Uremic toxins alter coagulation and fibrinolysis-related genes expression in human endothelial cells

Patients with chronic kidney disease (CKD) have an increased risk of thrombosis-related complications, such as venous thromboembolism [1]. These patients show prothrombotic state: increased blood tissue factor (TF) activity and elevated levels of fibrinogen or D-dimer [1,2]. However, the linkage between renal dysfunction and thrombogenicity remains unclear. The role of protein-bound uremic toxins (UTs) in cardiovascular complications is currently evaluated. In patients with CKD, thrombogenicity is associated with indolic uremic solutes, such as indoxyl sulfate (IS) and indole-3-acetic acid (IAA) [3,4].
Source: Thrombosis Research - Category: Hematology Authors: Tags: Letter to the Editors-in-Chief Source Type: research