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HERO ID
2056117
Reference Type
Journal Article
Subtype
Review
Title
Pathogenesis of vascular calcification in chronic kidney disease
Author(s)
Cozzolino, M; Brancaccio, D; Gallieni, M; Slatopolsky, E
Year
2005
Is Peer Reviewed?
1
Journal
Kidney International
ISSN:
0085-2538
EISSN:
1523-1755
Volume
68
Issue
2
Page Numbers
429-436
Language
English
PMID
16014020
DOI
10.1111/j.1523-1755.2005.00421.x
Web of Science Id
WOS:000230342500001
Abstract
Pathogenesis of vascular calcification in chronic kidney disease. Background. Hyperphosphatemia and hypercalcemia are independent risk factors for higher incidence of cardiovascular events in patients with chronic kidney disease. In addition to increased calcium-phosphate product, hyperphosphatemia accelerates the progression of secondary hyperparathyroidism with the concomitant bone loss, possibly linked to vascular calcium-phosphate precipitation. Results. The control of serum phosphate levels reduces vascular calcification not only by decreasing the degree of secondary hyperparathyroidism and calcium-phosphate product, but also by reducing the expression of proteins responsible for active bone mineral deposition in cells of the vasculature. The calcium and aluminum-free phosphate-binders provide a new and effective therapeutic tool in preventing vascular calcifications in chronic kidney disease in animal models and in hemodialysis patients. Conclusion. Additional investigations are necessary to examine the benefits of different phosphate-binders in reducing mortality from cardiovascular disease.
Keywords
vascular calcifications; hyperphosphatemia; kidney disease; calcium load; phosphate binders
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