Glomerular fibrin deposits may occur within vessels or in extracapillary crescents. Studies suggest that intravascular thrombosis is promoted by endothelial cell activation/injury, resulting in the release of endothelial-cell-derived tissue factor procoagulant, fibrinolytic inhibitors, platelet activating factor, and large multimers of von Willebrand factor. Fibrin in crescents may arise from coagulation of plasma in Bowman's space mediated by the release of tissue factor from infiltrating macrophages. Glomerular fibrin may be removed by fibrinolytic or phagocytic mechanisms or persist and lead to glomerular obsolescence. Suppression or elimination of factors that promote glomerular fibrin deposition and enhancement of mechanisms that remove glomerular fibrin may be important in the recovery from several forms of human kidney disease.