Bone Turnover and Vascular Calcification

Abstract

The impaired bone mineral metabolism followed byVascular Calcification (VC) will be presentat the beginning stage of Chronic Kidney Disease (CKD). VC can be considered as two major types, which are intimal calcification, associated with atherosclerosis, and medial calcification that involves damaged vascular smooth muscle cells (VSMCs), which leads to increase vascular stiffness and decrease vascular elasticity. Many factors control the mechanisms, and they are imbalances in serum calcium and phosphate, systemic inflammation, hyperparathyroidism, increased matrix degradation, VSMC apoptosis, decreased matrix glutamate protein, etc. These will make VSMCs Trans differentiation to phenotypic osteoblastic cells. In addition, patients with CKD usually have bone turnover problems. For a high turnover status, secondary hyperparathyroidism increases calcium and phosphate release from the bone, but for a low turnover status in a dynamic bone disorder, circulating phosphate and calcium cannot enter the bone to cause serum calcium and phosphate levels to frequently maintain at high levels. This is caused by the fact that the bone can no longer buffer the increases in phosphate and calcium load, and these conditions will cause the possibility of VC. Interestingly, the VC process will secrete sclerostin, a hormone that may act not only locally in the artery wall to reduce mineralization but also destroy bone mineralization. These problems will lead to reduced bone mass with a cycle between bone turnover and VC that only leads to problems. This article will describe the complex relationship between the rate of bone turnover and VC in CKD.