Abstract
Ethylene glycol is an infrequent but important cause of toxin-induced acute renal failure. Early detection is crucial so that appropriate therapy can be begun to ameliorate the profound metabolic acidosis of early toxicity and prevent the late complications of renal failure, central nervous system injury, respiratory depression, and cardiovascular collapse. Contemporary treatment of ethylene glycol intoxication has derived from our understanding of the pathophysiologic action of the toxin. Alcohol dehydrogenase catalyzes the degradation of ethylene glycol to glycolic acid. Glycolic acid contributes to the severe anion-gap metabolic acidosis common at presentation and is a metabolic intermediate for the subsequent formation . . .

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