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Eculizumab-induced reversal of dialysis-dependent kidney failure from C3 glomerulonephritis

C3 glomerulopathy (C3G) is characterized by C3 deposits with minimal immunoglobulin deposition caused by alternative complement pathway dysregulation. Unfortunately, no therapeutic intervention has consistently improved outcomes for patients with C3G. Eculizumab, a monoclonal antibody to C5, is curr...

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Detalles Bibliográficos
Autores principales: Inman, Melissa, Prater, Ginnie, Fatima, Huma, Wallace, Eric
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Oxford University Press 2015
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4515899/
https://www.ncbi.nlm.nih.gov/pubmed/26251714
http://dx.doi.org/10.1093/ckj/sfv044
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author Inman, Melissa
Prater, Ginnie
Fatima, Huma
Wallace, Eric
author_facet Inman, Melissa
Prater, Ginnie
Fatima, Huma
Wallace, Eric
author_sort Inman, Melissa
collection PubMed
description C3 glomerulopathy (C3G) is characterized by C3 deposits with minimal immunoglobulin deposition caused by alternative complement pathway dysregulation. Unfortunately, no therapeutic intervention has consistently improved outcomes for patients with C3G. Eculizumab, a monoclonal antibody to C5, is currently the only approved complement-specific agent with some efficacy in the treatment of C3 glomerulonephritis (C3GN). Here, we describe a patient with acute crescentic C3GN with no identified complement mutation or family history of renal disease who required dialysis for 6 months. Five months after initiation of eculizumab, she became dialysis independent, showing improvement is possible after adequate time on eculizumab.
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spelling pubmed-45158992015-08-06 Eculizumab-induced reversal of dialysis-dependent kidney failure from C3 glomerulonephritis Inman, Melissa Prater, Ginnie Fatima, Huma Wallace, Eric Clin Kidney J Contents C3 glomerulopathy (C3G) is characterized by C3 deposits with minimal immunoglobulin deposition caused by alternative complement pathway dysregulation. Unfortunately, no therapeutic intervention has consistently improved outcomes for patients with C3G. Eculizumab, a monoclonal antibody to C5, is currently the only approved complement-specific agent with some efficacy in the treatment of C3 glomerulonephritis (C3GN). Here, we describe a patient with acute crescentic C3GN with no identified complement mutation or family history of renal disease who required dialysis for 6 months. Five months after initiation of eculizumab, she became dialysis independent, showing improvement is possible after adequate time on eculizumab. Oxford University Press 2015-08 2015-06-15 /pmc/articles/PMC4515899/ /pubmed/26251714 http://dx.doi.org/10.1093/ckj/sfv044 Text en © The Author 2015. Published by Oxford University Press on behalf of ERA-EDTA. http://creativecommons.org/licenses/by-nc/4.0/ This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/4.0/), which permits non-commercial re-use, distribution, and reproduction in any medium, provided the original work is properly cited. For commercial re-use, please contact journals.permissions@oup.com
spellingShingle Contents
Inman, Melissa
Prater, Ginnie
Fatima, Huma
Wallace, Eric
Eculizumab-induced reversal of dialysis-dependent kidney failure from C3 glomerulonephritis
title Eculizumab-induced reversal of dialysis-dependent kidney failure from C3 glomerulonephritis
title_full Eculizumab-induced reversal of dialysis-dependent kidney failure from C3 glomerulonephritis
title_fullStr Eculizumab-induced reversal of dialysis-dependent kidney failure from C3 glomerulonephritis
title_full_unstemmed Eculizumab-induced reversal of dialysis-dependent kidney failure from C3 glomerulonephritis
title_short Eculizumab-induced reversal of dialysis-dependent kidney failure from C3 glomerulonephritis
title_sort eculizumab-induced reversal of dialysis-dependent kidney failure from c3 glomerulonephritis
topic Contents
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4515899/
https://www.ncbi.nlm.nih.gov/pubmed/26251714
http://dx.doi.org/10.1093/ckj/sfv044
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