Proximal renal tubular acidosis (type 2 RTA) is characterised by defective HCO3- reabsorption in the PCT. This directly impairs which transport mechanism?

• A All three of the above can be defective in proximal RTA ✓
• B Basolateral Na+/HCO3- cotransporter (NBCe1, SLC4A4)
• C Luminal carbonic anhydrase IV catalysing CO2 and H2O recombination
• D Na+/H+ exchanger NHE3 on the apical membrane of PCT cells

Explanation

Proximal RTA (type 2) can result from defects at multiple steps in proximal tubular bicarbonate reclamation. NHE3 (Na+/H+ exchanger 3) on the apical membrane secretes H+ into the lumen, which combines with filtered HCO3- to form H2CO3. Carbonic anhydrase IV (luminal) catalyses H2CO3 → CO2 + H2O, and carbonic anhydrase II (cytoplasmic) re-forms HCO3- inside the cell. NBCe1 (SLC4A4) on the basolateral membrane co-transports Na+ and HCO3- into the peritubular circulation. Mutations in CA II (causing combined proximal and distal RTA), NBCe1 (SLC4A4 mutations cause isolated proximal RTA with ocular abnormalities), or NHE3 dysfunction all impair proximal HCO3- reclamation.

Reference: Harper's Illustrated Biochemistry, 32nd ed.

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