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pubmed-article:17429198pubmed:abstractTextDuring haemodialysis (HD) the endothelium is the first organ to sense and to be impaired by mechanical and immunological stimuli. We hypothesized that a single HD session induces mobilization of endothelial progenitor cells (EPCs) and that cardiovascular risk factors may influence this process. We quantified EPCs at different maturational stages (CD34+, CD133+/VEGFR2+) in blood samples from 30 patients, during HD and on the interdialytic day, and in 10 healthy volunteers. Samples were drawn at the start of HD, 1, 2 and 3 h after, at the end of HD and at 24 h on the interdialytic day. Patients were divided into two groups based on a recent risk scoring system (SCORE project): low-risk (LR) and high-risk groups (HR). HD patients showed a significantly reduced basal number of EPCs with respect to healthy volunteers. In contrast, we observed increasing EPCs during HD whereas they diminished on the interdialytic day. The EPC number was directly correlated with HD time progression. The EPC number during HD was increased in the HR group with respect to the LR group. We had a direct correlation between risk score and number of EPCs. Cardiovascular risk factors influenced the mobilization of stem cells from the bone marrow. This feature could be the direct consequence of an augmented request of stem cells to respond to the most important endothelial impairment but could also show a defective capacity of EPCs to home in and repair the sites of vascular injury.lld:pubmed
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pubmed-article:17429198pubmed:copyrightInfoCopyright 2007 S. Karger AG, Basel.lld:pubmed
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pubmed-article:17429198pubmed:articleTitleEffects of haemodialysis on circulating endothelial progenitor cell count.lld:pubmed
pubmed-article:17429198pubmed:affiliationDepartment of Internal Medicine, University of Messina, Messina, Italy.lld:pubmed
pubmed-article:17429198pubmed:publicationTypeJournal Articlelld:pubmed
pubmed-article:17429198pubmed:publicationTypeComparative Studylld:pubmed
pubmed-article:17429198pubmed:publicationTypeResearch Support, Non-U.S. Gov'tlld:pubmed
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