Lupus Nephritis • • Varying presentations Immune complex formations e.g. Anti-dsDNA o These deposits in the mesangium and subendothelial space are proximal to the GBM and are therefore in communication with the vascular space o Complement activation (classical pathway) and generation of chemoattractants C3a and C5a results in the influx of neutrophils and mononuclear cells o Deposits in the subendothelial space also activate complement but cannot attract inflammatory cells because there is no access to the blood o Injury is limited to glomerular epithelium  proteinuria • Immune complex deposition o Upregulation and activation of adhesion molecules on endothelium that recruits proinflammatory leukocytes that initiate autoimmune injury o Activated glomerular cells, infiltrating macrophages and T cells produce inflammatory cytokines  E.g. TNF, IL-6, IFN, PDGF  This extends renal injury Classification of Lupus Nephritis • Class I: minimal mesangial o Minimal proteinuria, normal creatinine • Class II: mesangial proliferative o Microscopic haematuria and proteinuria • Class III: focal lupus o Haematuria, proteinuria, some HT • Class IV: diffuse lupus o Haematuria and proteinuria (most severe) • Class V: membranous lupus o Nephrotic syndrome • Class VI: advanced sclerosing lupus o Proteinuria, bland urine Treatment of lupus is guided by classification. Class IV has the best treatment response.