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

### **Pieter Evenepoel 1,2,\*, Sander Dejongh 1,2, Kristin Verbeke 3 and Bjorn Meijers 1,2**


Received: 30 March 2020; Accepted: 16 April 2020; Published: 29 April 2020

**Abstract:** 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 gu<sup>t</sup> 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 gu<sup>t</sup> dysbiosis in the bone–vascular axis may open avenues for novel therapeutics, including nutriceuticals.

**Keywords:** bone; vascular calcification; gut; CKD

**Key Contribution:** Gut dysbiosis is common in patients with CKD and is increasingly recognized to be involved in the pathogenesis of the bone-vascular axis.
