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Complement-Mediated Glomerular Diseases: A Tale of 3 Pathways
A renewed interest in the role of complement in the pathogenesis of glomerular diseases has improved our understanding of their basic, underlying physiology. All 3 complement pathways—classical, lectin, and alternative—have been implicated in glomerular lesions both rare (e.g., dense deposit disease...
Autores principales: | , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Elsevier
2016
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5678788/ https://www.ncbi.nlm.nih.gov/pubmed/29142924 http://dx.doi.org/10.1016/j.ekir.2016.06.005 |
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author | Bomback, Andrew S. Markowitz, Glen S. Appel, Gerald B. |
author_facet | Bomback, Andrew S. Markowitz, Glen S. Appel, Gerald B. |
author_sort | Bomback, Andrew S. |
collection | PubMed |
description | A renewed interest in the role of complement in the pathogenesis of glomerular diseases has improved our understanding of their basic, underlying physiology. All 3 complement pathways—classical, lectin, and alternative—have been implicated in glomerular lesions both rare (e.g., dense deposit disease) and common (e.g., IgA nephropathy). Here we review the basic function of these pathways and highlight, with a disease-specific focus, how activation can lead to glomerular injury. We end by exploring the promise of complement-targeted therapies as disease-specific interventions for glomerular diseases. |
format | Online Article Text |
id | pubmed-5678788 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2016 |
publisher | Elsevier |
record_format | MEDLINE/PubMed |
spelling | pubmed-56787882017-11-15 Complement-Mediated Glomerular Diseases: A Tale of 3 Pathways Bomback, Andrew S. Markowitz, Glen S. Appel, Gerald B. Kidney Int Rep Review A renewed interest in the role of complement in the pathogenesis of glomerular diseases has improved our understanding of their basic, underlying physiology. All 3 complement pathways—classical, lectin, and alternative—have been implicated in glomerular lesions both rare (e.g., dense deposit disease) and common (e.g., IgA nephropathy). Here we review the basic function of these pathways and highlight, with a disease-specific focus, how activation can lead to glomerular injury. We end by exploring the promise of complement-targeted therapies as disease-specific interventions for glomerular diseases. Elsevier 2016-07-01 /pmc/articles/PMC5678788/ /pubmed/29142924 http://dx.doi.org/10.1016/j.ekir.2016.06.005 Text en © 2016 International Society of Nephrology. Published by Elsevier Inc. http://creativecommons.org/licenses/by-nc-nd/4.0/ This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/). |
spellingShingle | Review Bomback, Andrew S. Markowitz, Glen S. Appel, Gerald B. Complement-Mediated Glomerular Diseases: A Tale of 3 Pathways |
title | Complement-Mediated Glomerular Diseases: A Tale of 3 Pathways |
title_full | Complement-Mediated Glomerular Diseases: A Tale of 3 Pathways |
title_fullStr | Complement-Mediated Glomerular Diseases: A Tale of 3 Pathways |
title_full_unstemmed | Complement-Mediated Glomerular Diseases: A Tale of 3 Pathways |
title_short | Complement-Mediated Glomerular Diseases: A Tale of 3 Pathways |
title_sort | complement-mediated glomerular diseases: a tale of 3 pathways |
topic | Review |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5678788/ https://www.ncbi.nlm.nih.gov/pubmed/29142924 http://dx.doi.org/10.1016/j.ekir.2016.06.005 |
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