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Phosphate, Microbiota and CKD

Phosphate is a key uremic toxin associated with adverse outcomes. As chronic kidney disease (CKD) progresses, the kidney capacity to excrete excess dietary phosphate decreases, triggering compensatory endocrine responses that drive CKD-mineral and bone disorder (CKD-MBD). Eventually, hyperphosphatem...

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Autores principales: Favero, Chiara, Carriazo, Sol, Cuarental, Leticia, Fernandez-Prado, Raul, Gomá-Garcés, Elena, Perez-Gomez, Maria Vanessa, Ortiz, Alberto, Fernandez-Fernandez, Beatriz, Sanchez-Niño, Maria Dolores
Formato: Online Artículo Texto
Lenguaje:English
Publicado: MDPI 2021
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8070653/
https://www.ncbi.nlm.nih.gov/pubmed/33924419
http://dx.doi.org/10.3390/nu13041273
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author Favero, Chiara
Carriazo, Sol
Cuarental, Leticia
Fernandez-Prado, Raul
Gomá-Garcés, Elena
Perez-Gomez, Maria Vanessa
Ortiz, Alberto
Fernandez-Fernandez, Beatriz
Sanchez-Niño, Maria Dolores
author_facet Favero, Chiara
Carriazo, Sol
Cuarental, Leticia
Fernandez-Prado, Raul
Gomá-Garcés, Elena
Perez-Gomez, Maria Vanessa
Ortiz, Alberto
Fernandez-Fernandez, Beatriz
Sanchez-Niño, Maria Dolores
author_sort Favero, Chiara
collection PubMed
description Phosphate is a key uremic toxin associated with adverse outcomes. As chronic kidney disease (CKD) progresses, the kidney capacity to excrete excess dietary phosphate decreases, triggering compensatory endocrine responses that drive CKD-mineral and bone disorder (CKD-MBD). Eventually, hyperphosphatemia develops, and low phosphate diet and phosphate binders are prescribed. Recent data have identified a potential role of the gut microbiota in mineral bone disorders. Thus, parathyroid hormone (PTH) only caused bone loss in mice whose microbiota was enriched in the Th17 cell-inducing taxa segmented filamentous bacteria. Furthermore, the microbiota was required for PTH to stimulate bone formation and increase bone mass, and this was dependent on bacterial production of the short-chain fatty acid butyrate. We review current knowledge on the relationship between phosphate, microbiota and CKD-MBD. Topics include microbial bioactive compounds of special interest in CKD, the impact of dietary phosphate and phosphate binders on the gut microbiota, the modulation of CKD-MBD by the microbiota and the potential therapeutic use of microbiota to treat CKD-MBD through the clinical translation of concepts from other fields of science such as the optimization of phosphorus utilization and the use of phosphate-accumulating organisms.
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spelling pubmed-80706532021-04-26 Phosphate, Microbiota and CKD Favero, Chiara Carriazo, Sol Cuarental, Leticia Fernandez-Prado, Raul Gomá-Garcés, Elena Perez-Gomez, Maria Vanessa Ortiz, Alberto Fernandez-Fernandez, Beatriz Sanchez-Niño, Maria Dolores Nutrients Review Phosphate is a key uremic toxin associated with adverse outcomes. As chronic kidney disease (CKD) progresses, the kidney capacity to excrete excess dietary phosphate decreases, triggering compensatory endocrine responses that drive CKD-mineral and bone disorder (CKD-MBD). Eventually, hyperphosphatemia develops, and low phosphate diet and phosphate binders are prescribed. Recent data have identified a potential role of the gut microbiota in mineral bone disorders. Thus, parathyroid hormone (PTH) only caused bone loss in mice whose microbiota was enriched in the Th17 cell-inducing taxa segmented filamentous bacteria. Furthermore, the microbiota was required for PTH to stimulate bone formation and increase bone mass, and this was dependent on bacterial production of the short-chain fatty acid butyrate. We review current knowledge on the relationship between phosphate, microbiota and CKD-MBD. Topics include microbial bioactive compounds of special interest in CKD, the impact of dietary phosphate and phosphate binders on the gut microbiota, the modulation of CKD-MBD by the microbiota and the potential therapeutic use of microbiota to treat CKD-MBD through the clinical translation of concepts from other fields of science such as the optimization of phosphorus utilization and the use of phosphate-accumulating organisms. MDPI 2021-04-13 /pmc/articles/PMC8070653/ /pubmed/33924419 http://dx.doi.org/10.3390/nu13041273 Text en © 2021 by the authors. https://creativecommons.org/licenses/by/4.0/Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/).
spellingShingle Review
Favero, Chiara
Carriazo, Sol
Cuarental, Leticia
Fernandez-Prado, Raul
Gomá-Garcés, Elena
Perez-Gomez, Maria Vanessa
Ortiz, Alberto
Fernandez-Fernandez, Beatriz
Sanchez-Niño, Maria Dolores
Phosphate, Microbiota and CKD
title Phosphate, Microbiota and CKD
title_full Phosphate, Microbiota and CKD
title_fullStr Phosphate, Microbiota and CKD
title_full_unstemmed Phosphate, Microbiota and CKD
title_short Phosphate, Microbiota and CKD
title_sort phosphate, microbiota and ckd
topic Review
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8070653/
https://www.ncbi.nlm.nih.gov/pubmed/33924419
http://dx.doi.org/10.3390/nu13041273
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