Renal tubular acidosis during therapy for diabetic ketoacidosis.
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.
D000136:Acid-Base Equilibrium; D000141:Acidosis, Renal Tubular / Q000097:blood / Q000209:etiology* / Q000378:metabolism; D000328:Adult; D001639:Bicarbonates / Q000097:blood / Q000494:pharmacology / Q000627:therapeutic use; D002245:Carbon Dioxide / Q000097:blood; D002712:Chlorides / Q000097:blood; D016883:Diabetic Ketoacidosis / Q000188:drug therapy*; D005260:Female; D006801:Humans; D006863:Hydrogen-Ion Concentration; D007328:Insulin / Q000627:therapeutic use*; D010100:Oxygen / Q000097:blood; D010313:Partial Pressure
D001639:Bicarbonates; D002712:Chlorides; D007328:Insulin; D002245:Carbon Dioxide; D010100:Oxygen