ABSTRACT
Fibrinogen, von Willebrand factor (vWF), and their receptors, glycoprotein (GP) Ib and the GPIIb-IIIa complex, play a vital role in normal hemostasis, by initiating and mediating the formation of platelet thrombi at site of vascular injury (35). The activationdependent receptor function of the GPIIb-IIIa complex is defective in uremia, as shown by decreased binding of both vWF and fibrinogen to stimulated platelets (36). While the number of GPIIb-IIIa receptors expressed on the platelet membrane is normal, their activation is impaired. In contrast, the vWF binding to gpIb is normal. Removal of substances present in uremic plasma markedly improved the GPIIb-IIIa defect, suggesting that dialyzable toxic substances are probably a major component of the altered platelet function in uremia.
