Deposition of calcium oxalate in the skin in two patients suffering from oxalosis caused by primary hyperoxaluria

1974 ◽  
Vol 250 (4) ◽  
pp. 323-350 ◽  
Author(s):  
L. H. Jansen ◽  
J. L. Groeneveld ◽  
J. B. Meer
2012 ◽  
Vol 138 (suppl 1) ◽  
pp. A002-A002
Author(s):  
Nadja Burns ◽  
Brian Castillo ◽  
Aditya Gupta ◽  
Brandy McKelvy ◽  
Sozos Papasozomenos

Author(s):  
Steven L. Daniel ◽  
Luke Moradi ◽  
Henry Paiste ◽  
Kyle D. Wood ◽  
Dean G. Assimos ◽  
...  

Oxalobacter formigenes , a unique anaerobic bacterium that relies solely on oxalate for growth, is a key oxalate-degrading bacterium in the mammalian intestinal tract. Degradation of oxalate in the gut by O. formigenes plays a critical role in preventing renal toxicity in animals that feed on oxalate-rich plants. The role of O. formigenes in reducing the risk of calcium oxalate kidney stone disease and oxalate nephropathy in humans is less clear, in part due to difficulties in culturing this organism, and the lack of studies which have utilized diets controlled in their content of oxalate. Herein, we review the literature on the 40 th anniversary of the discovery of O. formigenes , with a focus on its biology, its role in gut oxalate metabolism and calcium oxalate kidney stone disease, and potential areas of future research. Results from ongoing clinical trials utilizing O. formigenes in healthy volunteers and in patients with Primary Hyperoxaluria Type 1 (PH1), a rare but severe form of calcium oxalate kidney stone disease, will also be discussed. Information has been consolidated on O. formigenes strains and best practices to culture this bacterium, which should serve as a good resource for researchers.


2018 ◽  
Author(s):  
Robin S Chirackal ◽  
John C Lieske

Humans cannot degrade oxalate. Thus, oxalate that is generated in the liver and/or absorbed from the intestine must be eliminated by the kidneys. Among genetic causes, primary hyperoxaluria (PH) type 1 is the most common and occurs due to deficiency of hepatic peroxisomal alanine glyoxalate aminotransferase. PH2 is caused by deficiency of lysosomal glyoxalate reductase or hydroxypyruvate reductase, whereas PH3 results from deficiency of mitochondrial 4-hydroxy-2-oxoglutarate aldolase. Enteric hyperoxaluria is caused by excessive colonic oxalate absorption due to any type of fat malabsorption. The diagnosis of hyperoxaluria is based on the history, 24-hour urine studies, and genetic testing. Early diagnosis and timely intervention are essential. To treat PH, adequate fluid intake, inhibitors of calcium oxalate crystallization (citrate or neutral phosphorus), and pyridoxine-in responsive patients are all important. Intensive dialysis and prompt kidney or combined kidney-liver transplantation are essential to minimize systemic oxalosis if renal failure occurs. Dietary modifications (low fat, low oxalate, and adequate calcium) are key for enteric hyperoxaluria. Calcium can be used as an oxalate binder. Newer modalities including oxalate degrading bacteria, oral oxalate decarboxylase preparations, and inhibitory ribonucleic acids are all under investigation. This review contains 9 figures, 6 tables, and 90 references. Key Words: bariatric surgery, calcium oxalate, dialysis, enteric hyperoxaluria, fat malabsorption, genetic testing, kidney stone, nephrolithiasis, oxalate, oxalate decarboxylase, Oxalobacter formigenes, primary hyperoxaluria, pyridoxine, transplantation, urolithiasis


2016 ◽  
Vol 24 (4) ◽  
pp. 770-778 ◽  
Author(s):  
Chaitali Dutta ◽  
Nicole Avitahl-Curtis ◽  
Natalie Pursell ◽  
Marita Larsson Cohen ◽  
Benjamin Holmes ◽  
...  

2016 ◽  
Vol 89 (1) ◽  
pp. 250 ◽  
Author(s):  
José Antonio T. Poloni ◽  
Clotilde D. Garcia ◽  
Liane N. Rotta ◽  
Mark A. Perazella

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