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

被引:22
作者
Evenepoel, Pieter [1 ,2 ]
Dejongh, Sander [1 ,2 ]
Verbeke, Kristin [3 ]
Meijers, Bjorn [1 ,2 ]
机构
[1] KU Leuven Univ Leuven, Lab Nephrol, Dept Immunol & Microbiol, B-3000 Leuven, Belgium
[2] Univ Hosp Leuven, Dept Nephrol & Renal Transplantat, B-3000 Leuven, Belgium
[3] KU Leuven Univ Leuven, Translat Res Ctr Gastrointestinal Disorders TARGI, B-3000 Leuven, Belgium
关键词
bone; vascular calcification; gut; CKD; CHAIN FATTY-ACIDS; CORONARY-ARTERY CALCIFICATION; P-CRESYL SULFATE; OSTEOBLAST-SPECIFIC PROTEINS; NECROSIS-FACTOR-ALPHA; VITAMIN-K DEFICIENCY; BOUND UREMIC TOXINS; A RISK-FACTOR; INDOXYL SULFATE; HEMODIALYSIS-PATIENTS;
D O I
10.3390/toxins12050285
中图分类号
TS2 [食品工业];
学科分类号
0832 ;
摘要
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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页数:18
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