BACKGROUND: Vascular access failure is the most common cause of morbidity and hospitalization in haemodialysis (HD) patients. Although there are reports that anti-platelet agents can prevent vascular access thrombosis, the relationship between platelet activation and vascular access failure is not clear. The aim of this study was to investigate the role of platelet activation in recurrent vascular access failure. METHODS: The studied subjects were divided into three groups: group I included 23 HD patients with recurrent vascular access failure (native arteriovenous fistula <2 year survival or synthetic arteriovenous graft <1 year survival), group II included 15 HD patients with longer vascular access survival (>5 year survival) and group III included 10 healthy volunteers as controls. The expression of platelet activation markers (CD62P and fibrinogen receptor) and the numbers of platelet-derived microparticles were measured and compared between groups. RESULTS: CD62P-positive platelets were significantly higher in group I than in both group II (7.3+/-3.7 vs 3.5+/-1.3%; P<0.0005) and group III (2.9+/-0.9%; P<0.00005). Fibrinogen receptor-positive (PAC-1-positive) platelets were also significantly higher in group I than in group II (2.2+/-2.1 vs 0.9+/-0.7%; P<0.01) and group III (0.8+/-0.6%; P<0.01). CONCLUSIONS: A higher level of circulating activated platelets is associated with shorter survival of vascular access in HD patients. The higher level of circulating activated platelets may be a predictor of recurrent vascular access failure. The potential advantageous effects of anti-platelet therapy on this patient population warrant further investigation.
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Chuang et al. (2003) studied this question.
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