Which renal tubular acidosis (RTA) type is characterised by inability to lower urine pH below 5.5 despite systemic acidosis, and what is the primary defect?

• A Type 1 (distal) RTA; defective H+-ATPase or H+/K+-ATPase in alpha-intercalated cells of the collecting duct, impairing acid secretion ✓
• B Type 2 (proximal) RTA; failure of HCO3 reabsorption in the proximal tubule, leading to bicarbonate wasting
• C Type 4 RTA (hyperkalaemic); aldosterone deficiency or resistance reducing both K+ and H+ secretion
• D Type 3 RTA; mixed proximal and distal defect with inherited carbonic anhydrase II deficiency

Explanation

In Type 1 (distal) RTA, the primary defect is in the alpha-intercalated cells of the cortical and medullary collecting duct. Normally, these cells use H+-ATPase (and in some species H+/K+-ATPase) to secrete H+ into the tubular lumen against steep concentration gradients, producing urine pH as low as 4.5–5.0. In dRTA, this proton pump is non-functional (or back-leaks), so even during systemic acidosis the urine cannot be acidified below pH 5.5. Clinical features include: hyperchloraemic normal-AG metabolic acidosis, hypokalaemia (due to secondary aldosterone activation and distal K+ wasting), nephrocalcinosis, and nephrolithiasis (calcium phosphate stones). Type 2 RTA (option B) wastes bicarbonate but can still acidify urine below 5.5. Type 4 (option C) causes hyperkalaemia. Type 3 is rare.

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

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