ABSTRACT
This chapter describes the role of fibrinolysis in the pathogenesis of vascular and thromboembolic complications associated with diabetes mellitus. Thickening of the basement membrane, microthrombi, and vascular proliferation are the main pathological hallmarks of microangiopathy, which causes diabetic retinopathy, kidney disease, and polyneuropathy. The development of the atherosclerotic lesion is caused by multiple interacting factors, necessarily operative in each patient, and include disturbed lipid metabolism, release of mitogenic factors, endothelial cell damage leading to platelet hyperactivity, and disorders of the fibrin balance with persisting fibrin deposits. Endothelial cells produce a number of factors involved in the normal clotting and fibrinolysis mechanisms, such as prostacyclin, von Willebrand factor, tissue-type plasminogen activator, and plasminogen activator inhibitor. The mechanisms underlying the changes in coagulation factors taking place in diabetes are still uncertain. Endothelial fibrinolytic activity might be altered in diabetics by a different mechanism involving protein C.
