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Circulating Endothelial Progenitor Cells After Kidney Transplantation

Circulating endothelial progenitor cells (EPCs) promote vascular repair and maintain integrity of the endothelial monolayer. Reduced EPCs number has been associated with endothelial dysfunction in various cardiovascular diseases. Cardiovascular disease risk is higher in renal transplant patients (RT...

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Bibliographic Details
Published in:American journal of transplantation 2005-09, Vol.5 (9), p.2154-2159
Main Authors: Soler, María José, Martínez‐Estrada, Ofelia María, Puig‐Marí, Josep Maria, Marco‐Feliu, Didac, Oliveras, Anna, Vila, Joan, Mir, Marisa, Orfila, Antonia, Vilaró, Senén, Lloveras, Josep
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Language:English
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Summary:Circulating endothelial progenitor cells (EPCs) promote vascular repair and maintain integrity of the endothelial monolayer. Reduced EPCs number has been associated with endothelial dysfunction in various cardiovascular diseases. Cardiovascular disease risk is higher in renal transplant patients (RT) than the general population. We studied EPCs number and proliferation in RT, and examined the association with other cardiovascular risk factors such as reduced glomerular filtration rate (GFR) and LDL cholesterol. EPCs concentration was determined in 94 RT and 39 control subjects (C) by flow cytometry. EPCs proliferation was also studied after 7 days in culture. EPCs concentration was significantly reduced in RT versus C (median 33.5 [5–177] vs. 53 [9–257] EPCs/105 PMN cells, p = 0.006). EPCs proliferation was also reduced in RT versus C (mean ± SD; 372.7 ± 229.3 vs. 539.8 ± 291.3 EPCs × field, p = 0.003). In multiple regression analysis, GFR, HDL, LDL and body weight were independent predictors of EPCs concentration in RT (r2= 0.25, p < 0.001). EPCs number is reduced in RT, particularly in patients with reduced GFR. Moreover, EPCs from RT studied in vitro, showed reduced proliferation, which is a sign of functional impairment. These alterations may be involved in increased cardiovascular risk of RT.
ISSN:1600-6135
1600-6143
DOI:10.1111/j.1600-6143.2005.01010.x