mediators of inflammation (including complement, infiltrating leucocytes and cytokines), injure renal parenchyma and its networks. Inflammatory kidney injury results in the local release of kidney antigens via apoptosis and necrosis (Rovin & Parikh, 2014). These antigens, in combination with antigenpresenting dendritic cells, T cells and B cells are conditioned by intrarenal interferon-a (IFN-a) and other cytokines, which are likely to result in intrarenal creation of kidney-specific autoantibodies. This organ-specific autoimmunity may perpetuate kidney inflammation and cause future lupus nephritis flares. Therefore, treatment should focus on reducing inflammation of lupus nephritis and addressing organ-specific autoimmunity to prevent reactivation of lupus nephritis (Rovin & Parikh, 2014).