A 45-year-old man has Type 4 renal tubular acidosis (hyperkalaemic distal RTA) secondary to diabetic nephropathy. Which of the following is the MECHANISM and which drug CORRECTS both hyperkalaemia and acidosis?
- A Aldosterone deficiency/resistance causing impaired K+ and H+ secretion in collecting duct; fludrocortisone ✓
- B Defective H+-ATPase in collecting duct; fludrocortisone
- C Proximal bicarbonate wasting; sodium bicarbonate supplements
- D Carbonic anhydrase inhibition in proximal tubule; acetazolamide
Explanation
Type 4 RTA (hyporeninism-hypoaldosteronism or aldosterone resistance) is the most common RTA in adults, typically in diabetic nephropathy or obstructive uropathy. The mechanism is reduced aldosterone action in the cortical collecting duct, impairing both K+ secretion (→hyperkalaemia) and H+ secretion (→non-anion-gap metabolic acidosis). Fludrocortisone (a mineralocorticoid) corrects both abnormalities by restoring aldosterone receptor activity. Type 1 (distal) RTA involves defective H+-ATPase and presents with hypokalaemia. Type 2 (proximal) RTA involves bicarbonaturia.
Reference: Harrison's Principles of Internal Medicine, 21st ed.
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