Hyperchloremic metabolic acidosis in diabetes mellitus: a case report and discussion of pathophysiologic mechanisms.
A 21-year old woman with poorly controlled diabetes mellitus was examined for persistent hyperchloremic metabolic acidosis. There was no evidence of ingestion of hydrochloric acid or its equivalent. Gastrointestinal loss of bicarbonate was absent. Proximal tubular bicarbonate reabsorption and distal nephron hydrogen-ion secretion were normal. Ammonia and net acid excretions were high, and thus there was no obvious cause for this acidosis. Further study revealed a very large loss of beta-hydroxybutyrate in the urine that closely approximated net acid excretion. This loss of potential bicarbonate was the principal cause for the hyperchloremic metabolic acidosis. Phosphate, urate, and beta-hydroxybutyrate fractional excretions were all abnormally high. Generalized aminoaciduria was also present, but the renal handling of glucose and bicarbonate was normal. With improved control of her diabetes, the generalized aminoaciduria disappeared, the urine beta-hydroxybutyrate loss ceased, the fractional excretions of phosphate and urate approached normal, and the acidosis was rapidly corrected.
D000328:Adult; D000596:Amino Acids / Q000652:urine; D001639:Bicarbonates / Q000378:metabolism; D016883:Diabetic Ketoacidosis / Q000378:metabolism / Q000503:physiopathology*; D005260:Female; D006801:Humans; D006885:Hydroxybutyrates / Q000652:urine; D007684:Kidney Tubules / Q000503:physiopathology; D010710:Phosphates / Q000652:urine; D014527:Uric Acid / Q000652:urine
D000596:Amino Acids; D001639:Bicarbonates; D006885:Hydroxybutyrates; D010710:Phosphates; D014527:Uric Acid