Glomerular permeability: alteration in size- and charge-based barrier function in lupus nephritis.
To study alterations in glomerular permeability and their relation to immune deposits, anionic and cationic ferritins were systemically injected in immunosuppressed or untreated mice with lupus nephritis. Kidneys were studied by light, immunofluorescence and electron microscopy. In untreated mice with membranous and proliferative glomerulonephritis, ultrastructural analyses of tracer molecules in the capillary wall indicated that deposition of immune complexes (a) resulted in a focal, not generalized, alteration in the glomerular permeability properties; (b) induced disruption of size- and charge-based barriers at the vicinity of such immune deposits, and (c) induced leak of anionic protein, predominantly via residual slit pores, into the urinary space. When mice with immune complex disease were immunosuppressed with cyclophosphamide or methylprednisolone for 90 days, immune complexes were confined to the mesangium and glomerular structure and barrier (size- and charge-based) function were preserved.
D000818:Animals; D000936:Antigen-Antibody Complex / Q000032:analysis; D001485:Basement Membrane / Q000503:physiopathology*; D002199:Capillary Permeability; D003520:Cyclophosphamide / Q000494:pharmacology; D005260:Female; D005293:Ferritins / Q000494:pharmacology / Q000652:urine; D005921:Glomerulonephritis / Q000503:physiopathology / Q000652:urine; D007678:Kidney Glomerulus / Q000098:blood supply / Q000473:pathology / Q000503:physiopathology*; D008180:Lupus Erythematosus, Systemic / Q000503:physiopathology / Q000652:urine; D008775:Methylprednisolone / Q000494:pharmacology; D051379:Mice; D008814:Mice, Inbred NZB; D008854:Microscopy, Electron
D000936:Antigen-Antibody Complex; D003520:Cyclophosphamide; D005293:Ferritins; D008775:Methylprednisolone