A patient with type 4 renal tubular acidosis (hyperkalemic, hyperchloremic metabolic acidosis) most likely has dysfunction of which transporter or hormone pathway?

• A Carbonic anhydrase II deficiency in proximal tubule reducing HCO3- reabsorption
• B H+-ATPase failure in type A intercalated cells causing classic distal RTA
• C NHE3 dysfunction in the proximal tubule impairing bulk HCO3- reclamation
• D Aldosterone deficiency or resistance impairing principal cell Na+ absorption and H+/K+ secretion in the collecting duct ✓

Explanation

Type 4 RTA (hypoaldosteronism or aldosterone resistance) is characterised by hyperkalemia and hyperchloremic metabolic acidosis. Aldosterone normally stimulates principal cells to reabsorb Na+ (via ENaC), creating a lumen-negative potential that drives K+ and H+ secretion. In its absence or resistance, both K+ and H+ (via type A intercalated cell H+-ATPase) cannot be adequately secreted. The resulting hyperkalemia further suppresses ammoniagenesis, compounding acidosis. Type 2 RTA involves carbonic anhydrase II or NHE3; classic type 1 RTA involves H+-ATPase failure.

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

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