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dc.contributor.authorRodríguez García, Minerva-
dc.contributor.authorCabezas Rodríguez, Iván-
dc.contributor.authorLópez Ongil, Susana-
dc.contributor.authorDíaz López, J. Bernardino-
dc.contributor.authorCannata Andía, Jorge B.-
dc.date.accessioned2010-04-23T07:23:15Z-
dc.date.available2010-04-23T07:23:15Z-
dc.date.issued2010-
dc.identifier.citationMed Prin Pract.2010eng
dc.identifier.issn1423-0151-
dc.identifier.urihttps://ria.asturias.es/RIA/handle/123456789/374-
dc.description.abstractSeveral studies suggest that vascular calcifications play a main role in the cardiovascular disease, which is one of the main causes of mortality in CKD patients. Vascular calcification is determined by prevalent traditional, uraemia-related and non-traditional risk factors such as cardiovascular disease or pro-inflammatory molecules and occurs mainly in the arteries, which are classified in three types according to their size and structural characteristics. Several epidemiological studies have linked vascular calcifications to bone loss and fractures in chronic kidney disease patients and also in the general population, stressing the fact that both can share pathogenetic pathways. The mechanisms behind vascular calcification are complex and not yet fully understood. Phosphorus plays a main role, while other elements related to bone formation have been recently identified, including the BMP-Wnt-Msx-2 axis. The strategies to control vascular calcifications involve several measures, chief among them the control of hyperphosphatemia. Furthermore, it has been recently described that strategies focusing on both reducing bone resorption and increasing bone mineralization may decrease the risk of vascular calcifications.eng
dc.description.sponsorshipFondo de Investigaciones Sanitarias, REDinREN del ISCIII (Redes Temáticas de Investigación Cooperativa en Salud; RD06/0016/1013); FICYT (Fundación para el Fomento en Asturias de la Investigación Científica Aplicada y la Tecnología), and Fundación Renal Iñigo Álvarez de Toledo (Spain). The authors also would like to extend their appreciation to Marino Santirso for the language editing of this articleeng
dc.language.isoengeng
dc.publisherKargereng
dc.rights.urihttp://creativecommons.org/licenses/by/3.0/es/*
dc.rights.urihttp://creativecommons.org/licenses/by/3.0/es/*
dc.rights.urihttp://creativecommons.org/licenses/by/3.0/es/*
dc.rights.urihttp://creativecommons.org/licenses/by/3.0/es/*
dc.rights.urihttp://creativecommons.org/licenses/by/3.0/es/*
dc.rights.urihttp://creativecommons.org/licenses/by/3.0/es/*
dc.rights.urihttp://creativecommons.org/licenses/by/3.0/es/*
dc.rights.urihttp://creativecommons.org/licenses/by/3.0/es/*
dc.rights.urihttp://creativecommons.org/licenses/by/3.0/es/*
dc.rights.urihttp://creativecommons.org/licenses/by/3.0/es/*
dc.rights.urihttp://creativecommons.org/licenses/by/3.0/es/*
dc.rights.urihttp://creativecommons.org/licenses/by/3.0/es/*
dc.rights.urihttp://creativecommons.org/licenses/by/3.0/es/*
dc.rights.urihttp://creativecommons.org/licenses/by/3.0/es/*
dc.rights.urihttp://creativecommons.org/licenses/by/3.0/es/*
dc.rights.urihttp://creativecommons.org/licenses/by/3.0/es/*
dc.rights.urihttp://creativecommons.org/licenses/by/3.0/es/*
dc.rights.urihttp://creativecommons.org/licenses/by/3.0/es/*
dc.rights.urihttp://creativecommons.org/licenses/by/3.0/es/*
dc.rights.urihttp://creativecommons.org/licenses/by/3.0/es/*
dc.rights.urihttp://creativecommons.org/licenses/by/3.0/es/*
dc.rights.urihttp://creativecommons.org/licenses/by/3.0/es/*
dc.subjectVascular calcificationeng
dc.subjectCardiovascular diseaseeng
dc.titleVascular calcification: pathogenesis, epidemiology anda clinical impacteng
dc.typearticleeng
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