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Pathogenesis of vascular calcification in chronic kidney disease.
Kidney Int 2005; 68(2):429-36KI

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.

Authors+Show Affiliations

Department of Nephrology and Dialysis, Ospedale San Paolo, Milan, Italy. mariocozzolino@hotmail.comNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Review

Language

eng

PubMed ID

16014020

Citation

Cozzolino, Mario, et al. "Pathogenesis of Vascular Calcification in Chronic Kidney Disease." Kidney International, vol. 68, no. 2, 2005, pp. 429-36.
Cozzolino M, Brancaccio D, Gallieni M, et al. Pathogenesis of vascular calcification in chronic kidney disease. Kidney Int. 2005;68(2):429-36.
Cozzolino, M., Brancaccio, D., Gallieni, M., & Slatopolsky, E. (2005). Pathogenesis of vascular calcification in chronic kidney disease. Kidney International, 68(2), pp. 429-36.
Cozzolino M, et al. Pathogenesis of Vascular Calcification in Chronic Kidney Disease. Kidney Int. 2005;68(2):429-36. PubMed PMID: 16014020.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Pathogenesis of vascular calcification in chronic kidney disease. AU - Cozzolino,Mario, AU - Brancaccio,Diego, AU - Gallieni,Maurizio, AU - Slatopolsky,Eduardo, PY - 2005/7/15/pubmed PY - 2005/10/14/medline PY - 2005/7/15/entrez SP - 429 EP - 36 JF - Kidney international JO - Kidney Int. VL - 68 IS - 2 N2 - 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. SN - 0085-2538 UR - https://www.unboundmedicine.com/medline/citation/16014020/full_citation L2 - https://linkinghub.elsevier.com/retrieve/pii/S0085-2538(15)50863-6 DB - PRIME DP - Unbound Medicine ER -