BACKGROUND: Circulating bone marrow-derived endothelial progenitor cells (EPCs) promote vascular repair, and their number correlates with endothelial function and cardiovascular risk in humans. In uremic patients, the number of functionally active EPCs is reduced. Thus, we assessed EPCs in stable patients 6 months or more after renal transplantation. METHODS: We analyzed circulating CD34+ hematopoietic progenitor cells (HPCs) using flow cytometry and EPCs (in vitro assay) in 74 renal transplant patients (51.6+/-11.5 years; 46 males), 74 age-matched healthy subjects, and 29 patients with preterminal renal failure. RESULTS: EPC numbers were similar in renal transplant recipients and controls (232+/-92 vs. 250+/-103/high power field; n.s.), but were significantly higher than in uremic patients (160+/-97/high power field; P=0.004). In addition, transplant recipients had more HPCs than controls (2.71+/-1.65 vs. 1.99+/-1.12 /microl; P=0.004) and uremic patients (1.64+/-0.96/microl; P=0.001). EPCs in renal transplant recipients correlated significantly with graft function(that is, Cockcroft-Gault clearance [r=0.294; P=0.012]), but not with age or HPCs. Moreover, in the multiple regression analysis, graft function (r=0.332; P=0.01) and diastolic blood pressure (r=-0.278; P=0.03) were independent predictors of EPCs. In vitro, sera from renal transplant recipients with poor graft function significantly inhibited EPC differentiation compared with sera from patients with a clearance above 50 mL/min (151+/-54 vs. 274+/-94 EPCs/high power field; P=0.02). CONCLUSIONS: EPC numbers in stable renal transplant recipients are comparable to those found in healthy subjects. In addition, graft function is a significant determinant of EPCs. Prospective studies should explore whether improvement of EPCs influences cardiovascular risk in renal transplant recipients.
BACKGROUND: Circulating bone marrow-derived endothelial progenitor cells (EPCs) promote vascular repair, and their number correlates with endothelial function and cardiovascular risk in humans. In uremicpatients, the number of functionally active EPCs is reduced. Thus, we assessed EPCs in stable patients 6 months or more after renal transplantation. METHODS: We analyzed circulating CD34+ hematopoietic progenitor cells (HPCs) using flow cytometry and EPCs (in vitro assay) in 74 renal transplant patients (51.6+/-11.5 years; 46 males), 74 age-matched healthy subjects, and 29 patients with preterminal renal failure. RESULTS: EPC numbers were similar in renal transplant recipients and controls (232+/-92 vs. 250+/-103/high power field; n.s.), but were significantly higher than in uremicpatients (160+/-97/high power field; P=0.004). In addition, transplant recipients had more HPCs than controls (2.71+/-1.65 vs. 1.99+/-1.12 /microl; P=0.004) and uremicpatients (1.64+/-0.96/microl; P=0.001). EPCs in renal transplant recipients correlated significantly with graft function(that is, Cockcroft-Gault clearance [r=0.294; P=0.012]), but not with age or HPCs. Moreover, in the multiple regression analysis, graft function (r=0.332; P=0.01) and diastolic blood pressure (r=-0.278; P=0.03) were independent predictors of EPCs. In vitro, sera from renal transplant recipients with poor graft function significantly inhibited EPC differentiation compared with sera from patients with a clearance above 50 mL/min (151+/-54 vs. 274+/-94 EPCs/high power field; P=0.02). CONCLUSIONS: EPC numbers in stable renal transplant recipients are comparable to those found in healthy subjects. In addition, graft function is a significant determinant of EPCs. Prospective studies should explore whether improvement of EPCs influences cardiovascular risk in renal transplant recipients.
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