Next Article in Journal
Clostridium perfringens Epsilon-Toxin Impairs the Barrier Function in MDCK Cell Monolayers in a Ca2+-Dependent Manner
Next Article in Special Issue
Editorial on the Special Issue “Comorbidities in Chronic Kidney Disease”
Previous Article in Journal
The Occurrence of Potential Harmful Cyanobacteria and Cyanotoxins in the Obrzyca River (Poland), a Source of Drinking Water
Previous Article in Special Issue
Inflammation and Premature Ageing in Chronic Kidney Disease
Review

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

1
Laboratory of Nephrology, Department of Immunology and Microbiology, KU Leuven—University of Leuven, B-3000 Leuven, Belgium
2
Department of Nephrology and Renal Transplantation, University Hospitals Leuven, B-3000 Leuven, Belgium
3
Translational Research Center for Gastrointestinal Disorders (TARGID), KU Leuven—University of Leuven, B-3000 Leuven, Belgium
*
Author to whom correspondence should be addressed.
Toxins 2020, 12(5), 285; https://doi.org/10.3390/toxins12050285
Received: 30 March 2020 / Revised: 15 April 2020 / Accepted: 16 April 2020 / Published: 29 April 2020
(This article belongs to the Special Issue Comorbidities in Chronic Kidney Disease (CKD))
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. View Full-Text
Keywords: bone; vascular calcification; gut; CKD bone; vascular calcification; gut; CKD
Show Figures

Figure 1

MDPI and ACS Style

Evenepoel, P.; Dejongh, S.; Verbeke, K.; Meijers, B. The Role of Gut Dysbiosis in the Bone–Vascular Axis in Chronic Kidney Disease. Toxins 2020, 12, 285. https://doi.org/10.3390/toxins12050285

AMA Style

Evenepoel P, Dejongh S, Verbeke K, Meijers B. The Role of Gut Dysbiosis in the Bone–Vascular Axis in Chronic Kidney Disease. Toxins. 2020; 12(5):285. https://doi.org/10.3390/toxins12050285

Chicago/Turabian Style

Evenepoel, Pieter, Sander Dejongh, Kristin Verbeke, and Bjorn Meijers. 2020. "The Role of Gut Dysbiosis in the Bone–Vascular Axis in Chronic Kidney Disease" Toxins 12, no. 5: 285. https://doi.org/10.3390/toxins12050285

Find Other Styles
Note that from the first issue of 2016, MDPI journals use article numbers instead of page numbers. See further details here.

Article Access Map by Country/Region

1
Back to TopTop