What causes non-anion gap (AG) (hyperchloremic) metabolic acidosis in patients undergoing urinary diversion procedures?

Updated: Dec 08, 2020
  • Author: Christie P Thomas, MBBS, FRCP, FASN, FAHA; Chief Editor: Vecihi Batuman, MD, FASN  more...
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Hyperchloremic metabolic acidosis can develop in patients who undergo a urinary diversion procedure, such as a sigmoid bladder or an ileal conduit.

This occurs through 1 of the following 2 mechanisms:

The first is the intestinal mucosa has an apical Cl-/HCO3- exchanger. When urine is diverted to a loop of bowel (as in patients with obstructive uropathy), the chloride in the urine is exchanged for HCO3-. Significant loss of HCO3- can occur, with a concurrent increase in serum Cl- concentration.

The second is intestinal mucosa reabsorbs urinary NH4+, and the latter is metabolized in the liver to NH3 and H+. This is particularly likely to occur if urine contact time with the intestinal mucosa is prolonged, as when a long loop of bowel is used or when the stoma is obstructed and when sigmoid rather than ileal loop is used. Presumably, the creation of a continent bladder also increases HCO3- loss. This disorder is not observed very frequently anymore because short-loop incontinent ureteroileostomies are used now.

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