**1. Introduction**

Chronic kidney disease (CKD) is recognized as a major noncommunicable disease of growing epidemic dimensions worldwide. CDK–mineral and bone disorder (CKD–MBD) is one of the many complications associated with CKD. It represents a systemic disorder of mineral and bone metabolism due to CKD, manifested with either one or a combination of the following: (1) abnormalities of calcium, phosphorus (phosphate), parathyroid hormone, or vitamin D metabolism; (2) abnormalities in bone turnover, mineralization, volume, linear growth, or strength; and (3) vascular or other soft-tissue calcification. CKD–MBD explains, at least in part, the high morbidity and mortality of CKD patients [1].

Bone demineralization and vascular mineralization often concur in CKD, as in the general population. This contradictory association is often referred to as the 'calcification paradox' or the bone–vascular axis [2]. Mounting evidence indicates that CKD-associated gu<sup>t</sup> dysbiosis may be involved in the pathogenesis of the bone–vascular axis. The present review aims to update the current evidence on the role of gu<sup>t</sup> dysbiosis in the bone–vascular axis.
