期刊
CLINICAL JOURNAL OF THE AMERICAN SOCIETY OF NEPHROLOGY
卷 5, 期 2, 页码 227-234出版社
AMER SOC NEPHROLOGY
DOI: 10.2215/CJN.03260509
关键词
-
资金
- Fondo de Investigacion Sanitaria, Instituto de Salud Carlos III [FIS PI06/0724, PI06/0747, PI07/0204, PI08/1038, RD06/0016/0007]
- Junta de Andalucia [CM0008, TCRM0006/2006, P06-CVI-021.72, P08-CTS-3797]
- Fundacion Nefrologica
Background and objectives: We studied the relationship between microinflammation and endothelial damage in chronic kidney disease (CKD) patients on different dialysis modalities. Design, setting, participants, & measurements: Four groups of CKD stage 5 patients were studied: 1) 14 nondialysis CKD patients (CKD-NonD); 2) 15 hemodialysis patients (HD); 3) 12 peritoneal dialysis patients with residual renal function >1 ml/min (PD-RRF >1); and 4) 13 peritoneal dialysis patients with residual renal function <= 1 ml/min (PD-RRF <= 1). Ten healthy subjects served as controls. CD14(+)CD16(+) cells and apoptotic endothelial microparticles (EMPs) were measured by flow cytometry. Serum vascular endothelial growth factor (VEGF) was measured by ELISA. Results: CKD-NonD and HD patients had a higher percentage of CD14(+)CD16(+) monocytes than PD groups and controls. CD14(+)CD16(+) was similar in the PD groups, regardless of their RRF, and controls. The four uremic groups displayed a marked increase in apoptotic EMPs and VEGF compared with controls. Apoptotic EMPs and VEGF were significantly higher in HD patients than in CKD-NonD and both PD groups. However, there were no significant differences between CKD-NonD and the two PD groups. There was a correlation between CD14(+)CD16(+) and endothelial damage in CKD-NonD and HD patients, but not in PD and controls. Conclusions: There was an increase in CD14(+)CD16(+) only in CKD-NonD and HD patients. In these patients, there was a relationship between increased CD14(+)CD16(+) and endothelial damage. These results strongly suggest that other factors unrelated to the microinflammatory status mediated by CD14(+)CD16(+) are promoting the endothelial damage in PD, regardless of their RRF. Clin J Ain Soc Nephrol 5: 227-234, 2010. doi: 10.2215/CJN.03260509
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据