In summary, evidence exists that immunologically mediated renal diseases can be modulated by interfering with the mechanism of production of autoantibodies by specific antiidiotypic immunity. However, more studies are necessary to establish efficient and safe parameters from which to suggest such treatment in human immune nephritides. Although the evidence is still circumstantial, it is necessary to keep in mind that antiidiotypic antibodies may also add to glomerular immune deposits and potentially could contribute to the chronicity of some forms of immunologic nephritis. The fate of the majority of immunologic nephritides is a slow progression toward end-stage renal insufficiency. Although in most cases the etiology remains to be determined, it is generally felt that a better understanding of the initial immune dysregulation may lead to a greater possibility of control and cure. In this perspective, new directions of research, such as the one reviewed here, should be considered. Modulation of the damaging autoimmune responses in SLE or Goodpasture's Syndrome might be possible. For instance, the identification of a cross-reacting idiotype among anti-GBM antibodies would be the first step for a possible future use of natural or synthetic idiotypes for autovaccination purposes. Antiidiotype antibodies, particularly in the form of monoclonal chimaeric (mouse/human) hybridomas, could be utilized for passive immunosuppression, particularly in combination with plasmapheresis, with or without conventional immunosuppressive drugs. Clearly, this is part of a long-term process that may or may not be realized. The success of new forms of specific immunologic treatment for kidney diseases may ultimately depend upon ongoing efforts in the study of the new molecular aspects of regulation of potential nephritogenic immune responses.