Laboratory of Nephrology, Department of Immunology and Microbiology, KU Leuven-University of Leuven, B-3000 Leuven, Belgium.
Department of Nephrology and Renal Transplantation, University Hospitals Leuven, B-3000 Leuven, Belgium.
Toxins (Basel). 2020 Apr 29;12(5):285. doi: 10.3390/toxins12050285.
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.
患有慢性肾脏病(CKD)的患者骨质密度降低和血管钙化的风险增加。在 CKD 中,骨脱矿质和血管矿化经常同时发生,类似于在一般人群中观察到的情况。这种矛盾的关联通常被称为“钙化悖论”或“骨血管轴”。越来越多的证据表明,与 CKD 相关的肠道菌群失调可能参与了骨血管轴的发病机制。肠道屏障功能受损、从以糖解为主到以蛋白水解发酵为主的代谢转变以及维生素 K 生成减少,可能单独或协同作用,导致 CKD 患者的血管和骨骼病理生物学发生变化。更好地了解肠道菌群失调在骨血管轴中的作用可能为包括营养疗法在内的新型治疗方法开辟途径。