In vivo experiments (i.e., perfusion with MPO followed by nontoxic concentrations of hydrogen peroxide and chloride ions) revealed MPO-mediated glomerular disease resulting in glomerular morphologic changes, endothelial and mesangial cell injury, activation of platelets, and subsequent proliferative responses mimicking inflammatory and proliferative glomerulonephritis in humans [18]. This evidence concerns the gene MPO and proliferative glomerulonephritis.