The mechanisms of leukocyte entry into the kidney during inflammatory renal disease have recently received considerable attention. Chemotactic factors appear to play a central role in this process, not only by inducing leukocyte movement but also by enhancing endothelial and leukocyte adhesiveness and endothelial permeability. The evidence supporting the role of chemotactic factors in renal inflammation comes from three types of studies. (1) Cell culture studies have shown that renal parenchymal cells produce chemotactic factors in response to proinflammatory stimuli. (2) Immunohistochemical and in situ hybridization analyses of renal tissue from patients or experimental animals have demonstrated local renal expression of chemotactic factors in association with inflammatory disease. (3) Experiments designed to neutralize the chemoattractant activity of specific chemotactic factors in leukocyte-dependent models of renal injury have shown an attenuation of inflammatory infiltrates and a decrease in indices of renal damage. In this article, these data are reviewed for complement-derived chemotactic factors, the leukocyte-specific chemokines, and the interstitial chemoattractant osteopontin, and the possibilities of therapeutic interventions based on abrogating chemoattractant expression or function in human renal disease are considered.