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10.1056/NEJMoa0707330 http://scihub22266oqcxt.onion/10.1056/NEJMoa0707330 18337603!3030578!18337603     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=18337603&cmd=llinks): Failed to open stream: HTTP request failed! HTTP/1.1 429 Too Many Requests in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 215 Warning: imagejpeg(C:\Inetpub\vhosts\kidney.de\httpdocs\phplern\18337603.jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117       N+Engl+J+Med 2008 ; 358 (11): 1129-36 Nephropedia Template TP {{tp|p=18337603|t=2008. VEGF inhibition and renal thrombotic microangiopathy |pdf=|usr=}}{{18337603}} gab.com Text VEGF inhibition and renal thrombotic microangiopathy JO: N Engl J Med http://www.kidney.de/pget.php?&tw=1&pmid=18337603 #FOAvip The glomerular microvasculature is particularly susceptible to injury in thrombotic microangiopathy, but the mechanisms by which this occurs are unclear. We report the cases of six patients who were treated with bevacizumab, a humanized monoclonal antibody against vascular endothelial growth factor (VEGF), in whom glomerular disease characteristic of thrombotic microangiopathy developed. To show that local reduction of VEGF within the kidney is sufficient to trigger the pathogenesis of thrombotic microangiopathy, we used conditional gene targeting to delete VEGF from renal podocytes in adult mice; this resulted in a profound thrombotic glomerular injury. These observations provide evidence that glomerular injury in patients who are treated with bevacizumab is probably due to direct targeting of VEGF by antiangiogenic therapy. Twit Text FOAVip VEGF inhibition and renal thrombotic microangiopathy ????N Engl J Med http://www.kidney.de/pget.php?&tw=1&pmid=18337603 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=18337603 #FOAvip English Wikipedia <ref>{{Cite pmid|18337603}}</ref> VEGF inhibition and renal thrombotic microangiopathy #MMPMID18337603 Eremina V; Jefferson JA; Kowalewska J; Hochster H; Haas M; Weisstuch J; Richardson C; Kopp JB; Kabir MG; Backx PH; Gerber HP; Ferrara N; Barisoni L; Alpers CE; Quaggin SE N Engl J Med 2008[Mar]; 358 (11): 1129-36 PMID18337603show ga The glomerular microvasculature is particularly susceptible to injury in thrombotic microangiopathy, but the mechanisms by which this occurs are unclear. We report the cases of six patients who were treated with bevacizumab, a humanized monoclonal antibody against vascular endothelial growth factor (VEGF), in whom glomerular disease characteristic of thrombotic microangiopathy developed. To show that local reduction of VEGF within the kidney is sufficient to trigger the pathogenesis of thrombotic microangiopathy, we used conditional gene targeting to delete VEGF from renal podocytes in adult mice; this resulted in a profound thrombotic glomerular injury. These observations provide evidence that glomerular injury in patients who are treated with bevacizumab is probably due to direct targeting of VEGF by antiangiogenic therapy. |Aged[MESH] |Angiogenesis Inhibitors/*adverse effects/therapeutic use[MESH] |Animals[MESH] |Antibodies, Monoclonal, Humanized[MESH] |Antibodies, Monoclonal/*adverse effects/therapeutic use[MESH] |Bevacizumab[MESH] |Female[MESH] |Gene Targeting[MESH] |Humans[MESH] |Kidney Glomerulus/blood supply/*drug effects/pathology[MESH] |Male[MESH] |Mice[MESH] |Mice, Knockout[MESH] |Microcirculation/drug effects[MESH] |Middle Aged[MESH] |Neoplasms/drug therapy[MESH] |Podocytes/*metabolism[MESH] |Proteinuria/chemically induced[MESH] |RNA, Messenger/metabolism[MESH] |Renal Circulation[MESH] |Signal Transduction[MESH] |Thrombosis/*chemically induced[MESH]VEGF inhibition and renal thrombotic microangiopathy (epmc).pdf DeepDyve Pubget Overpricing