diffuse proliferative glomerulonephritis

DPGN results from subendothelial deposition of immune complexes (DNA-anti-DNA) that activate complement, leading to diffuse endocapillary and mesangial proliferation involving >50% of glomeruli. On light microscopy, glomeruli show a 'wire-loop' appearance due to thickened capillary walls from subendothelial deposits. Immunofluorescence reveals granular 'full-house' staining (IgG, IgA, IgM, C3, C1q). Electron microscopy shows subendothelial and mesangial electron-dense deposits, sometimes with tubuloreticular inclusions (suggestive of high interferon activity). Clinically, patients present with hematuria, red cell casts, proteinuria (often nephrotic-range), hypertension, and declining renal function—classic nephritic-nephrotic overlap syndrome. It is the most common and severe form of lupus nephritis (ISN/RPS Class IV), and can also rarely occur post-infectious (though PSGN is typically less diffuse and self-limited in children). Diagnosis is confirmed via renal biopsy given the aggressive nature; low complement (C3, C4) and elevated anti-dsDNA titers support active lupus nephritis. Treatment involves aggressive immunosuppression (corticosteroids plus cyclophosphamide or mycophenolate mofetil) to prevent progression to end-stage renal disease. Prognosis is guarded without treatment, with a significant risk of progressing to chronic kidney disease.