Type 4 renal tubular acidosis (hyperkalemic distal RTA) is caused by aldosterone deficiency or resistance. The resulting hyperkalemia itself worsens the acidosis through which additional mechanism?

• A Excess K⁺ competes with H⁺ for secretion by the H⁺/K⁺-ATPase in collecting duct type A cells
• B Hyperkalemia inhibits renal ammoniagenesis in the proximal tubule, reducing NH₃ available for H⁺ buffering in collecting duct ✓
• C High serum K⁺ stimulates chloride channel CFTR opening, reducing H⁺ secretion
• D Hyperkalemia activates thiazide-sensitive NaCl cotransporter, reducing distal tubule H⁺ secretion

Explanation

Hyperkalemia independently worsens metabolic acidosis by impairing renal ammoniagenesis. In the proximal tubule, NH₄⁺ (formed from glutamine) is the primary urinary buffer that allows net acid excretion. Hyperkalemia suppresses the enzyme phosphate-dependent glutaminase and reduces NH₃/NH₄⁺ production, drastically limiting titration of secreted H⁺ in the medullary collecting duct. This vicious cycle — aldosterone deficiency → hyperkalemia → reduced ammoniagenesis → worsening acidosis — is the hallmark of type 4 RTA. H⁺/K⁺-ATPase actually uses K⁺ reabsorption coupled to H⁺ secretion, so hyperkalemia would reduce the driving force for this exchanger.

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

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