A patient with chronic respiratory acidosis (pH 7.31, PaCO₂ 68 mmHg, HCO₃⁻ 34 mEq/L) has been stable for 3 weeks. The primary renal compensatory mechanism involves increased activity of which tubular protein?
- A Pendrin (SLC26A4) in type B intercalated cells to secrete bicarbonate
- B Basolateral Cl⁻/HCO₃⁻ exchanger (AE1) in type A intercalated cells to retain Cl⁻
- C Apical H⁺-ATPase and basolateral NBCe1 in the proximal tubule and type A intercalated cells ✓
- D NKCC2 in thick ascending limb to increase sodium reabsorption and alkaline load
Explanation
In chronic respiratory acidosis, the kidneys compensate by maximally retaining bicarbonate. This involves upregulation of H⁺ secretion via apical vacuolar H⁺-ATPase (and H⁺/K⁺-ATPase) in proximal tubule and type A intercalated cells of collecting duct, generating new HCO₃⁻ that exits basolaterally via the electrogenic sodium-bicarbonate cotransporter NBCe1. For each H⁺ secreted, one new HCO₃⁻ is added to blood. Pendrin in type B cells secretes HCO₃⁻ (relevant in alkalosis). Basolateral AE1 in type A cells exchanges Cl⁻ for HCO₃⁻, retaining HCO₃⁻, but NBCe1 drives the bulk of bicarbonate retention.
Reference: Guyton & Hall, Textbook of Medical Physiology, 14th ed.
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