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.
Točna etiologija proturječnih hemostatskih poremećaja u terminalnom stadiju bubrežne bolesti, tj. tromboze i sklonosti krvarenju, nije u potpunosti razjašnjena. Poremećena funkcija trombocita u bolesnika s bubrežnim zatajenjem nije uzrokovana povišenom koncentracijom ureje, premda prisutnost fragmenata fibrinogena može spriječiti vezivanje normalnog fibrinogena, odnosno stvaranje agregata tromobocita. Na poremećaj hemostaze kod bolesnika s bubrežnim zatajenjem može utjecati i izbor nadomjesnog bubrežnog liječenja. Bolesnici na hemodijalizi imaju povećani rizik tromboze prvenstveno zbog oslobađanja tromboksana A2 i ADP -a u cirkulaciju, kao i zbog degranulacije trombocita. U stanovitoj mjeri trombociti se aktiviraju i prolaskom krvi kroz sustav crpki, dok moguću ulogu imaju i mikromjehurići. Transplantacija bubrega je metoda izbora u liječenju bolesnika s bubrežnim zatajenjem. Imunosupresivna terapija je povezana s povećanim rizikom razvoja trombembolijskih komplikacija. Imajući u vidu dugotrajnu potrebu za imunosupresivnim liječenjem kod bolesnika s transplantiranim bubregom potrebna su daljnja istraživanja radi utvrđivanja mogućeg povoljnog učinka različitih imunosupresiva u odnosu na agregaciju trombocita.