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. 1975 Feb 22;112(4):463–466.

Renal tubular acidosis during therapy for diabetic ketoacidosis.

R Giammarco, M B Goldstein, M L Halperin, B J Stinebaugh
PMCID: PMC1956182  PMID: 234290

Abstract

A young woman presented with typical diabetic ketoacidosis. Five hours after insulin had been given hyperchloremic metabolic acidosis developed. This could not be attributed to gastrointestinal loss of bacarbonate, ingestion of HCI or carbonic anhydrase inhibitor, or the administered fluids and electrolytes. The combination of hyperchloremic metabolic acidosis and a urine pH of 5.6 during acidemia prompted specific studies that established the presence of disorders of renal acidification. A transient defect of hydrogen ion secretion in the distal nephron was suggested by the decrease in urine-blood Pco-2 gradient after administration of sodium bicarbonate. Proximal renal tubular acidosis was indicated by the reduced bicarbonate threshold that persisted for approximately 7 weeks.

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Selected References

These references are in PubMed. This may not be the complete list of references from this article.

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