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A 53-year-old man on hemodialysis suffered from short bowel syndrome after subtotal colectomy and partial resection of the small intestine. Laboratory tests showed multiple electrolyte disorders and enlarged sodium and chloride ion (Cl(−)) gaps despite treatment with large volume of sodium chloride replacement via central venous infusion. Blood gas analysis showed slightly high bicarbonate ion levels and metabolic alkalosis was suspected, which is uncommon in end stage kidney disease. The measurement of electrolytes in feces from ileostomy showed relatively high Cl(−) excretion. The loss of Cl(−) to feces may have caused the metabolic alkalosis; thus, additional Cl(−) replacement may have been necessary.

A 47-year-old man presented with severe hypokalemic paralysis and respiratory failure. A large amount of potassium was administered along with providing intensive care, and his condition improved. Hypokalemia was attributed to increased urinary potassium excretion. A kidney biopsy was performed to make a definitive histological diagnosis. It revealed acute tubulointerstitial nephritis (TIN). After the diagnosis, prednisolone was administered, and the TIN gradually improved. From the clinical course and laboratory findings, the TIN was presumed to be an autoimmune disorder. Further specific autoantibody tests were positive for anti-mitochondrial antibody (AMA), which has been gaining increasing attention in regard to TIN. In addition, all previous cases of TIN associated with AMA have affected females. The detailed pathogenetic mechanisms are as yet unclear and require further investigation.