The rejection process refers primarily to the destruction of foreign tissues by host immune mechanisms. This process affects host lymphoid tissue profoundly and alters the migration patterns of lymphocytes in recipients of organ allografts [8]. It has been shown that specifically sensitized lymphocytes traffic both to and from the transplant [9, 10]. A considerable amount of knowledge has been gathered on the preferential migration pathways of lymphocytes through lymphoid and mucosa-associated lymphoid organs [1, 15]. The factors regulating lymphocyte migration through non-lymphoid tissue in normal conditions are not well known and even less well understood in the context of graft rejection. In this article we described for the first time migration in a recipient non-lymphoid organ (heart) and it's potentially harmful effects in causing parenchymal damage during renal allograft rejection in the rat model. These lesions were detected during the process of developing a model of chronic renal allograft rejection. The pathogenesis of these cardiac lesions is not fully understood but possible mechanisms include upregulation of homing receptors/adhesion molecules, breakdown of peripheral tolerance and involvement of cross-reacting anti-endothelial antibodies.