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Information Journal Paper

Title

VASCULAR CALCIFICATION IN CHRONIC KIDNEY DISEASE MECHANISMS AND CLINICAL IMPLICATION

Pages

  285-299

Abstract

 Vascular calcification is a well-known complication of chronic kidney disease and one of the main predictors for increased cardiovascular morbidity and mortality in these patients. It may happen in 2 main types of intimal calcification, as a part of diffuse atherosclerosis, and medial calcification, which is generally focal in distribution, unrelated to atherosclerotic risk factors, and seen in younger hemodialysis patients. Pathogenesis may be genetic, mineral metabolism related, or nonmineral metabolism related. Increased calcium, phosphorus, and calcium-phosphorus product, decreased parathyroid hormone level, and overzealous use of active vitamin D supplements are the main mineral metabolism-related mechanisms of vascular calcification. Other mechanisms are formation of matrix vesicles and cellular apoptosis, with generation of hydroxyapatite crystals within vesicles and apoptotic bodies. The interplay of various activator proteins of vascular calcification such as bone morphogenetic proteins and receptor activator of nuclear factor-kappa B ligand, or inhibitor proteins like matrix Gla protein, bone morphogenetic protein-7, osteopontin, osteoprotegerin, fetuin-A, Smad6, and pyrophosphate are important in establishment of vascular calcification. Vascular calcification is related to all-cause and cardiovascular mortality both in general population and dialysis patients. Minimizing traditional risk factors of vascular calcification, prevention of hypercalcemia, and avoidance of high doses of calcium-based phosphate binders and vitamin D analogues are important measures for prevention or attenuation of progression of vascular calcification. Sevelamer and cinacalcet may prevent progression of vascular calcification. With the evolving knowledge of the pathogenesis of vascular calcification, we can look forward to emergence of novel therapies for this complication in the future.

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  • Cite

    APA: Copy

    OSSAREH, SHAHRZAD. (2011). VASCULAR CALCIFICATION IN CHRONIC KIDNEY DISEASE MECHANISMS AND CLINICAL IMPLICATION. IRANIAN JOURNAL OF KIDNEY DISEASES (IJKD), 5(5), 285-299. SID. https://sid.ir/paper/309338/en

    Vancouver: Copy

    OSSAREH SHAHRZAD. VASCULAR CALCIFICATION IN CHRONIC KIDNEY DISEASE MECHANISMS AND CLINICAL IMPLICATION. IRANIAN JOURNAL OF KIDNEY DISEASES (IJKD)[Internet]. 2011;5(5):285-299. Available from: https://sid.ir/paper/309338/en

    IEEE: Copy

    SHAHRZAD OSSAREH, “VASCULAR CALCIFICATION IN CHRONIC KIDNEY DISEASE MECHANISMS AND CLINICAL IMPLICATION,” IRANIAN JOURNAL OF KIDNEY DISEASES (IJKD), vol. 5, no. 5, pp. 285–299, 2011, [Online]. Available: https://sid.ir/paper/309338/en

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