In type 1 (distal) renal tubular acidosis, the patient cannot acidify urine below pH 5.5. The fundamental defect involves failure of which membrane protein in alpha-intercalated cells of the collecting duct?

• A Na⁺-K⁺-ATPase on the basolateral membrane
• B H⁺-ATPase (V-type proton pump) on the apical membrane ✓
• C Carbonic anhydrase type II in the cytoplasm
• D AE1 (band 3 protein) Cl⁻/HCO₃⁻ exchanger on the basolateral membrane

Explanation

Type 1 (distal) RTA results from impaired H⁺ secretion by alpha-intercalated cells; the most common mechanism is loss-of-function of the apical V-type H⁺-ATPase, preventing urine pH from falling below 5.5. Mutations in the basolateral AE1 (Cl⁻/HCO₃⁻ exchanger) also cause autosomal dominant/recessive forms by impairing HCO₃⁻ exit and indirectly H⁺ secretion. Type 2 (proximal) RTA involves impaired HCO₃⁻ reabsorption in the proximal tubule. Type 4 RTA involves aldosterone deficiency/resistance causing hyperkalemia and acidosis.

Reference: Guyton & Hall, Textbook of Medical Physiology, 14th ed.

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