This study was designed to determine whether systemic amyloidosis is an additional risk factor for hemostatic abnormalities in hemodialysis patients and to evaluate local alterations of the hemostatic process within the patent-functional native arteriovenous fistula (AVF). Concentrations of in vivo molecular hemostatic markers, including prothrombin fragment(1+2) (PF 1.2), thrombin-antithrombin III complex (TAT) and plasmin-alpha(2)-antiplasmin complex (PAP) were determined in plasma samples taken simultaneously from AVFs and contralateral upper extremity large veins of hemodialysis patients associated with and without systemic amyloidosis. Seven amyloid (2 women, 5 men, aged 34 +/- 6 years), and 13 non-amyloid patients (4 women, 9 men, aged 36 +/- 7 years) on maintenance hemodialysis and 20 healthy volunteers (8 women, 12 men, aged 36 +/- 9 years) were in eluded in the study. Peripheral vein PF 1.2 and TAT levels showed no difference between amyloid and non-amyloid patient groups, but both were significantly higher than control group. PF 1.2 and TAT levels were also found to be elevated in fistulas when compared with that of peripheral vein in both amyloid and non-amyloid patient groups. Determination of PAP in peripheral veins of each group revealed significantly higher levels in amyloid hemodialysis patients than in non-amyloid patients and controls. PAP levels were significantly higher in fistulas of amyloid patients than in non-amyloid patients. In conclusion, this study confirms enhanced coagulation and fibrinolysis in hemodialysis patients and excessive fibrinolysis in amyloid patients with remarkable contribution of AVF on enhanced coagulation and fibrinolysis.