In Type 1 (distal) Renal Tubular Acidosis (dRTA), the patient cannot acidify the urine below pH 5.5 despite systemic acidosis. Serum electrolytes show hyperchloraemia and hypokalaemia. The biochemical defect responsible for hypokalaemia in dRTA is:
- A Failure to secrete H+ creates a more electronegative lumen, increasing Na+ reabsorption via ENaC with compensatory K+ wasting ✓
- B Impaired H+/K+-ATPase in the collecting duct unable to secrete potassium
- C Alkaline urine activates aldosterone synthase, driving excessive kaliuresis
- D Metabolic acidosis shifts potassium into cells via K+/H+ exchange
Correct answer: A. Failure to secrete H+ creates a more electronegative lumen, increasing Na+ reabsorption via ENaC with compensatory K+ wasting
Explanation
In distal RTA, impaired H+-ATPase (or Cl-/HCO3- exchanger, or carbonic anhydrase II) in alpha-intercalated cells prevents H+ secretion into the collecting duct lumen. This results in less positive lumen charge (reduced electrochemical gradient), yet enhanced Na+ absorption via ENaC generates a more electronegative lumen potential — this drives compensatory K+ secretion through ROMK channels. Systemic acidosis also triggers secondary hyperaldosteronism, further promoting K+ loss and Na+ retention, exacerbating hypokalaemia.
Reference: Harper's Illustrated Biochemistry, 32nd ed.
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