Rejection of renal allografts in man and animals is most frequently induced by cell-mediated immunity, the morphologic hallmark of which is the infiltration of the graft by mononuclear cells. In some presensitized recipients rejection may be mediated by humoral transplantation antibodies, and this is characterized clinically by a rapid tempo of rejection and morphologically by accumulation of polymorphonuclear neutrophils and renal cortical necrosis. In recipients treated with immunosuppressive drugs, most renal allografts function well for over 1 yr. However, late deterioration is observed in many grafts. This may take the form of proliferative glomerulonephritis with accumulation of immunoglobulin and complement along glomerular basement membranes. This glomerular lesion of the graft may be of immunologic nature without being rejection. In many instances the glomerular lesion may be due to recurrence of the original disease of the recipient. In other instances it may represent a de novo immunologic process induced by the response to antigens shared by the graft and recipient as evidenced by animal experiments. The glomerular lesion in the graft may also be caused by humoral transplantation antibodies. Therefore, the final outcome of the renal transplantation may to a great extent depend on the strength of transplantation antibody response, being more favorable for low than high responders.