In renal tubular acidosis type 4 (hyperkalemic distal RTA), the primary defect involves which mechanism?
- A Carbonic anhydrase II deficiency causing failure of bicarbonate reclamation in proximal tubule
- B Aldosterone deficiency or resistance causing reduced ENaC activity, impaired H⁺ secretion, and impaired K⁺ secretion in the collecting duct ✓
- C H⁺-ATPase (vacuolar) deficiency in type A intercalated cells causing inability to acidify urine
- D HCO3⁻/Cl⁻ anion exchanger (AE1) defect in type A intercalated cells
Explanation
Type 4 RTA is characterized by hyperkalemia, hyperchloremic (normal anion gap) metabolic acidosis, and urine pH that can be appropriately acidic. The defect is hypoaldosteronism or aldosterone resistance (e.g., in diabetic nephropathy, obstructive uropathy, NSAIDs, ACE inhibitors). Aldosterone normally drives ENaC activity in principal cells, creating a lumen-negative potential that drives both K⁺ secretion (ROMK) and H⁺ secretion (H⁺-ATPase in intercalated cells). Without this potential, both are impaired, causing hyperkalemia and acidosis. CA II defect causes type 3 RTA, H⁺-ATPase defect causes type 1 RTA, AE1 defect also causes type 1.
Reference: Guyton & Hall, Textbook of Medical Physiology, 14th ed.
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