Are calcium oxalate crystals involved in the mechanism of acute renal failure in ethylene glycol poisoning?

2009 ◽  
Vol 47 (9) ◽  
pp. 859-869 ◽  
Author(s):  
Kenneth McMartin
1980 ◽  
Vol 16 (4) ◽  
pp. 479-486 ◽  
Author(s):  
W. Godolphin ◽  
E. P. Meagher ◽  
H. D. Sanders ◽  
J. Frohlich

2018 ◽  
Vol 58 (4) ◽  
pp. 257-260 ◽  
Author(s):  
Janos Bokor ◽  
Krisztina Danics ◽  
Eva Keller ◽  
Zoltan Szollosi

Ethylene glycol (EG) may be acutely toxic following ingestion. In fatal cases, microscopic examination of urine and kidney specimens can establish a post-mortem diagnosis of EG poisoning. We describe the main renal histopathologic changes during different stages of EG poisoning, which might be helpful when dating the EG poisoning itself. A single-centre retrospective study conducted on all EG poisoning cases demonstrated that in an early stage of EG poisoning, fine dust-like crystals were deposited to the tubular cell basement membrane, followed by internalisation of calcium oxalate crystals into the epithelial cells. Later, the crystals formed larger aggregates within the epithelial cells. As the changes became advanced, pronounced tubular epithelial damage occurred, with detachment of epithelial cells from the basement membrane. In the final stage, coarse calcium oxalate crystals were recognised in the tubular lumen, with cellular debris from damaged epithelial cells. Our study shows that the time-dependent histological changes described follow the clinical stages of EG poisoning and may therefore provide a rough estimate of the time of EG ingestion before death.


PEDIATRICS ◽  
1952 ◽  
Vol 10 (6) ◽  
pp. 660-666
Author(s):  
L. YING CHOU ◽  
W. L. DONOHUE

A case is reported of renal failure in a boy subsequent to recurrent calcium oxalate urinary calculi. The post mortem disclosed widespread deposits in the tissues of calcium oxalate crystals. These were particularly prominent in the kidneys and bone marrow. It is suggested that this is the end result of an "inborn error of metabolism" in which there was an excessive formation of oxalic acid.


2017 ◽  
Vol 377 (15) ◽  
pp. 1467-1467 ◽  
Author(s):  
Mohamad Hanouneh ◽  
Teresa K. Chen

2016 ◽  
Vol 4 (1) ◽  
pp. 33-35
Author(s):  
Rajat Das Gupta ◽  
Debashis Datta ◽  
Debashis Datta ◽  
Suranjan Kumar.

Background: The concentrated juice made from Averrhoa bilimbi is rich in oxalic acid. It can cause acute oxalate nephropathy by blocking the tubules with calcium oxalate crystals. Case: An elderly woman was admitted to the hospital with a history of swelling of the legs, facial puffiness, and abdominal distention. Her biochemical study revealed features of acute renal failure. She gave history of taking half liter of bilimbi juice. Renal biopsy confirmed it was a case of acute oxalic nephropathy, which made it the second case of acute oxalic nephropathy due to ingestion of bilimbi juice ever reported from Bangladesh. Conclusion: It is not safe to consume high oxalate-containing fruits in large quantities.


2017 ◽  
Vol 68 (7) ◽  
pp. 1591-1594 ◽  
Author(s):  
Cristina Furnica ◽  
Anton Knieling ◽  
Simona Irina Damian ◽  
Madalina Diac ◽  
Sofia David ◽  
...  

Ethylene glycol intoxication is potentially fatal and associated with typical clinical, laboratory and histopathological findings. The authors present the case of a 57-year-old male with a history of chronic alcoholism and who accidentally ingested approximately 1 litter of antifreeze solution. The patient was discovered comatose in his house and addressed to the emergency department with a Glasgow coma score of 3, severe metabolic acidosis, acute renal failure, atrial fibrillation and liver dysfunction. Despite reanimation manoeuvres and haemodialysis for 2 h the patient deceased 5 h after hospital admission. Necropsy examination revealed a stomach with oedematous walls, mucosa erosions and signs of bleeding together with a disorganised, granular single kidney with unidentifiable corticomedullary border. Histopathological examination displayed typical findings in the kidney such as autolytic changes of the epithelium and abundant calcium oxalate crystals in the lumen of the proximal tubules. Ethylene glycol intoxication is frequent in our country and its metabolites glycoaldehyde, glycolic acid, glyoxylic acid and oxalic acid are responsible for the severe metabolic acidosis and formation of calcium oxalate crystals in various organs and leading to severe multiple organ dysfunction and death. Forensic pathologists should be aware of clinical and biological manifestations as well as of typical histopathological findings as ethylene glycol is commonly ingested accidentally or used in homicidal/autolytical attempts.


2010 ◽  
Vol 30 (1) ◽  
pp. 108-111
Author(s):  
Jill Vanmassenhove ◽  
Raymond Vanholder ◽  
Ramses Forsyth ◽  
Annemieke Dhondt

Primary hyperoxaluria type 1 (PH1) is a rare metabolic disorder caused by a defect in glyoxylate metabolism attributable to low or absent activity of the liver-specific peroxisomal enzyme alanine/glyoxylate aminotransferase. This defect leads to enhanced conversion of glyoxylate to poorly soluble oxalate, which is then excreted into the urine. This process may lead to deposition of calcium oxalate crystals in many tissues as well as in the kidneys, resulting in nephrolithiasis, nephrocalcinosis, and/or renal failure.We present a 39-year-old patient with end-stage renal failure due to PH1, who was admitted with symptoms of feeling bloated, vomiting, diarrhea, and abdominal pain related to encapsulating peritoneal sclerosis (EPS). He had been treated with peritoneal dialysis for a total period of 5 years.EPS is a rare condition characterized by fibrosis and adhesions of the peritoneum to loops of the small intestine and has been described secondary to treatment with peritoneal dialysis. It also occurs in a variety of other clinical conditions such as autoimmune diseases and peritoneal and intra-abdominal malignancies.The calcium oxalate crystals found in the peritoneal fascia of this particular patient may suggest a causative relationship between crystal deposits and evolution to fibrosis and sclerosis of the peritoneum. The degree of impact of the peritoneal dialysis treatment itself on the development of EPS, however, is uncertain.


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