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 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.
Highlights
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, 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
Summary
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. 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 gut 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 gut dysbiosis in the bone–vascular axis
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