This review focuses on the role of two cytokines, platelet-derived growth factor and transforming growth factor-beta, in glomerular injury. The most recent in vitro and in vivo evidence for the role of platelet-derived growth factor and transforming growth factor-beta in glomerular hypercellularity and matrix expansion is summarized. In vitro studies utilizing cultured glomerular cells continue to provide valuable information as to the mechanism by which these cytokines result in glomerular injury. Upregulation of both cytokines and their receptors have been demonstrated during the course of experimental proliferative glomerulonephritis. Neutralization studies using specific antibodies in vivo established a causative role in glomerular pathology. Studies should be extended to humans and other animal models of renal disease. Practical approaches to modify biologic effects of cytokines in vivo should also be sought.