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 TNF, favor glomerular thrombogenic properties through enhancement of
thromboplastin synthesis and of
plasminogen activator inhibitor PAI-1, and through decrease in
thrombomodulin activity. In some diseases, intraglomerular
fibrin formation appears to be favored by increased glomerular prothrombotic properties, for example: augmented
thromboplastin activity in immune
glomerulonephritides and in
Shwartzman phenomenon, excessive
thromboxane A2 synthesis, and decreased fibrinolytic activity in severe renal allograft rejection. In other diseases glomerular hemostasis appears to function homeostatically, for example, in
thrombin-induced
disseminated intravascular coagulation with enhancement of fibrinolytic 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.