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10.1093/ckj/sfy066 http://scihub22266oqcxt.onion/10.1093/ckj/sfy066 31198222!6543964!31198222     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=31198222&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       Clin+Kidney+J 2019 ; 12 (3): 338-347 Nephropedia Template TP {{tp|p=31198222|t=2019. Atypical hemolytic uremic syndrome: a syndrome in need of clarity |pdf=|usr=}}{{31198222}} gab.com Text Atypical hemolytic uremic syndrome: a syndrome in need of clarity JO: Clin Kidney J http://www.kidney.de/pget.php?&tw=1&pmid=31198222 #FOAvip Atypical hemolytic uremic syndrome (aHUS) is a thrombotic microangiopathy (TMA) originally understood to be limited to renal and hematopoietic involvement. Whereas aberrations in complement regulatory proteins (CRPs), C3 or complement factor B (CFB) are detected in approximately 60% of patients, a complement-derived pathogenesis that reflects dysregulation of the alternative pathway (AP) of complement activation is present in approximately 90% of patients. aHUS remains a diagnosis of exclusion. The discovery of a disintegrin and metalloproteinase with a thrombospondin type 1 motif, member 13 (ADAMTS13) and its utility in the diagnosis of thrombotic thrombocytopenic purpura (TTP) has resulted in the appreciation that cases of aHUS have been inappropriately diagnosed as TTP. Thus there has been an evolving appreciation of clinical manifestations of aHUS that renders the appellation aHUS misleading. This article will review the pathogenesis and the evolving clinical presentations of aHUS, present a hypothesis that there can be a phenotypic expression of aHUS due to a complement storm in a disorder where direct endothelial damage occurs and discuss future areas of research to more clearly define the clinical spectrum and management of aHUS. Twit Text FOAVip Atypical hemolytic uremic syndrome: a syndrome in need of clarity ????Clin Kidney J http://www.kidney.de/pget.php?&tw=1&pmid=31198222 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=31198222 #FOAvip English Wikipedia <ref>{{Cite pmid|31198222}}</ref> Atypical hemolytic uremic syndrome: a syndrome in need of clarity #MMPMID31198222 Berger BE Clin Kidney J 2019[Jun]; 12 (3): 338-347 PMID31198222show ga Atypical hemolytic uremic syndrome (aHUS) is a thrombotic microangiopathy (TMA) originally understood to be limited to renal and hematopoietic involvement. Whereas aberrations in complement regulatory proteins (CRPs), C3 or complement factor B (CFB) are detected in approximately 60% of patients, a complement-derived pathogenesis that reflects dysregulation of the alternative pathway (AP) of complement activation is present in approximately 90% of patients. aHUS remains a diagnosis of exclusion. The discovery of a disintegrin and metalloproteinase with a thrombospondin type 1 motif, member 13 (ADAMTS13) and its utility in the diagnosis of thrombotic thrombocytopenic purpura (TTP) has resulted in the appreciation that cases of aHUS have been inappropriately diagnosed as TTP. Thus there has been an evolving appreciation of clinical manifestations of aHUS that renders the appellation aHUS misleading. This article will review the pathogenesis and the evolving clinical presentations of aHUS, present a hypothesis that there can be a phenotypic expression of aHUS due to a complement storm in a disorder where direct endothelial damage occurs and discuss future areas of research to more clearly define the clinical spectrum and management of aHUS. ?Atypical hemolytic uremic syndrome: a syndrome in need of clarity (epmc).pdf DeepDyve Pubget Overpricing