In a patient with chronic metabolic acidosis, urinary ammonium excretion rises several-fold above baseline within days. The adaptive process responsible is:
- A Upregulation of glutamine deamidation and glutamate deamination in proximal tubular cells ✓
- B Conversion of filtered creatinine to ammonium in the collecting duct lumen
- C Increased hepatic conversion of ammonia to glutamine for urinary delivery
- D Passive diffusion of arterial ammonia into the distal nephron along its gradient
Explanation
Chronic acidosis induces enzymes of proximal tubular ammoniagenesis: each glutamine molecule metabolized yields two NH4+ and two new bicarbonate ions that are returned to the blood. Urinary NH4+ excretion can rise from roughly 30 to over 300 mEq/day, and it is quantitatively the dominant adaptive route for net acid excretion because titratable acid is capped by available phosphate. Hepatic glutamine uptake actually falls in systemic acidosis to spare substrate for the kidney.
Reference: Robbins and Cotran Pathologic Basis of Disease, 10th ed.
High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP
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