In type 4 renal tubular acidosis (RTA), what is the PRIMARY mechanism causing the hyperchloremic non-anion-gap metabolic acidosis?
- A Aldosterone deficiency or resistance → impaired H⁺ and K⁺ secretion in the collecting duct → reduced NH4⁺ excretion and hyperkalemia ✓
- B Proximal tubule failure to reabsorb HCO3⁻ → HCO3⁻ wasting in urine
- C Absent distal H⁺-ATPase pump leading to inability to acidify urine below pH 5.3
- D Carbonic anhydrase II deficiency preventing H2CO3 dissociation in both proximal and distal nephron
Explanation
Type 4 RTA results from hypoaldosteronism (or tubular resistance to aldosterone, as in diabetic nephropathy or drugs like ACE inhibitors). Aldosterone is required for principal cell Na⁺ reabsorption, which generates the negative lumen potential that drives H⁺ secretion by intercalated cells and K⁺ secretion. Without aldosterone, H⁺ secretion decreases, but more critically, the NH4⁺ excretion pathway is impaired because hyperkalemia (from lost K⁺ secretion) suppresses renal ammoniagenesis. The resultant impaired net acid excretion causes non-anion-gap acidosis. Option B is type 2 (proximal) RTA. Option C is type 1 (distal) RTA. Option D is a rare autosomal recessive syndrome.
Reference: Guyton & Hall, Textbook of Medical Physiology, 14th ed.
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