How does loss of HCO3- via the GI tract cause non-anion gap (AG) (hyperchloremic) metabolic acidosis?

Updated: Dec 08, 2020
  • Author: Christie P Thomas, MBBS, FRCP, FASN, FAHA; Chief Editor: Vecihi Batuman, MD, FASN  more...
  • Print

The secretions of the GI tract, with the exception of the stomach, are relatively alkaline, with high concentrations of base (50-70 mEq/L). Significant loss of lower GI secretions results in metabolic acidosis, especially when the kidneys are unable to adapt to the loss by increasing net renal acid excretion.

Such losses can occur in diarrheal states, fistula with drainage from the pancreas or the lower GI tract, and sometimes vomiting if it occurs as a result of intestinal obstruction. When pancreatic transplantation is performed, the pancreatic duct is sometimes diverted into the recipient bladder, from where exocrine pancreatic secretions are lost in the final urine. Significant loss also occurs in patients who abuse laxatives, which should be suspected when the etiology for non-AG metabolic acidosis is not clear.

Urine pH will be less than 5.3, with a negative urine AG reflecting normal urine acidification and increased NH4+ excretion. However, if distal Na+ delivery is limited because of volume depletion, the urine pH cannot be lowered maximally.

Replacing the lost HCO3- on a daily basis can treat this form of metabolic acidosis.

Did this answer your question?
Additional feedback? (Optional)
Thank you for your feedback!