Abstract
The case of a 64-year-old man who started hemodialysis at the age of 31 years is presented. The patient began experiencing diarrhea in July 2013 and presented with a circumferential protruding lesion and an ulcer in the ascending colon. An examination of the biopsy sample showed inflammatory cell infiltration. The patient revealed a positive result of an interferon-γ release assay test and was diagnosed with intestinal tuberculosis. Treatment with antituberculous drugs was initiated, but was ineffective. Four months later, the patient also developed ileus and consequently underwent right hemicolectomy, ileostomy, and mucous fistula. Postoperatively, the patient exhibited hypotension, hyperkalemia, and metabolic acidosis. The cause of the acidosis was considered to be massive diarrhea, and it improved after the administration of sodium bicarbonate and other treatments. However, the hyperkalemia persisted even after ion-exchange resin treatment. One year later, a stoma reversal was performed, and the patient’s serum potassium level subsequently decreased. As his hyperkalemia improved promptly after the stoma reversal, it was considered that it had been caused reduced potassium excretion in the colon. This case highlights the importance of a compensatory mechanism for increasing intestinal potassium excretion in hemodialysis patients.
