin) in type B intercalated cells of the collecting duct
Explanation
In respiratory alkalosis, the kidney compensates by excreting HCO3- to lower plasma levels. This occurs via upregulation of pendrin (SLC26A4), the Cl-/HCO3- exchanger on the apical surface of type B intercalated cells in the cortical collecting duct. Pendrin secretes HCO3- into the lumen in exchange for Cl-, effectively excreting the excess bicarbonate. NHE3 downregulation also contributes by reducing proximal tubular HCO3- reabsorption, but the type B intercalated cell via pendrin is the primary effector of net HCO3- secretion.
Reference: Guyton & Hall, Textbook of Medical Physiology, 14th ed.
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