title: Imbalance between detached circulating endothelial cells and endothelial progenitor cells in chronic kidney disease.
abstract: BACKGROUND
  Patients with chronic kidney disease (CKD) display endothelial dysfunction and are at a high risk for atherosclerotic cardiovascular disease (CVD). Recent studies suggest that circulating detached endothelial cells (CECs) and stimulated endothelial progenitor cells (EPCs) from the bone marrow may reflect endothelial damage.
  
  
  METHODS
  We correlated the levels of CECs expressing the endothelial cell inflammation marker (MICA+ cells) and EPCs (Tie-2+ or VEGFR-2+ cells) in a population of 19 (55 +/- 3 years; 42% males) patients with advanced CKD (median glomerular filtration rate 8 ml/min). In addition, the levels of CD-31+ cells were investigated. Twenty healthy age- (49 +/- 2 years) and gender- (50% men) matched subjects served as controls.
  
  
  RESULTS
  CECs expressing MICA were increased (7.6 +/- 2.7 vs. 1.6 +/- 0.3%; p < 0.05) in CKD patients, however EPCs expressing Tie-2 or VEGFR-2 were significantly decreased (0.16 +/- 0.07 vs. 0.53 +/- 0.15%; p < 0.05, and 0.42 +/- 0.10 vs. 2.80 +/- 0.72%; p < 0.01, respectively) as compared to controls. Furthermore, we also found that the levels of CD-31+ cells were significantly elevated (22.8 +/- 4.2 vs. 9.4 +/- 0.8%; p < 0.01) in CKD patients. Patients on angiotensin-converting enzyme (ACE) inhibitors tended (p = 0.06) to have higher levels of VEGFR-2+ cells (0.57 +/- 0.14 vs. 0.16 +/- 0.11%).
  
  
  CONCLUSIONS
  Our results suggest that there is a marked imbalance between the CEC and EPC numbers in patients with CKD. Further research is needed to evaluate the independent role of inflammatory endothelial markers as well as the effects of ACE inhibitors on mobilization of EPCs in patients with advanced CKD.
authors.affiliation: Division of Renal Medicine and Baxter Novum, Karolinska Institutet, Karolinska University Hospital at Huddinge, Stockholm, Sweden.
authors.forename: Ernesto
authors.initials: E
authors.lastname: Rodríguez-Ayala
authors.forename: Qiang
authors.initials: Q
authors.lastname: Yao
authors.forename: Carolina
authors.initials: C
authors.lastname: Holmén
authors.forename: Bengt
authors.initials: B
authors.lastname: Lindholm
authors.forename: Suchitra
authors.initials: S
authors.lastname: Sumitran-Holgersson
authors.forename: Peter
authors.initials: P
authors.lastname: Stenvinkel
mesh_terms: D002452:Cell Count; D042783:Endothelial Cells / Q000473:pathology*; D005260:Female; D015395:Histocompatibility Antigens Class I / Q000378:metabolism; D006801:Humans; D007676:Kidney Failure, Chronic / Q000473:pathology / Q000503:physiopathology*; D008297:Male; D008875:Middle Aged; D019408:Platelet Endothelial Cell Adhesion Molecule-1 / Q000378:metabolism; D042787:Receptor, TIE-2 / Q000378:metabolism; D013234:Stem Cells / Q000473:pathology*; D040301:Vascular Endothelial Growth Factor Receptor-2 / Q000378:metabolism
chemical_list: D015395:Histocompatibility Antigens Class I; C099187:MHC class I-related chain A; D019408:Platelet Endothelial Cell Adhesion Molecule-1; D042787:Receptor, TIE-2; D040301:Vascular Endothelial Growth Factor Receptor-2