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A model of in situ immune complex glomerulonephritis in the rat employing cationized ferritin.
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1980
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Glomerular DiseaseRenal PathologyImmunologyPathologyAnti-ferritin AntibodyPlanted AntigenInflammationGlomerulonephritisRenal FunctionElectron MicroscopyIga GlomerulonephritisAcute Kidney InjuryChronic Kidney DiseaseAutoimmune DiseaseLupus NephritisAutoimmunityRenal PathophysiologyUrologyGlomerulopathyMedicineNephrologyKidney Research
In the model described here the ability of cationized (basic) ferritin to bind to the glomerular basement membrane and act as a planted antigen was exploited. This planted antigen was accessible to circulating antibody resulting in in situ immune complex formation. Perfusion of cationized ferritin (isoelectric point greater than 9.5) directly into the renal arteries, followed by intravenous injection of anti-ferritin antibody resulted in induction of glomerulonephritis with heavy proteinuria lasting for about 3 weeks. Fine granular deposition of antigen, antibody and rat C3 along the glomerular capillary walls was seen by immunofluorescence. Electron microscopy revealed the presence of subepithelial deposits containing ferritin; the foot processes were fused. This demonstrates the potential role of basic antigens in the pathogenesis of in situ immune complex glomerulonephritis.