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Abstract: PO0945

Dysregulation of Fibrinolytic Process Contributes to the Thrombotic and Bleeding Complications in ESRD Patients

Session Information

Category: Dialysis

  • 701 Dialysis: Hemodialysis and Frequent Dialysis

Authors

  • Siddiqui, Fakiha, Loyola University Health System, Maywood, Illinois, United States
  • Bansal, Vinod K., Loyola University Health System, Maywood, Illinois, United States
  • Iqbal, Omer M., Loyola University Health System, Maywood, Illinois, United States
  • Bontekoe, Emily, Loyola University Health System, Maywood, Illinois, United States
  • Fareed, Jawed, Loyola University Health System, Maywood, Illinois, United States
Background

End stage renal disease (ESRD) is a complex syndrome involving both cellular and humoral mechanisms. Both thrombotic and bleeding complications are observed which may result in cardiovascular and cerebrovascular adverse outcomes. Fibrinolytic system placed an important role in the regulation of hemostatic process. A comprehenhesive profiling of the components of fibrinolytic process may provide additional understanding of the bleeding and thrombotic complications in ESRD.

Methods

Citrated whole blood samples were collected from a cohort of ESRD patients (n=95). Normal citrated plasmas were obtained from healthy male and female individuals. These samples were analyzed for prothrombin time (PT), activated partial thromboplastin time (aPTT), prothrombinase-induced clotting time (PiCT) and thrombin time (TT) using clot based technique. Fibrinolytic parameters such as urokinase type plasminogen acticator (uPA), plasminogen activator inhibitor-1 antigen (PAI-1A), and D-Dimer were measured by using ELISA method. Funtional PAI-1 was measured by using an amydolytic method. All results were compiled as group means ± SEM and respective ratios were calculated.

Results

All of the clotting results showed varying levels of elevated values in comparison to normal plasma. uPA levels showed wide variations and were increased (1.6 fold). D-Dimer was markedly increased in the ESRD patients (11.53 fold). Both functional (1.2 fold) and antigenic (3.07 fold) levels of PAI-1 were increased. Interestingly, the PAI-1 antigen levels was much higher in contrast to the functional levels suggesting a progressive consumption of this mediator.

Conclusion

These results suggest that the overall hemostatic system in ESRD patients is dysregulated due to the imbalance of the inhibitors such as PAI-1. The persistent activation of fibrinolysis is due to the increase production of uPA which facilitates endogenous fibrinolysis resulting in the elevation of D-Dimer. The generation of fibrinolytic enzymes results in increased fibrin/fibrinogen degradation products which may contribute to the observed intrinsic and extrinsic coagulation defects as measured by the elevation of PT and aPTT. Monitoring of fibrinolytic parameters along with clotting test may be helpful in the risk stratification and prediction of adverse outcomes in ESRD patients