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1 Department of Medicine, Division of Nephrology, Toronto General Hospital, Toronto, ON, Canada
2 Department of Surgery, Division of Cardiac Surgery, Toronto General Hospital, Toronto, ON, Canada
* To whom correspondence should be addressed. E-mail: christopher.chan{at}uhn.on.ca.
Cardiovascular disease is the principal cause of death in end-stage renal disease (ESRD) patients. Endothelial progenitor cells (EPCs) play a critical role in vascular repair, and improving EPC biology represents a novel therapeutic target. Three groups of age and gender matched patients were studied: (1) 10 healthy control; (2) 12 conventional hemodialysis (CHD) patients and (3) 10 nocturnal hemodialysis (NHD) patients. EPC number and migratory function were assessed. Left ventricular mass index (LVMI) was derived and correlations between EPC biology, uremic clearance and LVMI were made. Compared to controls, EPC number and function were markedly impaired in CHD patients [(3.48 ± 1.2 vs. 0.86 ± 0.20 % per 50,000 cells, p<0.05) and (18.8 ± 2.64 vs. 3.75 ± 0.34 cells per HPF, p<0.05) respectively]. In contrast, EPC number and function were normal in NHD patients [(3.48 ± 1.17 vs. 3.83 ± 0.77[NHD] % per 50,000 cells) and (18.8 ± 2.6 vs. 22.2 ± 2.4 [NHD] cells per HPF) respectively]. Among ESRD patients, EPCs number and function inversely correlated to predialysis urea concentration (r = - 0.40; r = -0.57), LVMI (r = - 0.41; -0.46) and systolic blood pressure (r= - 0.58; r = -0.44). We demonstrate that NHD is associated with restoration of abnormal EPC biology in ESRD. Given the increasing importance of EPCs in the repair and restoration of cardiovascular function, these data have important clinical implications for vascular risk in ESRD patients.
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