ANIMAL models have long served as an introduction to understanding the possible mechanisms responsible for human immune renal injury. Exploration of these models has refined and expanded our knowledge of the ways in which nephritogenic antigen and antibody interactions can lead to phlogogenic immune deposit formation, mediator activation, and relatively nonselective damage to surrounding renal structures, thereby producing pathophysiological changes.1,2 In addition, antibody reactions capable of inducing selective glomerular (or tubular) cell damage have been recently defined. Cellular immune reactions are clearly important in tubulointerstitial injury, and studies continue to define cellular immune contributions to glomerular injury. The humoral and cellular mediation pathways that magnify antibody-induced injury are increasingly defined, and the cells of the glomerulus itself are being investigated as contributors of phlogogenic mediator molecules.
The elucidation of the mechanisms of human immune renal injury, unfortunately, lags behind the understanding of the experimental models of both glomerulonephritis and
Curtis B. Wilson. Immune Aspects of Renal Diseases. JAMA. 1987;258(20):2957–2961. doi:10.1001/jama.1987.03400200163020