Macrophages convert proinflammatory or anti-inflammatory signals of tissue microenvironments into response mechanisms. These response mechanisms largely derive from evolutionary conserved defense programs of innate host defense, wound healing, and tissue homeostasis. Hence, in many settings these programs lead to renal inflammation and tissue remodeling (ie, glomerulonephritis and sclerosis or interstitial nephritis and fibrosis). There is abundant experimental evidence that blocking macrophage recruitment or macrophage activation can ameliorate renal inflammation and fibrosis. In this review we discuss experimental tools to target renal macrophage recruitment by using antagonists against selectins, chemokines, integrins, or other important cytokines that mediate renal injury via macrophage recruitment, some of these already having been used in clinical trials.