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Comparative Study
. 2010 Feb;5(2):227-34.
doi: 10.2215/CJN.03260509. Epub 2010 Jan 7.

Effect of different dialysis modalities on microinflammatory status and endothelial damage

Affiliations
Comparative Study

Effect of different dialysis modalities on microinflammatory status and endothelial damage

Ana Merino et al. Clin J Am Soc Nephrol. 2010 Feb.

Abstract

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 <or=1 ml/min (PD-RRF <or=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.

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Figures

Figure 1.
Figure 1.
Representative flow cytometry analysis. (A) CD14 monocytes (G1) were assessed using an SSC-Height/CD14-PerCP dot plot and backgated (G2) within the FCS-Height/SSC-Height (B). Subsequently, CD14+CD16+ monocytes within the G2 population were assessed using CD16-FITC/CD14-PerCP dot plot (C, D, E, F). Representative histograms of CD14+CD16+ expression in different CKD patients and a healthy subject (C, D, E, F). The region represents CD14+CD16+ monocytes from controls, chronic kidney disease patients (CKD-NonD), hemodialysis patients (HD), and peritoneal dialysis patients (PD).
Figure 2.
Figure 2.
Serum VEGF concentrations were measured by ELISA in control, chronic kidney disease (CKD-NonD), hemodialysis (HD), and peritoneal dialysis with RRF >1 ml/min (PD-RRF >1) patients, and peritoneal dialysis with RRF ≤1 ml/min (PD-RRF ≤1) patients. Values are shown as mean ± standard deviation. *P < 0.05 versus controls, CKD-NonD, PD-RRF >1, PD-RRF ≤1. #P < 0.05 versus controls.
Figure 3.
Figure 3.
Apoptotic EMPs in platelet-free plasma from control, chronic kidney disease (CKD-NonD), hemodialysis (HD), and peritoneal dialysis with RRF >1 ml/min (PD-RRF >1) patients, and peritoneal dialysis with RRF ≤1 ml/min (PD-RRF ≤1) patients. Apoptotic EMPs were measured by flow cytometry. Apoptotic EMPs are expressed as events per microliter. *P < 0.05 versus controls, CKD-NonD, PD-RRF > 1, PD-RRF ≤ 1. #P < 0.05 versus controls.
Figure 4.
Figure 4.
Correlation between CD14+CD16+ cells and serum VEGF concentration or apoptotic EMPs. (A) Percentages of CD14+CD16+ cells were correlated with serum VEGF concentrations in each group. (B) Percentages of CD14+CD16+ cells were correlated with the numbers of apoptotic EMPs in the controls, CKD-NonD, HD, and PD groups. We have shown only a single PD graph because both PD groups displayed similar results.

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