In type 4 (hyperkalaemic) renal tubular acidosis, the pathophysiology centres on:

• A Failure of alpha-intercalated cells to secrete H+ due to carbonic anhydrase II deficiency
• B Impaired proximal tubule HCO3- reabsorption with HCO3- wasting in urine
• C Aldosterone deficiency or resistance impairing K+ excretion and NH4+ formation/excretion in collecting duct ✓
• D Urinary NH3 trapping by acid pH causing NH4+ excretion defect

Explanation

Type 4 RTA (hyperreninaemic or hyporeninnaemic hypoaldosteronism) is caused by aldosterone deficiency (Addison's, heparin, ACE inhibitors, NSAIDs) or tubular resistance (diabetic nephropathy, obstructive uropathy). Aldosterone drives K+ excretion and stimulates NH3 synthesis/NH4+ secretion in the collecting duct — critical for net acid excretion. Without adequate aldosterone effect, hyperkalaemia develops, NH4+ production falls, and the kidneys fail to excrete the daily acid load, causing a normal anion gap (hyperchloraemic) metabolic acidosis. Type 1 RTA involves alpha-intercalated cell failure; Type 2 involves proximal HCO3- wasting.

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

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Written and medically reviewed by the StethoPrep medical team.