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The development of atypical hemolytic uremic syndrome depends on complement C5

The development of atypical hemolytic uremic syndrome depends on complement C5

http://www.wikidata.org/entity/Q28300378

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Atypical hemolytic uremic syndrome Eculizumab: a review of its use in atypical haemolytic uraemic syndrome Haemolytic uraemic syndrome.The interaction between factor H and Von Willebrand factor.Three kidneys, two diseases, one antibody?Complement-mediated injury and protection of endothelium: lessons from atypical haemolytic uraemic syndrome Thrombotic microangiopathy and associated renal disorders.Use of eculizumab for atypical haemolytic uraemic syndrome and C3 glomerulopathies.Complement regulation in renal disease models Successful treatment of DEAP-HUS with eculizumab.Atypical HUS associated with severe, unexpected antibody-mediated rejection post kidney transplant.Complement functional tests for monitoring eculizumab treatment in patients with atypical hemolytic uremic syndrome.Dynamics of complement activation in aHUS and how to monitor eculizumab therapy Molecules Great and Small: The Complement System.Atypical hemolytic uremic syndrome post-kidney transplantation: two case reports and review of the literature Partial Complement Factor H Deficiency Associates with C3 Glomerulopathy and Thrombotic Microangiopathy.Prevention and treatment of atypical haemolytic uremic syndrome after kidney transplantation.Investigating mechanisms of chronic kidney disease in mouse models Loss of properdin exacerbates C3 glomerulopathy resulting from factor H deficiency.Dense deposit disease and C3 glomerulopathy Update on hemolytic uremic syndrome: Diagnostic and therapeutic recommendations.C3 dysregulation due to factor H deficiency is mannan-binding lectin-associated serine proteases (MASP)-1 and MASP-3 independent in vivo.C3 glomerulonephritis and CFHR5 nephropathy.Progress in the development of animal models of acute kidney injury and its impact on drug discovery.Spectrum of anemia after kidney transplantation: pathophysiology and therapeutic implications.Endothelial cells: source, barrier, and target of defensive mediators.Treatment of atypical uraemic syndrome in the era of eculizumab Early Terminal Complement Blockade and C6 Deficiency Are Protective in Enterohemorrhagic Escherichia coli-Infected Mice.Invasive meningococcal disease in three siblings with hereditary deficiency of the 8(th) component of complement: evidence for the importance of an early diagnosis Efficacy of Targeted Complement Inhibition in Experimental C3 Glomerulopathy.Cisplatin-induced haemolytic uraemic syndrome associated with a novel intronic mutation of CD46 treated with eculizumab Factor H C-Terminal Domains Are Critical for Regulation of Platelet/Granulocyte Aggregate Formation.A case of atypical hemolytic uremic syndrome in a second renal transplant.C3 Glomerulopathy.Atypical hemolytic uremic syndrome Hemolytic uremic syndrome

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P2860

The development of atypical hemolytic uremic syndrome depends on complement C5

http://www.wikidata.org/entity/Q28300378

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2011 nî lūn-bûn

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2011 թուականի Յունուարին հրատարակուած գիտական յօդուած

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2011 թվականի հունվարին հրատարակված գիտական հոդված

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2011年の論文

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2011年論文

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2011年論文

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2011年論文

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2011年論文

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2011年论文

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name

The development of atypical hemolytic uremic syndrome depends on complement C5

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The development of atypical hemolytic uremic syndrome depends on complement C5

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The development of atypical hemolytic uremic syndrome depends on complement C5

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The development of atypical hemolytic uremic syndrome depends on complement C5

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The development of atypical hemolytic uremic syndrome depends on complement C5

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The development of atypical hemolytic uremic syndrome depends on complement C5

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The development of atypical hemolytic uremic syndrome depends on complement C5

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Journal of the American Society of Nephrology

P1476

The development of atypical hemolytic uremic syndrome depends on complement C5

@en

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Danielle Paixão-Cavalcante

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Franco Tedesco

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H Terence Cook

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Kirsten L Rose

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Marina Botto

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P2860

Factor I is required for the development of membranoproliferative glomerulonephritis in factor H-deficient mice

Complement. First of two parts

Thrombotic microangiopathy, hemolytic uremic syndrome, and thrombotic thrombocytopenic purpura

Hepatocyte nuclear factor 1alpha controls the expression of terminal complement genes

The molecular basis of familial hemolytic uremic syndrome: mutation analysis of factor H gene reveals a hot spot in short consensus repeat 20.

Clustering of missense mutations in the C-terminal region of factor H in atypical hemolytic uremic syndrome.

Factor H mutations in hemolytic uremic syndrome cluster in exons 18-20, a domain important for host cell recognition

The genetics and pathogenesis of haemolytic uraemic syndrome and thrombotic thrombocytopenic purpura.

Cutting edge: localization of the host recognition functions of complement factor H at the carboxyl-terminal: implications for hemolytic uremic syndrome.

Structural and functional characterization of factor H mutations associated with atypical hemolytic uremic syndrome

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137-45

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scholarly article

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1604228

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10.1681/ASN.2010050451

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P433

1

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22

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Elena Goicoechea de Jorge

Matthew C Pickering

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2011-01-01T00:00:00Z

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21148255

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3014042

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