| Literature DB >> 17136112 |
Abstract
Vascular calcification is not just a hallmark of uremic arterio- and atherosclerosis, but also a significant cardiovascular risk factor in patients with chronic kidney disease. In contrast to the previous assumption that vascular calcification predominantly occurs by passive precipitation of calcium and phosphate ions, recent research led to the insight that extraosseous calcification is a highly regulated process. High serum phosphate and calcium levels may induce a process of osteogenic 'bone-like' differentiation of vascular smooth muscle cells, while deficiencies of calcification inhibitors or a disturbed balance towards calcification inducers may have a relevant pathophysiological influence on the initiation and progression of calcified lesions. This overview summarizes some of the best explored novel risk factors for disturbances of calcium and phosphate homeostasis and points to the integral role of hyperphosphatemia as a modifiable key trigger in calcification processes.Entities:
Mesh:
Year: 2006 PMID: 17136112 DOI: 10.1038/sj.ki.5001996
Source DB: PubMed Journal: Kidney Int Suppl ISSN: 0098-6577 Impact factor: 10.545