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Gut microbiota and inflammation in chronic kidney disease patients

Inflammation is a multifactorial phenotype that in chronic kidney disease is associated with adverse patient outcomes. Recently, alterations in gut microbiota composition and intestinal barrier have been associated with inflammation and oxidative stress in CKD patients. Vanholder and Glorieux recent...

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Detalles Bibliográficos
Autores principales: Mafra, Denise, Fouque, Denis
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Oxford University Press 2015
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4440473/
https://www.ncbi.nlm.nih.gov/pubmed/26034597
http://dx.doi.org/10.1093/ckj/sfv026
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author Mafra, Denise
Fouque, Denis
author_facet Mafra, Denise
Fouque, Denis
author_sort Mafra, Denise
collection PubMed
description Inflammation is a multifactorial phenotype that in chronic kidney disease is associated with adverse patient outcomes. Recently, alterations in gut microbiota composition and intestinal barrier have been associated with inflammation and oxidative stress in CKD patients. Vanholder and Glorieux recently critically reviewed [Clin Kidney J (2015) 8 (2): 168-179] the current understanding of the role of gut microbiota in the production of uraemic toxins and the therapeutic implications. Where do we stand now? The basic mechanisms of the gut-kidney crosstalk must still be clarified. In addition, the efficacy and safety of therapeutic strategies to modulate the gut microbiota in order to decrease uraemic toxin production and inflammation in chronic kidney disease should be evaluated. Finally, an impact of such strategies on hard outcomes should be demonstrated before incorporation into routine clinical practice.
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spelling pubmed-44404732015-06-01 Gut microbiota and inflammation in chronic kidney disease patients Mafra, Denise Fouque, Denis Clin Kidney J Contents Inflammation is a multifactorial phenotype that in chronic kidney disease is associated with adverse patient outcomes. Recently, alterations in gut microbiota composition and intestinal barrier have been associated with inflammation and oxidative stress in CKD patients. Vanholder and Glorieux recently critically reviewed [Clin Kidney J (2015) 8 (2): 168-179] the current understanding of the role of gut microbiota in the production of uraemic toxins and the therapeutic implications. Where do we stand now? The basic mechanisms of the gut-kidney crosstalk must still be clarified. In addition, the efficacy and safety of therapeutic strategies to modulate the gut microbiota in order to decrease uraemic toxin production and inflammation in chronic kidney disease should be evaluated. Finally, an impact of such strategies on hard outcomes should be demonstrated before incorporation into routine clinical practice. Oxford University Press 2015-06 2015-05-06 /pmc/articles/PMC4440473/ /pubmed/26034597 http://dx.doi.org/10.1093/ckj/sfv026 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
Mafra, Denise
Fouque, Denis
Gut microbiota and inflammation in chronic kidney disease patients
title Gut microbiota and inflammation in chronic kidney disease patients
title_full Gut microbiota and inflammation in chronic kidney disease patients
title_fullStr Gut microbiota and inflammation in chronic kidney disease patients
title_full_unstemmed Gut microbiota and inflammation in chronic kidney disease patients
title_short Gut microbiota and inflammation in chronic kidney disease patients
title_sort gut microbiota and inflammation in chronic kidney disease patients
topic Contents
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4440473/
https://www.ncbi.nlm.nih.gov/pubmed/26034597
http://dx.doi.org/10.1093/ckj/sfv026
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