Lupus nephritis is a serious organ-threatening manifestation of systemic lupus erythematosus (SLE) in which autoantibodies, particularly anti-double-stranded DNA (anti-dsDNA) antibodies, form immune complexes that deposit in the glomeruli and trigger complement activation, inflammation, and progressive kidney damage. SLE is a chronic autoimmune disease in which the immune system loses tolerance to self-antigens, producing autoantibodies against nuclear components (antinuclear antibodies or ANA). The most pathogenic autoantibodies in lupus nephritis are anti-dsDNA antibodies, which bind to DNA released from apoptotic cells, forming circulating immune complexes. These complexes deposit in different locations within the glomerulus depending on their size and charge: mesangial deposits (mild disease, Class I-II), subendothelial deposits (proliferative disease, Class III-IV, the most severe forms), and subepithelial deposits (membranous disease, Class V). Once deposited, immune complexes activate the classical complement pathway (C1q, C4, C2, C3), recruiting inflammatory cells and generating the membrane attack complex (C5b-9) that directly damages podocytes and the glomerular basement membrane. This complement consumption is why serum C3 and C4 levels fall during active nephritis -- they are being consumed faster than the liver can produce them. Class...