2017 Volume 60 Issue 10 Pages 726-731
A 55-year-old man had type I diabetes mellitus pointed out 24 years earlier, and insulin intensive therapy had been given. Because his symptoms of nausea and vomiting had appeared from one week before his hospitalization, we first suspected diabetic keto-acidosis and performed an arterial blood gas assay. The data revealed the development of significant anion gap non-increased-type metabolic acidosis. Bladder urinary tract full extraction and ileal conduit reconstruction had been performed for the treatment of bladder cancer one year earlier, so we considered the disorder of acid excretion in the kidney to be due to diabetic nephropathy or renal tubular acidosis; however, several tests failed to confirm this etiology. Because his intestinal peristalsis had been reduced by diabetic neuropathy, the excretion of bicarbonate was enhanced by urinary retention. In addition, urinary acid excretion by the kidney was affected due to diabetic nephropathy, which might have induced his acidosis. The patient was treated with bicarbonate administration, and all symptoms disappeared. However, the continuous administration of bicarbonate has been needed, based on a blood gas analysis one year later. We should therefore recognize that metabolic acidosis can be induced by urinary diversion through the ileum in patients with diabetic complications.