Importance of platelet aggregation in patients with end-stage renal disease

The exact etiology of the conflicting hemostatic disorder in the advanced stage of chronic renal disease, i.e. prothrombotic versus bleeding tendency, is not completely understood. Abnormal platelet function in patients with renal failure is not caused by high concentrations of urea, although the presence of fibrinogen fragments may prevent binding of normal fibrinogen and formation of platelet aggregates. Hemostatic abnormalities in end-stage kidney disease may be affected, to some extent, by the choice of renal replacement therapy. Patients on hemodialysis have an increased risk of thrombotic events, primarily due to the release of thromboxane A2 and adenosine diphosphate into the circulation, as well as platelet degranulation. Some activation of platelets occurs due to the exposure of blood to the roller pump segment, but microbubbles may also play a role. Renal transplantation is the treatment of choice for patients with end-stage renal disease. Immunosuppressive therapy is associated with an increased risk of thromboembolic complications. Additional research is required to identify the potential benefits of different immunosuppressive therapies in relation to platelet aggregation, keeping in mind the long- term need for immunosuppression in renal transplant patients.