title: Altered glomerular permeability in the early phase of immune complex nephritis.
abstract: We investigated the pathogenesis of increased glomerular permeability in Balb/c mice after 5 weeks of administration of a polyclonal B cell activator (bacterial lipopolysaccharide). The glomerular transfer of anionic ferritin across the capillary walls and the urinary excretion of serum albumin served as probes of glomerular permeability; anionic groups of the glomerular basement membrane were assessed by the binding of cationized ferritin, and glomeruli were studied by light, immunofluorescence, and electron microscopy. The mice developed circulating immune complexes, proteinuria, and a proliferative glomerulonephritis, with mesangial and capillary loop deposits of immunoreactants. Increased transfer of anionic ferritin molecules occurred across capillary walls with and without demonstrable electron-dense deposits; detachments of visceral epithelium were not seen, and epithelial transport of anionic ferritin was negligible. Loss of anionic groups was extensive in glomerular capillary loops with and without associated electron-dense deposits. The findings indicate that an increase in glomerular permeability may precede the deposition of immunoreactants in the capillary wall; that filtration of macromolecules can occur across capillary walls with or without demonstrable immune deposits; and that loss of anionic groups of the glomerular basement membrane and enhanced filtration of macromolecules can occur in the absence of focal detachments of the visceral epithelium.
mesh_terms: D000818:Animals; D005260:Female; D005921:Glomerulonephritis / Q000503:physiopathology*; D007105:Immune Complex Diseases / Q000503:physiopathology*; D007678:Kidney Glomerulus / Q000473:pathology / Q000503:physiopathology*; D051379:Mice; D008807:Mice, Inbred BALB C; D010539:Permeability; D011507:Proteinuria / Q000209:etiology