[Kidney tubule dysfunction caused by acetic acid].
Two patients admitted after ingestion of 80% acetic acid are described. Only the first patient developed haemolysis, slight intravascular coagulation and oliguric kidney insufficiency. They were treated with a nasogastric tube and total parenteral feeding. During the first week after admission urinary excretion of beta 2-microglobulin, alanine-aminopeptidase and N-acetyl-glucosaminidase was significantly increased. The patients remained haemodynamically stable and did not develop fever. The above-mentioned elevated excretions returned to normal levels. Both patients showed similar patterns of tubular proteinuria. The observations in the second patient suggest a direct toxic effect of acetic acid on the proximal tubule of the kidney.
Schardijn
G H
GH
Kastelein
J J
JJ
Statius van Eps
L W
LW
D000085:Acetates / Q000506:poisoning*; D019342:Acetic Acid; D000118:Acetylglucosaminidase / Q000652:urine; D058186:Acute Kidney Injury / Q000139:chemically induced*; D000293:Adolescent; D000328:Adult; D000626:Aminopeptidases / Q000652:urine; D018826:CD13 Antigens; D004941:Esophagitis / Q000139:chemically induced; D005260:Female; D005756:Gastritis / Q000139:chemically induced; D006461:Hemolysis / Q000187:drug effects; D006801:Humans; D007684:Kidney Tubules / Q000187:drug effects*; D008297:Male; D001613:beta 2-Microglobulin / Q000652:urine
D000085:Acetates; D001613:beta 2-Microglobulin; D000118:Acetylglucosaminidase; D000626:Aminopeptidases; D018826:CD13 Antigens; D019342:Acetic Acid
Niertubulusfunctiestoornissen door azijnzuur.