CHARLES C. BAILEY JR., M.D.; ROBERT W. STEINER, M.D.
To the editor: Oh and colleagues (1) reported a series of patients in whom hyperchloremic metabolic acidosis developed during the recovery phase of diabetic ketoacidosis. They speculated that elevated renal excretion of beta-hydroxybutyrate anion could have been responsible for loss of potentially regenerated bicarbonate and maintenance of a normal anion gap. Alternatively, Fisher (2) has suggested that hyperchloremic metabolic acidosis could result from proximal tubule bicarbonate wasting secondary to hypophosphatemia. We have documented a transient renal acidification defect that may have contributed to the development of hyperchloremic metabolic acidosis in a patient with insulin-treated diabetic ketoacidosis.
A 27-year-old white woman
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BAILEY CC, STEINER RW. Renal Acidification Defect in Diabetic Ketoacidosis. Ann Intern Med. 1980;92:263. doi: 10.7326/0003-4819-92-2-263_2
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Published: Ann Intern Med. 1980;92(2_Part_1):263.
Cardiology, Coronary Risk Factors, Diabetes, Endocrine and Metabolism, Nephrology.
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Print ISSN: 0003-4819 | Online ISSN: 1539-3704
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