Prognoses for the next few years suggest a further increase in the number of patients requiring different forms of renal replacement selleck inhibitor therapy, including patients receiving haemodialysis, especially among patients with diabetes, arterial hypertension as well as the elderly ones [4].In recent years, the indications for treatment with oral anticoagulants (OACs) as well as their use have increased significantly [5]. This phenomenon included both the entire population of patients with CKD and patients receiving haemodialysis [6]. The continuously growing population of patients receiving haemodialysis as a result of the increasing prevalence of the aforementioned lifestyle diseases or social and demographic factors associated with them has an undoubted impact on this fact.

Attempts to find new applications for OACs in this group of patients are, however, not less important. Although they are based on a number of prospective, randomised studies in the general population, there are no such studies in the group of patients receiving haemodialysis [7]. Attempts to apply the results of studies carried out in the general population, from which patients with end-stage renal failure are usually excluded to begin with, to patients receiving haemodialysis are not only unjustified but sometimes have downright negative influence on the effectiveness of treatment and patients’ safety.2. Chronic Kidney Disease and Haemostasis DisordersAs renal failure progresses, increasingly significant disturbances occur in the process of blood coagulation.

At the initial stages of CKD, mostly as a result of disorders of the plasma coagulation system and fibrinolysis (e.g., decreased levels of protein C and antithrombin III, elevated concentrations of fibrinogen, von Willebrand factor, factor VIII, elevated concentration of plasminogen activator inhibitor-1 (PAI-1), decreased concentration of tissue plasminogen activator (t-PA)), prothrombotic processes, clinically expressed as hypercoagulation, dominate [8, 9]. As glomerular filtration rate (GFR) decreases and renal failure progresses, uraemic bleeding diathesis, characteristic of end-stage renal failure and patients during dialysis therapy, worsens. At the end stages of CKD, the accumulating uraemic toxins, both low-molecular-weight (e.g., urea, phenol and guanidinosuccinic acid) and medium-molecular-weight ones (e.g.

, RGD polypeptides), affect mostly platelet function, inhibiting their adhesion and aggregation and releasing platelet factors, such as serotonin or thromboxane A2 [10, 11]. These phenomena mostly lead to platelet haemostasis disorders. Uraemic toxins and proinflammatory cytokines, frequently co-occurring lipid disorders or arterial hypertension damage endothelium Carfilzomib and in this way disrupt also vascular haemostasis. As a result of their stimulation, endothelial cells produce large amounts of prostacyclin (PGI2) and nitric oxide (NO) [12].