The reviewed information implicates immune mechanisms in a variety of renal glomerular and tubulointerstitial diseases. Antibodies reactive with intrinsic structural or planted endogenous or exogenous antigens, and with circulating endogenous or exogenous antigens can initiate inflammatory capillary injury by localization in glomerular capillary tufts or along tubular basement membranes. This results in activation of mediator systems, including complement, neutrophils and other leukocytes, amines, peptides, and proteases, which result in vascular and tissue alterations. In some instances, nonimmune activation of complement (for instance, by the properdin system) and other mediators of vascular injury may be involved. A role of cellularly mediated immunologic injury in glomerular disease is not clear and remains the subject of considerable current research. More clearly, there is involvement of lymphocytes in tubulointerstitial and interstitial diseases as well as allograft rejection reactions. A rich armamentarium of in-vitro immunologic tests for specific antibodies, immune-complexes, serum complement levels, and renal tissue analysis provides opportunity for enhanced precision of diagnosis and monitoring progress of disease or treatment. Unfortunately, at the present time, there are not many effective therapies specific for most renal glomerular diseases; perhaps in the future better identification of offending environmental or host antigens will result in more effective prevention and treatment. Application of knowledge concerning renal glomerular diseases to the study of hypersensitivity induced tubulointerstitial injury has resulted in increasing understanding of the pathogenesis of interstitial inflammatory disease of the kidney.