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The Role of Gut Dysbiosis in the Bone–Vascular Axis in Chronic Kidney Disease

Patients with chronic kidney disease (CKD) are at increased risk of bone mineral density loss and vascular calcification. Bone demineralization and vascular mineralization often concur in CKD, similar to what observed in the general population. This contradictory association is commonly referred to...

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Autores principales: Evenepoel, Pieter, Dejongh, Sander, Verbeke, Kristin, Meijers, Bjorn
Formato: Online Artículo Texto
Lenguaje:English
Publicado: MDPI 2020
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7290823/
https://www.ncbi.nlm.nih.gov/pubmed/32365480
http://dx.doi.org/10.3390/toxins12050285
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author Evenepoel, Pieter
Dejongh, Sander
Verbeke, Kristin
Meijers, Bjorn
author_facet Evenepoel, Pieter
Dejongh, Sander
Verbeke, Kristin
Meijers, Bjorn
author_sort Evenepoel, Pieter
collection PubMed
description Patients with chronic kidney disease (CKD) are at increased risk of bone mineral density loss and vascular calcification. Bone demineralization and vascular mineralization often concur in CKD, similar to what observed in the general population. This contradictory association is commonly referred to as the ‘calcification paradox’ or the bone–vascular axis. Mounting evidence indicates that CKD-associated gut dysbiosis may be involved in the pathogenesis of the bone–vascular axis. A disrupted intestinal barrier function, a metabolic shift from a predominant saccharolytic to a proteolytic fermentation pattern, and a decreased generation of vitamin K may, alone or in concert, drive a vascular and skeletal pathobiology in CKD patients. A better understanding of the role of gut dysbiosis in the bone–vascular axis may open avenues for novel therapeutics, including nutriceuticals.
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spelling pubmed-72908232020-06-17 The Role of Gut Dysbiosis in the Bone–Vascular Axis in Chronic Kidney Disease Evenepoel, Pieter Dejongh, Sander Verbeke, Kristin Meijers, Bjorn Toxins (Basel) Review Patients with chronic kidney disease (CKD) are at increased risk of bone mineral density loss and vascular calcification. Bone demineralization and vascular mineralization often concur in CKD, similar to what observed in the general population. This contradictory association is commonly referred to as the ‘calcification paradox’ or the bone–vascular axis. Mounting evidence indicates that CKD-associated gut dysbiosis may be involved in the pathogenesis of the bone–vascular axis. A disrupted intestinal barrier function, a metabolic shift from a predominant saccharolytic to a proteolytic fermentation pattern, and a decreased generation of vitamin K may, alone or in concert, drive a vascular and skeletal pathobiology in CKD patients. A better understanding of the role of gut dysbiosis in the bone–vascular axis may open avenues for novel therapeutics, including nutriceuticals. MDPI 2020-04-29 /pmc/articles/PMC7290823/ /pubmed/32365480 http://dx.doi.org/10.3390/toxins12050285 Text en © 2020 by the authors. 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 (http://creativecommons.org/licenses/by/4.0/).
spellingShingle Review
Evenepoel, Pieter
Dejongh, Sander
Verbeke, Kristin
Meijers, Bjorn
The Role of Gut Dysbiosis in the Bone–Vascular Axis in Chronic Kidney Disease
title The Role of Gut Dysbiosis in the Bone–Vascular Axis in Chronic Kidney Disease
title_full The Role of Gut Dysbiosis in the Bone–Vascular Axis in Chronic Kidney Disease
title_fullStr The Role of Gut Dysbiosis in the Bone–Vascular Axis in Chronic Kidney Disease
title_full_unstemmed The Role of Gut Dysbiosis in the Bone–Vascular Axis in Chronic Kidney Disease
title_short The Role of Gut Dysbiosis in the Bone–Vascular Axis in Chronic Kidney Disease
title_sort role of gut dysbiosis in the bone–vascular axis in chronic kidney disease
topic Review
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7290823/
https://www.ncbi.nlm.nih.gov/pubmed/32365480
http://dx.doi.org/10.3390/toxins12050285
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