Three monocyte-related determinants of atherosclerosis in haemodialysis

被引:17
作者
Jacobson, SH [1 ]
Thylén, P
Lundahl, J
机构
[1] Karolinska Hosp, Dept Nephrol, SE-17176 Stockholm, Sweden
[2] Karolinska Hosp, Dept Clin Immunol, SE-17176 Stockholm, Sweden
[3] Karolinska Inst, Stockholm, Sweden
关键词
adhesion molecules; atherosclerosis; chemotaxis; haemodialysis; inflammation;
D O I
10.1093/ndt/15.9.1414
中图分类号
R3 [基础医学]; R4 [临床医学];
学科分类号
1001 ; 1002 ; 100602 ;
摘要
Background. It has been suggested that monocyte-related inflammatory mediators play a role in atherosclerosis. Haemodialysis induces phenotypic changes in adhesion molecule expression on monocytes. Soluble vascular cell adhesion molecule-1 (sVCAM-1), an adhesion molecule involved in monocyte recruitment, has been proposed to correlate with the extent of atherosclerosis in humans. Monocyte chemotactic protein-1 (MCP-1) functions as a monocyte-specific chemoattractant. Methods. We studied monocyte count, CD11b/CD18 expression on monocytes, MCP-1, and sVCAM-1 in nine patients on either cuprophane or polysulphone haemodialysis (n=18 treatments) at times 0 (before haemodialysis), 3 h (end of haemodialysis), 4, 6, 8 and 24 h after start of treatment, as well as in 18 healthy subjects. Results. Monocyte CD11b/CD18 expression increased with both membranes (P<0.001) during and after dialysis compared to before treatment. The concentrations of sVCAM-1 and MCP-1 were higher in patients compared to those in controls both before, during and after haemodialysis (P<0.001 at all time points). There were correlations between the expression of CD11b/CD18 on monocytes and the interdialytic concentrations of sVCAM-1 (r=0.76, P<0.001) and MCP-1 (r=0.54, P<0.05) and between MCP-1 and sVCAM-1 before and after haemodialysis (P<0.05). Conclusion. Patients on haemodialysis have an increased systemic chemotactic activity for monocytes, unphysiological phenotypic alterations in CD11b/CD18 expression during and after dialysis, and increased sVCAM-1 and MCP-1 concentrations. Prospective studies are needed to establish the role of these abnormalities in the pathogenesis of atherosclerosis in haemodialysis patients.
引用
收藏
页码:1414 / 1419
页数:6
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