In humans cryoglobulinemic glomerulonephritis (CGGN) may develop in the course of systemic cryoglobulinemia (CG) and is often associated with hepatitis C virus infection. It is believed that the glomerular injury in CG results from the deposition of immune complexes, but exact sequence of events in this process is unknown. Experimental models of CGGN provide an important tool to study pathogenesis of this type injury. This review describes two mouse models of CGGN and their use in understanding the role of various molecules involved in regulation of inflammatory and fibrosis pathways, such as complement components, Fc receptors, growth factors, and others; as well as illustrates their role in testing novel approaches of treatment in this type of renal injury. (Folia Histochemica et Cytobiologica 2011; Vol. 49, No. 4, pp. 537-546).