VWF and Hypoalbuminemia: As a consequence, hypoalbuminemia resulted in the excessive production of TXA2 and endoperoxides, leading to platelet hyperreactivity.17 In addition, hypoalbuminemia also led to the compensatory synthesis of fibrinogen and von Willebrand factors (vWFs) in the liver, resulting in hyperfibrinogenemia that promoted platelet hyperreactivity (Figure 2B, top right).14 Hypercholesterolemia was one of the metabolic consequences of NS, which was confirmed as the promotor of platelet biogenesis and activation.