Finally, in the setting of IBD, generally it is accompanied by hyperoxaluria. There are a number of potential mechanisms for this; decreased metabolism of oxalate by oxalobacter formigenes, decreased calcium binding to oxalate because of the relatively increased binding of calcium to malabsorbed fat in the GI tract. In any case, in order to have hyperoxaluria, it is necessary to have a functioning large bowel. In this case, the patient’s urinary oxalate was 28 which is in the low normal range and not suggestive of hyperoxaluria. Thus, the diagnosis is high output of alkaline fluid from an ileostomy.
The treatment in this case is to increase fluids and treat with a combination of sodium and potassium citrate. Even a small rise in urine pH would significantly reduce the risk of uric acid stones while the citrate and increased volume should reduce the calcium oxalate stone risk.