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World J Nephrol. Apr 6, 2012; 1(2): 43-53
Published online Apr 6, 2012. doi: 10.5527/wjn.v1.i2.43
Vascular calcification in chronic kidney disease: Pathogenesis and clinical implication
Sinee Disthabanchong
Sinee Disthabanchong, Division of Nephrology, Department of Medicine, Faculty of Medicine, Ramathibodi Hospital, Mahidol University, Bangkok 10400, Thailand
Author contributions: Disthabanchong S solely contributed to this paper.
Supported by The Kidney Foundation of Thailand
Correspondence to: Sinee Disthabanchong, MD, Associate Professor of Medicine, Division of Nephrology, Department of Medicine, Faculty of Medicine, Ramathibodi Hospital, Mahidol University, 270 Rama VI Rd, Phayathai, Bangkok 10400, Thailand. sineemd@hotmail.com
Telephone: +66-2-2011116 Fax: +66-2-2011400
Received: September 2, 2011
Revised: October 21, 2011
Accepted: February 10, 2012
Published online: April 6, 2012
Abstract

Cardiovascular disease is the leading cause of death among patients with chronic kidney disease (CKD). Vascular calcification (VC) is one of the independent risk factors associated with cardiovascular disease and cardiovascular mortality in both the general population and CKD patients. Earlier evidence revealed substantially higher prevalence of VC in young adults on chronic hemodialysis compared to the general population in the same age range, indicating the influence of CKD-related risk factors on the development of VC. Pathogenesis of VC involves an active, highly organized cellular transformation of vascular smooth muscle cells to bone forming cells evidenced by the presence of bone matrix proteins in the calcified arterial wall. VC occurs in both the intima and the media of arterial wall with medial calcification being more prevalent in CKD. In addition to traditional cardiovascular risks, risk factors specific to CKD such as phosphate retention, excess of calcium, history of dialysis, active vitamin D therapy in high doses and deficiency of calcification inhibitors play important roles in promoting the development of VC. Non-contrast multi-slice computed tomography has often been used to detect coronary artery calcification. Simple plain radiographs of the lateral lumbar spine and pelvis can also detect VC in the abdominal aorta and femoral and iliac arteries. Currently, there is no specific therapy to reverse VC. Reduction of calcium load, lowering phosphate retention using non-calcium containing phosphate binders, and moderate doses of active vitamin D may attenuate progression. Parenteral sodium thiosulfate has also been shown to delay VC progression.

Keywords: Coronary calcification; Cardiovascular; Vascular smooth muscle cells; Osteoblast; Bone; Phosphate; Vitamin D