Glomerular fibrin deposition is a common histopathological finding in a variety of glomerular diseases and suggests the intraglomerular activation of the coagulation system. The activation of thrombin is the last step in the coagulation cascade. On the basis of its ability to modulate several cell functions through the activation of different receptors and intracellular-signaling pathways, thrombin could be considered as a growth factor more than as a simple coagulation factor. Indeed, this multifunctional serine protease may represent the link between the activation of the coagulation cascade and the inflammatory and profibrotic response at the glomerular level. This review will focus on the potential role of thrombin in the pathogenesis of glomerular damage and on the mechanisms underlying the cellular effects of this serine protease.