Vascular calcification: mechanisms and management

Br J Cardiol 2008;15:316-21 Leave a comment
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Chronic kidney disease (CKD) is thought to affect approximately one in 10 people. Patients with CKD have significantly increased cardiovascular morbidity and mortality in comparison with the general population. This is thought to occur from a combination of increased atherosclerotic disease and medial calcification of arterial walls. Vascular calcification (VC) is recognised as an active, cell-mediated process with similarities to osteogenesis. Numerous systemic and local factors have been identified as inhibitors of calcification including fetuin-A, matrix Gla protein and pyrophosphate. There is also increasing evidence that increased serum phosphorus, serum calcium x phosphorus product, and/or calcium load is associated with increased VC.

Current treatment strategies focus on the correction of markers of mineral metabolism bone disease such as phosphate, calcium, parathyroid hormone and vitamin D. The use of agents such as bisphosphonates and cinacalcet show promise, but further data are awaited before their widespread use as a treatment for VC can be advocated. Imaging techniques currently used to assess VC are also discussed. Research into the mechanisms underlying VC are still being investigated and further insight into these mechanisms will lead to the development of therapeutic agents, which could improve cardiovascular outcomes in patients.

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