A patient with chronic kidney disease and sustained metabolic acidosis shows markedly increased renal ammonium excretion. Which substrate and cellular process account for this adaptive response?
- A Deamination of alanine in the thick ascending limb, driven by glucocorticoids
- B Metabolism of glutamine in the proximal tubule, producing ammonium and bicarbonate, upregulated by chronic acidosis ✓
- C Urease-mediated hydrolysis of filtered urea in the collecting duct lumen
- D Transamination of pyruvate in alpha-intercalated cells, generating ammonium for luminal secretion
Correct answer: B. Metabolism of glutamine in the proximal tubule, producing ammonium and bicarbonate, upregulated by chronic acidosis
Explanation
Chronic acidosis induces glutaminase and related enzymes in proximal tubular mitochondria, increasing uptake and metabolism of glutamine. Each glutamine molecule yields two ammonium ions, secreted into the lumen mostly as NH4+ exchanged for sodium on NHE3, and two new bicarbonate ions returned to blood via the basolateral cotransporter. This response can rise severalfold over days and is the dominant adaptive route for excreting fixed acid. Intercalated cells handle titratable acid and proton pumping, not ammoniagenesis, and urea hydrolysis does not occur in the human kidney.
Reference: Vander's Renal Physiology, 8th ed.
High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP
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