Acute glomemlonephritis can cause acute renal failure. Activated neutrophils and monocytes are major eflectors of glomerulonephritic renal failure. Adhesion molecules, granule enzymes, reactive oxygen radicals, lipid metabolites, and cytokines of activated neutrophils and monocytes mediate glomerular capillary constriction, occlusion, and destruction. Injurious products and biologically active mediators released by activated leukocytes have profound fictional eflects on mesangial cells and endothelial cells, which in turn participate in the disturbance of glomerularfinc-tion, for example, by altering capillary diameter and surface area. f i e glomerular injlammatory events result in decreased glomerular capillary ultrajiltraton coefl-cient and glomerular jiltration rate, as well as other functional perturbations.