Impaired platelet function plays a central role in the pathogenesis of
uremic bleeding tendency. Platelet membrane glycoproteins are fundame
ntal for normal platelet function. Their role for normal platelet phys
iology and pathophysiology of uremic platelet dysfunction is discussed
. Platelet from patients with end-stage renal failure have a defective
receptor function of the glycoprotein IIb-IIIa complex. This results
in defective fibrinogen binding to the platelet surface and consequent
ly in impaired platelet aggregation. Moreover, the role of von Willebr
and Factor-GPIb interaction in uremic bleeding tendency is discussed.
Uremic platelets also show a quantitative and qualitative defect of th
e alpha-granule glycoprotein thrombospondin which may impair consolida
tion of the platelet plug at the site of vascular injury.