Introduction. The severity of ethylene glycol toxicity is related to the metabolic acidosis resulting from the biotransformation of ethylene glycol into toxic metabolites. Glycolic acid causes severe acidosis and oxalate precipitates as calcium oxalate in the kidneys and other tissues. Case Report. An adult male was taken to the local hospital by the team rescue and was apparently unconscious; severe metabolic acidosis and renal failure led to death a few hours after the arrival. Confocal laser scanning microscopy demonstrated oxalate crystals deposition within the tubular epithelial cells and widespread necrosis of the tubular epithelium in the proximal tubules. Toxicological examinations revealed ethylene glycol; the blood level was 250 mg/L and in urine the concentration was 0.3%. Discussion. In cases of ethylene glycol poisoning, calcium oxalate may be excreted not only as dihydrate crystals, but also as monohydrate crystals. Direct toxicity, cortical edema, and inhibition of mitochondrial activity, as evidenced by decreased succinate dehydrogenase activity, are possible mechanisms of crystal damage. Since calcium oxalate monohydrate crystals are transported intracellularly by kidney cells, the renal toxicity of ethylene glycol may result from inhibition of mitochondrial respiratory function in proximal tubular cells by calcium oxalate monohydrate crystals. Conclusions. The histologic diagnosis of acute renal failure secondary to ethylene glycol poisoning depends on the recognitions of the changes of acute tubular damage in association with calcium oxalate crystals deposition within the tubular epithelial cells and the widespread necrosis of the tubular epithelium in the proximal tubules. Copyright © Informa Healthcare USA, Inc.

Calcium oxalate crystals in acute ethylene glycol poisoning: A confocal laser scanning microscope study in a fatal case

Pomara C.;D'Errico S.;Fineschi V.
2008-01-01

Abstract

Introduction. The severity of ethylene glycol toxicity is related to the metabolic acidosis resulting from the biotransformation of ethylene glycol into toxic metabolites. Glycolic acid causes severe acidosis and oxalate precipitates as calcium oxalate in the kidneys and other tissues. Case Report. An adult male was taken to the local hospital by the team rescue and was apparently unconscious; severe metabolic acidosis and renal failure led to death a few hours after the arrival. Confocal laser scanning microscopy demonstrated oxalate crystals deposition within the tubular epithelial cells and widespread necrosis of the tubular epithelium in the proximal tubules. Toxicological examinations revealed ethylene glycol; the blood level was 250 mg/L and in urine the concentration was 0.3%. Discussion. In cases of ethylene glycol poisoning, calcium oxalate may be excreted not only as dihydrate crystals, but also as monohydrate crystals. Direct toxicity, cortical edema, and inhibition of mitochondrial activity, as evidenced by decreased succinate dehydrogenase activity, are possible mechanisms of crystal damage. Since calcium oxalate monohydrate crystals are transported intracellularly by kidney cells, the renal toxicity of ethylene glycol may result from inhibition of mitochondrial respiratory function in proximal tubular cells by calcium oxalate monohydrate crystals. Conclusions. The histologic diagnosis of acute renal failure secondary to ethylene glycol poisoning depends on the recognitions of the changes of acute tubular damage in association with calcium oxalate crystals deposition within the tubular epithelial cells and the widespread necrosis of the tubular epithelium in the proximal tubules. Copyright © Informa Healthcare USA, Inc.
2008
Calcium oxalate crystals; Confocal microscopy; Ethylene glycol; Fatal case; Poisoning; Urine analysis
File in questo prodotto:
File Dimensione Formato  
Calcium oxalate crystals in acute ethylene glycol poisoning.pdf

solo gestori archivio

Tipologia: Versione Editoriale (PDF)
Licenza: NON PUBBLICO - Accesso privato/ristretto
Dimensione 602.81 kB
Formato Adobe PDF
602.81 kB Adobe PDF   Visualizza/Apri

I documenti in IRIS sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.

Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/20.500.11769/544202
Citazioni
  • ???jsp.display-item.citation.pmc??? ND
  • Scopus 44
  • ???jsp.display-item.citation.isi??? ND
social impact