Immune complex-induced defects in glomerular basement membrane charge can be "repaired" despite continuing glomerular disease.
There have been conflicting reports over whether or not glomerular immune complex deposits cause proteinuria by neutralizing the glomerular basement membrane anionic charge. We investigated whether the reported discrepancies could arise as a result of repair of the charge layer, in the face of continuing antigen deposition, and how rapidly this repair could be effected. We used a chronic serum sickness model of glomerulonephritis which consistently produces a nephrotic syndrome stable over 8 weeks. Charge distribution was demonstrated by the polyethyleneimine (PEI) method. Subepithelial electron dense deposits were associated with defects in the charge layer of the lamina rara externa at 2 and 4 weeks, but at 8 weeks many of the deposits had become surrounded by a new charge layer. This finding is of relevance to the interpretation of similar studies on human material.
D000818:Animals; D001485:Basement Membrane / Q000648:ultrastructure*; D005921:Glomerulonephritis / Q000473:pathology*; D007105:Immune Complex Diseases / Q000473:pathology*; D007678:Kidney Glomerulus / Q000648:ultrastructure; D008297:Male; D008854:Microscopy, Electron; D009404:Nephrotic Syndrome / Q000473:pathology; D011094:Polyethyleneimine; D051381:Rats; D011919:Rats, Inbred Strains; D013997:Time Factors
D011094:Polyethyleneimine