SLE is characterized by an accumulation of apoptotic material due to its poor clearance (9) (i). This leads to an immune response against chromatin (ii) and to increased expression and binding of apoptotic-chromatin antigens to kidney glomerular structures (iii). Antibodies against apoptotic-chromatin antigens (in particular anti-dsDNA and anti-nucleosome antibodies) may form immune complexes in the kidney with their specific planted antigens or may be entrapped on glomerular structures as immune complexes preformed in the circulation (iv). Immune complex deposition/formation eventually leads to immune-mediated tissue inflammation and damage (v). Local factors may also increase the susceptibility of renal tissue to damage (vi): Chromatin antigens may accumulate in the kidney tissue because of reduced DNAse-mediated chromatin degradation (11), and immune-mediated inflammation may itself increase vessel permeability, consequently increasing diffusion of the autoantigens themselves and of the soluble and cellular mediators of the autoimmune response. In this context, the lack of the potentially protective effect of kinins may represent an additional mechanism contributing to renal tissue damage. Ag, antigen.