Role of platelet factor 4-heparin complex antibody (HIT antibody) in the pathogenesis of thrombotic episodes in patients on hemodialysis.

Heparin-induced thrombocytopenia (HIT) is a severe complication in patients on hemodialysis (HD). It has been reported that platelet factor-4 (PF-4)-heparin complex antibody (HIT antibody) plays an important role in the pathogenesis of this serious complication. In the present study, we investigated the role of HIT antibody in the pathogenesis of thrombotic complications including shunt failure, cerebrovascular disease (CVD) and atherosclerosis in patients on dialysis. Plasma concentration of HIT antibody in patients on HD was 0.143+/-0.008 (n=105). This was significantly higher in patients on continuous ambulatory peritoneal dialysis (CAPD: 0.087+/-0.006, p=0.0008, n=22) and in non-dialysis patients (0.113+/-0.011, p=0.0011, n=12). There was a significant negative correlation between HIT antibody and the duration of dialysis. However, no significant correlation was found between HIT antibody and other factors including age, dose of heparin, platelet count and hemoglobin. There was a significant correlation between the number of failed arteriovenous fistula and HIT antibody levels. In addition, in patients with a history of CVD, plasma concentrations of HIT antibody were significantly higher compared with patients without CVD (CVD(+): 0.200+/-0.029 vs. (-): 0.127+/-0.005, p<0.0001). It is possible that genetic factors may also play a role in the expression of HIT antibody. From these data, it appears possible that HIT antibody plays an important role in the pathogenesis of thrombosis in patients on HD. Further studies are needed to clarify the role of HIT antibody in the pathogenesis of thrombotic episodes in these patients.