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The clinical features and causes of hyperchloremic acidosis in diabetics were examined in three patients. All of them had a history of diabetes mellitus of more than 10 years and were complicated with advanced retinopathy, neuropathy including autonomic nerve involvement, severe to moderate nephropathy and hypertension. Both case 1 (59-year-old male) and case 2 (44-year-old male) showed hyperkalemia, aciduria (pH5.0) and hyporeninemic hypoaldosteronemia. These clinical features corresponed to the renal tubular acidosis type IV described by Sebastian et al. Potassium load by hemolysis (case 2) and rapid depletion of plasma volume by spironolactone and furosemide (cases 1 and 2) were considered to be triggers of the acidosis. It is thought that hyperkalemia provoked a severe decrease in ammonium production by the distal tubules of these patients which were already impaired, and that hypovolemia and spironolactone promoted their hyporeninemic hypoaldosteronism. Case 3 (46-year-old male) showed the hypokalemic type of hyperchloremic acidosis triggered by acetazolamide which was administered for his glaucoma. Although acetazolamide was the direct cause of this acidosis, it is suspected that some renal abnormality such as in the two above patients was another contributory factor. Their acidosis was normalized by the oral administration of NaHCO3 and removal of the probable triggers.<BR>These findings suggest that in advanced diabetics, rapid depletion of plasma volume by spironolactone and/or administration of acetazolamide may present a hazard which leads to severe metabolic acidosis.
- 一般社団法人 日本糖尿病学会の論文
一般社団法人 日本糖尿病学会 | 論文
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