Sequential Studies of Glomerular Crescent Formation in Rabbits with Anti-Glomerular Basement Membrane(GBM) Antibody Induced Glomerulonephritis(GN).
- Author:
Hye Seon AHN
;
Jung Woo NOH
;
Moon Hyang PARK
- Publication Type:Original Article
- Keywords:
Anti-GBM antibody;
Crescent;
Glomerulonephritis;
Rabbit;
Histologic changes
- MeSH:
Animals;
Atrophy;
Bowman Capsule;
Capillaries;
Collagen;
Endothelial Cells;
Epithelial Cells;
Fibrin;
Fibroblasts;
Fibrosis;
Glomerulonephritis;
Guinea Pigs;
Immunoglobulin G;
Microscopy;
Myofibroblasts;
Rabbits*
- From:Korean Journal of Pathology
1997;31(3):219-232
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
To investigate the mechanism of crescent formation, sequential pathologic changes from the New Zealand White rabbits with anti-GBM antibody induced GN by administration of guinea pig anti-GBM IgG were studied by light (LM), immunofluorescent (IF) and electron (EM) microscopy. Although no glomerular changes were observed in LM, swelling of the endothelial cells and the epithelial cells were noted in EM by day 2. By day 7, early and cellular crescents were evident. Proteinaceous materials and fibrins were noted in the glomerular capillary lumina (GCL) and Bowman's space (BS) associated with segmental hypercellularity. The GBM damage became progressively severe, followed by focal detachment of the visceral epithelial cells from the GBM. At day 14, fibrin strands, mononuclear cells and collagen fibrils were present between the proliferating extracapillary cells. At day 31, fibrocellular crescents were predominated. Elongated spindle cells, morphologically resembling myofibroblasts, were noted near the Bowman's capsule (BC). A degree of tubular atrophy, interstitial fibrosis, and inflammatory infiltrates increased as it did with fibrous organization of crescent. Intense linear IF staining for IgG and C3 were seen throughout the experiments along the GBM. In conclusion, the progression of crescent from an early "proteinaceous" stage through cellular, fibrocellular and fibrous stages was well documented in this study. Inflammatory cells and coagulation mechanism may activate the initiation of the GBM damage at the early stage. Activated periglomerular mononuclear cells may also cause disruption of BC which facilitates entry of activated periglomerular cells and fibroblasts into BS leading to progressive fibrous crescent formation.
