title: Circulating endothelial progenitor cells after kidney transplantation.
abstract: 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/10(5) 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 x 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.
authors.affiliation: Nephrology Department, Hospital del Mar, Universitat Autònoma de Barcelona, Barcelona, Spain. m-soler@northwestern.edu
authors.forename: María José
authors.initials: MJ
authors.lastname: Soler
authors.forename: Ofelia María
authors.initials: OM
authors.lastname: Martínez-Estrada
authors.forename: Josep Maria
authors.initials: JM
authors.lastname: Puig-Marí
authors.forename: Didac
authors.initials: D
authors.lastname: Marco-Feliu
authors.forename: Anna
authors.initials: A
authors.lastname: Oliveras
authors.forename: Joan
authors.initials: J
authors.lastname: Vila
authors.forename: Marisa
authors.initials: M
authors.lastname: Mir
authors.forename: Antonia
authors.initials: A
authors.lastname: Orfila
authors.forename: Senén
authors.initials: S
authors.lastname: Vilaró
authors.forename: Josep
authors.initials: J
authors.lastname: Lloveras
mesh_terms: D000071916:AC133 Antigen; D000328:Adult; D015703:Antigens, CD / Q000096:biosynthesis; D018952:Antigens, CD34 / Q000096:biosynthesis; D001835:Body Weight; D002318:Cardiovascular Diseases / Q000473:pathology; D002319:Cardiovascular System / Q000473:pathology; D049109:Cell Proliferation; D042783:Endothelial Cells / Q000166:cytology*; D005260:Female; D005434:Flow Cytometry; D005919:Glomerular Filtration Rate; D006023:Glycoproteins / Q000096:biosynthesis; D006801:Humans; D007166:Immunosuppressive Agents / Q000494:pharmacology / Q000627:therapeutic use; D007676:Kidney Failure, Chronic; D016030:Kidney Transplantation; D017493:Leukocyte Common Antigens / Q000096:biosynthesis; D016014:Linear Models; D008075:Lipoproteins, HDL / Q000378:metabolism; D008077:Lipoproteins, LDL / Q000378:metabolism; D008297:Male; D008875:Middle Aged; D009504:Neutrophils / Q000378:metabolism; D010455:Peptides; D012044:Regression Analysis; D012737:Sex Factors; D013234:Stem Cells / Q000166:cytology*; D013997:Time Factors
chemical_list: D000071916:AC133 Antigen; D015703:Antigens, CD; D018952:Antigens, CD34; D006023:Glycoproteins; D007166:Immunosuppressive Agents; D008075:Lipoproteins, HDL; D008077:Lipoproteins, LDL; D010455:Peptides; D017493:Leukocyte Common Antigens