Recent studies using experimental models of glomerular disease have not only elucidated the pathophysiologic basis of glomerular disease, but have also identified potential new treatments. In this review, we will provide examples of how cytokines and cytokine antagonists may be used in the future treatment of glomerular disease. Treatments will be presented for each of the pathophysiologic phases of disease, beginning with the etiology, the development of a nephritogenic immune response, the mechanisms by which glomerular injury occurs, the response of the glomerulus to injury that results in cell proliferation and matrix expansion, and the factors that lead to healing or scarring. Special emphasis is placed on the cytokines interleukin 1 beta and tumor necrosis factor alpha, which are proinflammatory cytokines that potentiate neutrophil-and monocyte-mediated glomerular injury, and on the growth factors platelet-derived growth factor and transforming growth factor beta, which are involved in cell proliferation and matrix expansion that occur as glomerular cells respond to injury. The identification of the specific mediators involved in glomerular disease should provide new therapies that are more specific and less toxic than current conventional immunosuppressive regimens.