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dc.contributor.authorRodríguez-García, Minerva-
dc.contributor.authorCabezas-Rodríguez, Iván-
dc.contributor.authorLópez-Ongil, Susana-
dc.contributor.authorDíaz-López, Bernardino-
dc.contributor.authorCannata Andía, Jorge B.-
dc.date.accessioned2013-03-19T10:13:29Z-
dc.date.available2013-03-19T10:13:29Z-
dc.date.issued2011-
dc.identifier.citationMed Princ Pract.2011;20:203–212eng
dc.identifier.issn1011-7571-
dc.identifier.urihttps://ria.asturias.es/RIA/handle/123456789/2603-
dc.description.abstractVascular calcification plays a major role in cardiovascular disease, which is one of the main causes of mortality in chronic kidney disease patients. Vascular calcification is determined by prevalent traditional and uraemia-related (non-traditional) risk factors. It occurs mainly in the arteries, which are classified into three types according to their size and structural characteristics. In addition, vascular calcification has been associated with bone loss and fractures in chronic kidney disease patients and the general population, stressing the fact that both disorders can share pathogenetic pathways. The strategies to control vascular calcification involve several measures, chief among them the control of hyperphosphataemia. Furthermore, it has been recently described that strategies that reduce bone resorption and increase bone mineralization may decrease the risk of vascular calcifications;however, this approach still remains controversial. The mechanisms involved in vascular calcification are complex and not yet fully understood. Phosphorus plays a major role,while other factors related to bone formation have been recently identified.eng
dc.description.sponsorshipThe authors wish to thank the Fondo de Investigaciones Sanitarias, REDinREN del ISCIII (Redes Temáticas de Investigación Cooperativa en Salud; RD06/0016/1013), FYCIT (Fundación para el Fomento en Asturias de la Investigación Científica Aplicada y la Tecnología) and Fundación Renal Iñigo Álvarez de Toledo (Spain)eng
dc.language.isoengeng
dc.publisherKarger AGeng
dc.relation.ispartofMedical Principles and Practiceeng
dc.relation.haspart20eng
dc.relation.isreferencedbySí, esta versión ha sido citadaeng
dc.rights.urihttp://creativecommons.org/licenses/by/3.0/es/*
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dc.rights.urihttp://creativecommons.org/licenses/by/3.0/es/*
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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/*
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dc.rights.urihttp://creativecommons.org/licenses/by/3.0/es/*
dc.rights.urihttp://creativecommons.org/licenses/by-nc-sa/3.0/deed.eseng
dc.source203;212-
dc.subjectVascular calcificationeng
dc.subjectChronic kidney diseaseeng
dc.subjectSecondary hyperparathyroidismeng
dc.subjectBone loss vascular-bone linkseng
dc.subject.classificationPublicadoeng
dc.titleVascular Calcification in Patients with Chronic Kidney Disease: Types, Clinical Impact and Pathogenesiseng
dc.typearticleeng
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