A patient with chronic diarrhea develops a hyperchloremic, non-anion gap metabolic acidosis. What is the most likely mechanism?

• A. Loss of bicarbonate with potassium depletion
• B. Impaired renal ammoniagenesis
• C. Bicarbonate loss with chloride retention
• D. Increased intestinal acid production

Answer: (C)

Chronic diarrheal loss of bicarbonate creates a hyperchloremic, non‑anion gap metabolic acidosis. The gut fluids are rich in bicarbonate, so when a large volume is lost in stool, circulating base decreases. To keep electrical neutrality, serum chloride rises to compensate for the missing bicarbonate, producing hyperchloremia while the anion gap stays normal. This combination—loss of bicarbonate with a concurrent rise in chloride—is the hallmark mechanism behind the acidosis in chronic diarrhea.

Other options describe different scenarios: impaired renal ammoniagenesis would cause acidosis from reduced acid excretion at the kidney, not from GI bicarbonate loss; increased intestinal acid production isn’t the typical driver of this pattern; and bicarbonate loss with potassium depletion isn’t the primary explanation for the hyperchloremic, non‑anion gap picture seen with diarrheal bicarbonate loss.