Nephrol Dial Transplant (2000) 15: 1414-1419
© 2000 European Renal Association-European Dialysis and Transplant Association
Three monocyte-related determinants of atherosclerosis in haemodialysis
1 Departments of Nephrology, 2 Clinical Immunology, Karolinska Hospital and Karolinska Institute, Stockholm, Sweden
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.
Keywords: adhesion molecules; atherosclerosis; chemotaxis; haemodialysis; inflammation
Correspondence and offprint requests to: Dr Stefan H. Jacobson MD PhD, Director, Department of Nephrology, Karolinska Hospital, SE-171 76 Stockholm, Sweden.
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