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Kidney Int. 2005 Aug;68(2):429-36.

Pathogenesis of vascular calcification in chronic kidney disease.

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1
Department of Nephrology and Dialysis, Ospedale San Paolo, Milan, Italy. mariocozzolino@hotmail.com

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.

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