This paper reviews current concepts of glomerular immune injury of both inflammatory and
noninflammatory types. In noninflammatory lesions induced by antibody alone or C5b-9, the
glomerular epithelial cell appears to be the principal target of injury. Similar mechanisms are
probably operative in human diseases such as minimal change nephrotic syndrome and
membranous nephropathy. In inflammatory lesions, circulating effector cells including
neutrophils, macrophages, platelets, and probably lymphocytes as well as resident …