Glomeruli possess a complex hemostasis system with prothrombotic (procoagulant, antifibrinolytic) and antithrombotic (anticoagulant, fibrinolytic) properties that can act locally on platelet adhesion or aggregation, on plasmatic coagulation pathways, and on fibrinolysis. In vitro, inflammatory mediators, such as XVF, favor glomerular thrombogenic properties through enhancement of thromboplastin synthesis and of plasminogen activator inhibitor PAI-1, and through decrease in thrombomdulin ac-tivity. In some diseases, intraglomerular Jibrin formation appears to be favored by increased glomerular prothrombotic properties, for example: augmented thromboplnstin activity in immune glomerulonephritides and in Shwartzman phenomenon, excessive thromboxane A2 synthesis, and decreased fibrinolytic activity in severe renal allografr rejection. In other diseases glomerular hemostasis appears to function homeostatically, for example, in thrombin-induced disseminated intravascular coagulation with enhancement offibrinolytic activity favoring fibrin dissolution. Novel methods allowing the study of glomerular hemostatic activities in renal biopsy fragments should help to understand the mechanisms of fibrin deposition in human diseases and to treat it on a logical basis.