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dc.contributor.authorGracia, Marta
dc.contributor.authorBetriu i Bars, M. Àngels
dc.contributor.authorMartínez Alonso, Montserrat
dc.contributor.authorArroyo, David
dc.contributor.authorAbajo, María
dc.contributor.authorFernández i Giráldez, Elvira
dc.contributor.authorValdivielso Revilla, José Manuel
dc.date.accessioned2018-04-25T07:36:04Z
dc.date.available2018-04-25T07:36:04Z
dc.date.issued2016-02
dc.identifier.issn1555-9041
dc.identifier.urihttp://hdl.handle.net/10459.1/63139
dc.description.abstractBackground and objectives Ultrasonographic detection of subclinical atheromatosis is a noninvasive method predicting cardiovascular events. Risk factors predicting atheromatosis progression in CKD are unknown. Predictors of atheromatosis progression were evaluated in patients with CKD. Design, setting, participants, & measurements Our multicenter, prospective, observational study included 1553 patients with CKD (2009-2011). Carotid and femoral ultrasounds were performed at baseline and after 24 months. A subgroup of 476 patients with CKD was also randomized to undergo ultrasound examination at 12 months. Progression of atheromatosis was defined as an increase in the number of plaque territories analyzed by multivariate logistic regression. Results Prevalence of atheromatosis was 68.7% and progressed in 59.8% of patients after 24 months. CKD progression was associated with atheromatosis progression, suggesting a close association between pathologies. Variables significantly predicting atheromatosis progression, independent from CKD stages, were diabetes and two interactions of age with ferritin and plaque at baseline. Given that multiple interactions were found between CKD stage and age, phosphate, smoking, dyslipidemia, body mass index, systolic BP (SBP), carotid intima-n-iedia thickness, plaque at baseline, uric acid, cholesterol, 25-hydroxy vitamin D (250H vitamin D), and antiplatelet and phosphate binders use, the analysis was stratified by CKD stages. In stage 3, two interactions (age with phosphate and plaque at baseline) were found, and smoking, diabetes, SBP, low levels of 25OH vitamin D, and no treatment with phosphate binders were positively associated with atheromatosis progression. In stages 4 and 5, three interactions (age with ferritin and plaque and plaque with smoking) were found, and SBP was positively associated with atheromatosis progression. In dialysis, an interaction between body mass index and 25OH vitamin D was found, and age, dyslipidemia, carotid intima-media thickness, low cholesterol, ferritin, and uric acid were positively associated with atheromatosis progression. Conclusions Atheromatosis progression affects more than one half of patients with CKD, and predictive factors differ depending on CKD stage.
dc.description.sponsorshipThe work presented here was funded by a research grant from Abbvie,the Spanish Government, and Fondos Europeos de Desarrollo, European Funds for Regional Development (FEDER) funds Thematic Networks for Collaborative Research (RETIC) grant RD12/0021/0026 and Fund for Sanitary Research (FIS) grant PS10/00946
dc.format.mimetypeapplication/pdf
dc.language.isoeng
dc.publisherAmerican Society of Nephrology
dc.relation.isformatofVersió postprint del document publicat a: https://doi.org/10.2215/CJN.01240215
dc.relation.ispartofClinical Journal of The American Society of Nephrology, 2016, vol. 11, num. 2, p. 287-296
dc.rights(c) American Society of Nephrology, 2016
dc.subjectAtherosclerosis
dc.subjectChronic kidney disease
dc.subjectCardiovascular disease
dc.subjectVitamin D deficiency
dc.titlePredictors of Subclinical Atheromatosis Progression over 2 Years in Patients with Different Stages of CKD
dc.title.alternativePredictors of subclinical atheromatosis progression in patients at diferent stages of chronic kidney disease after two years of follow-up. The Nefrona study
dc.typeinfo:eu-repo/semantics/article
dc.date.updated2018-04-25T07:36:05Z
dc.identifier.idgrec023813
dc.type.versioninfo:eu-repo/semantics/acceptedVersion
dc.rights.accessRightsinfo:eu-repo/semantics/openAccess
dc.identifier.doihttps://doi.org/10.2215/CJN.01240215


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