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ISSN: 2161-0959

Journal of Nephrology & Therapeutics
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Review Article

Bone Turnover and Vascular Calcification

Pei-Chen Wu1, Cai-Mei Zheng2, Min-Tser Liao3, Chia-Chao Wu4, Kuo-Cheng Lu5 and Wen-Chih Liu6*

1Department of Internal Medicine, Division of Nephrology, Da Chien General Hospital, Miaoli County, Taiwan

2Department of Internal Medicine, Division of Nephrology, Shuang Ho Hospital, Taipei Medical University, Taipei, Taiwan

3Department of Pediatrics, Taoyuan Armed Forces General Hospital, Taoyuan, Taiwan

4Department of Medicine, Division of Nephrology, Tri-Service General Hospital, National Defense Medical Center, Taipei, Taiwan

5Department of Medicine, Division of Nephrology, Cardinal Tien Hospital, School of Medicine, Fu-Jen Catholic University, New Taipei City, Taiwan

6Department of Internal Medicine, Division of Nephrology, Yonghe Cardinal Tien Hospital, New Taipei City, Taiwan

*Corresponding Author:
Wen-Chih Liu
Department of Internal Medicine, Division of Nephrology
Cardinal Tien Hospital, Yonghe Branch, 80 Zhongxing St.
Yonghe Dist., New Taipei City 234, Taiwan
Fax: +886-2-29218270
E-mail: [email protected]

Received Date: April 23, 2014; Accepted Date: May 28, 2014; Published Date: June 05, 2014

Citation: Wu PC, Zheng CM, Liao MT, Wu CC, Lu KC, et al. (2014) Bone Turnover and Vascular Calcification. J Nephrol Ther 4:171. doi:10.4172/2161-0959.1000171

Copyright: © 2014 Wu PC, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

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.

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