Endothelial activation is central to the pathophysiology of glomerulonephritis, vasculitis, allograft rejection, ischemia-reperfusion injury and thrombotic angiopathies. Major advances in endothelial biology during the past year have emphasized the importance of selectin, mucin, integrin, and immunoglobulin-like adhesion molecules in leukocyte trafficking in glomerular inflammation, and have defined novel mechanisms by which leukocyte-endothelial cell interactions are regulated by inflammatory mediators and cytokines. These breakthroughs have already spawned experimental immunosuppressive strategies that should antecede the development of novel, potent and specific therapies for common renal diseases.