The kidney, particularly the glomerulus, is vulnerable to immune and inflammatory injury via a variety of humoral and cellular mechanisms. In lupus nephritis, both arms of the adaptive effector response, together with innate effectors, can be prominent participants. Furthermore, in systemic lupus erythematosus (SLE) there is reactivity to multiple autoantigens that can be planted in glomeruli, be deposited as components of circulating immune complexes, or be intrinsic to the glomerulus itself.

Other forms of autoimmune renal disease are characterised by autoimmunity to a more restricted range of autoantigens. Thus, examining effector mechanisms in autoimmune diseases such as myeloperoxidase anti-neutrophil associated glomerulonephritis (MPO-ANCA) associated nephritis and autoimmune anti-glomerular basement membrane (GBM) disease can take arguably a more reductionist approach compared to lupus nephritis.

Published and unpublished data in studies in experimental models of these forms of renal vasculitis will be discussed, focusing on the role of cell mediated responses and renal injury in these diseases. The potential relevance of these studies to SLE and lupus nephritis will be highlighted.