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10.1097/MNH.0000000000000229

http://scihub22266oqcxt.onion/10.1097/MNH.0000000000000229
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C4891250!4891250!27191349
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suck abstract from ncbi


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pmid27191349      Curr+Opin+Nephrol+Hypertens 2016 ; 25 (4): 363-71
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  • Oxalate, inflammasome, and progression of kidney disease #MMPMID27191349
  • Ermer T; Eckardt KU; Aronson PS; Knauf F
  • Curr Opin Nephrol Hypertens 2016[Jul]; 25 (4): 363-71 PMID27191349show ga
  • Purpose of review: Oxalate is an end product of metabolism excreted via the kidney. Excess urinary oxalate, whether from primary or enteric hyperoxaluria, can lead to oxalate deposition in the kidney. Oxalate crystals are associated with renal inflammation, fibrosis and progressive renal failure. It has long been known that as glomerular filtration rate (GFR) becomes reduced in chronic kidney disease (CKD), there is striking elevation of plasma oxalate. Taken together, these findings raise the possibility that elevation of plasma oxalate in CKD may promote renal inflammation and more rapid progression of CKD independent of primary etiology. Recent findings: The inflammasome has recently been identified to play a critical role in oxalate-induced renal inflammation. Oxalate crystals have been shown to activate the nucleotide-binding domain, leucine-rich repeat inflammasome 3 (also known as NALP3, NLRP3 or cryopyrin), resulting in release of Interleukin-1? and macrophage infiltration. Deletion of inflammasome proteins in mice protects from oxalate-induced renal inflammation and progressive renal failure. Summary: The findings reviewed in this article expand our understanding of the relevance of elevated plasma oxalate levels leading to inflammasome activation. We propose that inhibiting oxalate-induced inflammasome activation, or lowering plasma oxalate, may prevent or mitigate progressive renal damage in CKD, and warrants clinical trials.
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