New advances in understanding the treatment of glomerulonephritis.
Glomerulonephritis is the commonest cause of renal failure, yet there is little understanding as to its etiology except that immunological mechanisms are thought to be important. This has considerably hampered efforts to develop appropriate treatment. Only in rapidly progressive nephritis (RPGN) has clear progress been made as a result a radical improvement in prognosis obtained. In some forms of RPGN aberrant immunological mechanisms have been identified and their components characterized. The best defined are those in which auto-immune responses are generated and lead directly or indirectly to renal injury. As yet, only humoral auto-immune responses are easy to characterize in man; technical difficulties surround attempts to identify cellular auto-immune reactants. However, both can be investigated in animal experimental models. This presentation will focus on the more recent studies of the auto-immune responses in human RPGN and the possible contribution that these (together with those derived from animal studies) make towards a better understanding of the treatment of glomerulonephritis.
D001323:Autoantibodies / Q000032:analysis; D001324:Autoantigens / Q000276:immunology; D001327:Autoimmune Diseases / Q000276:immunology*; D001485:Basement Membrane / Q000276:immunology; D002851:Chromatography, High Pressure Liquid; D003593:Cytoplasm / Q000276:immunology; D005921:Glomerulonephritis / Q000276:immunology*; D014890:Granulomatosis with Polyangiitis / Q000276:immunology; D006801:Humans; D007677:Kidney Function Tests; D007678:Kidney Glomerulus / Q000276:immunology; D009504:Neutrophils / Q000276:immunology; D011863:Radioimmunoassay; D014657:Vasculitis / Q000276:immunology
D001323:Autoantibodies; D001324:Autoantigens