In a patient with type 4 renal tubular acidosis (hyperkalemic hyperchloremic metabolic acidosis), which specific mechanism is PRIMARILY responsible for the hyperkalemia?

• A Aldosterone deficiency or resistance impairing principal cell K+ secretion in the cortical collecting duct ✓
• B Reduced Na+/K+-ATPase activity in the cortical collecting duct
• C Increased distal delivery of potassium from the loop of Henle
• D Metabolic acidosis directly inhibiting renal K+ excretion via H-K ATPase activation

Explanation

Type 4 RTA results from hypoaldosteronism (e.g., from diabetic nephropathy, ACE inhibitors) or aldosterone resistance (e.g., in obstructive uropathy, trimethoprim). Aldosterone normally drives K+ secretion via ENaC and ROMK channels in principal cells of the cortical collecting duct. Without aldosterone action, K+ accumulates in plasma — causing hyperkalemia. The hyperkalemia itself then suppresses NH4+ production, reducing ammonium excretion and causing non-anion gap metabolic acidosis. Options A, C, and D are not the primary mechanisms in type 4 RTA.

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

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