Systemic Lupus Erythematosus Advanced

Systemic lupus erythematosus (SLE) is a chronic multisystem autoimmune disease characterized by production of pathogenic autoantibodies against nuclear antigens, immune complex deposition in tissues, and complement activation leading to inflammation and organ damage. The pathogenesis involves loss of immune tolerance to self-antigens: defective clearance of apoptotic cells exposes nuclear antigens (dsDNA, histones, Sm, RNP), which are processed by dendritic cells and presented to autoreactive T and B lymphocytes. Activated B cells produce autoantibodies — particularly anti-dsDNA antibodies — that form immune complexes with their target antigens. These immune complexes deposit in blood vessel walls, glomeruli, skin, joints, and serosal surfaces, activating the complement cascade (C3, C4 consumption) and recruiting inflammatory cells. Lupus nephritis (the most serious common manifestation) results from immune complex deposition in the glomerulus, classified by ISN/RPS classes I-VI based on biopsy pattern. Class III (focal proliferative) and Class IV (diffuse proliferative) are the most aggressive and require immunosuppressive therapy with mycophenolate mofetil or cyclophosphamide induction followed by maintenance therapy. The NP must understand that SLE is characterized by periods of flare and remission, involves virtually any organ...