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Am J Physiol Renal Physiol 296: F1314-F1322, 2009. First published April 1, 2009; doi:10.1152/ajprenal.90755.2008
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Endothelial progenitor cell dysfunction in patients with progressive chronic kidney disease

Guido Krenning,1 Patricia Y. W. Dankers,1 Johannes W. Drouven,1 Femke Waanders,2 Casper F. M. Franssen,2,3 Marja J. A. van Luyn,1 Martin C. Harmsen,1,* and Eliane R. Popa1,*

1Stem Cell and Tissue Engineering Research Group, Department of Pathology and Medical Biology, 2Division of Nephrology, Department of Internal Medicine, and 3Dialysis Center Groningen, University Medical Center Groningen, University of Groningen, Groningen, The Netherlands

Submitted 18 December 2008 ; accepted in final form 31 March 2009

Endothelial progenitor cells (EPC) contribute to repair and maintenance of the vascular system, but in patients with chronic kidney disease (CKD), the number and function of EPC may be affected by kidney dysfunction. We assessed numbers and the angiogenic function of EPC from patients with CKD in relation to disease progression. In a cross-sectional, prospective study, 50 patients with varying degrees of CKD, including 20 patients undergoing dialysis and 10 healthy controls, were included. Mononuclear cells were isolated, and circulating EPC were quantified by flow cytometry based on expression of CD14 and CD34. EPC were cultured on fibronectin-coated supramolecular films of oligocaprolactone under angiogenic conditions to determine their angiogenic capacity and future use in regenerative medicine. CKD patients had normal numbers of circulating CD14+ EPC but reduced numbers of circulating CD34+ EPC. Furthermore, EPC from patients with CKD displayed functional impairments, i.e., hampered adherence, reduced endothelial outgrowth potential, and reduced antithrombogenic function. These impairments were already observed at stage 1 CKD and became more apparent when CKD progressed. Dialysis treatment only partially ameliorated EPC impairments in patients with CKD. In conclusion, EPC number and function decrease with advancing CKD, which may hamper physiological vascular repair and can add to the increased risk for cardiovascular diseases observed in CKD patients.

cardiovascular disease; CD34; CD14; hemodialysis; peritoneal dialysis


Address for reprint requests and other correspondence: E. R. Popa, Stem Cell and Tissue Engineering Research Group, Dept. of Pathology and Medical Biology, Univ. Medical Center Groningen, Univ. of Groningen, Hanzeplein 1 (EA11), NL-9713GZ, Groningen, The Netherlands (e-mail: e.r.popa{at}med.umcg.nl)






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