scholarly journals Immunohistochemical characterization of glomerular inflammatory cells and expression of adhesion molecules in anti-glomerular basement membrane (anti-GBM) glomerulonephritis induced in WKY rats with monoclonal anti-GBM antibodies of different subclasses

2006 ◽  
Vol 56 (2) ◽  
pp. 55-61 ◽  
Author(s):  
Tadashi Kado ◽  
Takayuki Kohda ◽  
Shinichi Okada ◽  
Atsushi Hayashi ◽  
Yasushi Utsunomiya ◽  
...  
Keyword(s):  
Basement Membrane ◽  
Adhesion Molecules ◽  
Glomerular Basement Membrane ◽  
Inflammatory Cells ◽  
Wky Rats

scholarly journals Differentiating Glomerular Inflammation from Fibrosis in a Bone Marrow Chimera for Rat Anti-Glomerular Basement Membrane Glomerulonephritis

2015 ◽  
Vol 42 (1) ◽  
pp. 42-53
Author(s):  
Cindy Zhou ◽  
Kristie Lou ◽  
Kiana Tatum ◽  
Jeremiah Funk ◽  
Jean Wu ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Basement Membrane ◽  
Glomerular Basement Membrane ◽  
Critical Role ◽  
Inflammatory Cells ◽  
Wky Rats ◽  
Persistent Inflammation ◽  
Fibrotic Process ◽  
Wistar Kyoto ◽  
End Stage

Background: Many types of glomerulonephritis (GN) undergo tandem connected phases: inflammation and fibrosis. Fibrosis in human GNs leads to irreversible end-stage disease. This study investigated how these 2 phases were controlled. Methods: Using a rat anti-glomerular basement membrane GN model, we established bone marrow (BM) chimeras between GN-resistant Lewis (LEW) and GN-susceptible Wistar Kyoto (WKY) rats. Glomerular inflammation and fibrosis were compared between chimeras. Results: LEW's BM to WKY chimeras with or without co-transfer of host WKY's T cells were GN-resistant. On the other hand, WKY's BM to LEW (LEWWKY) chimeras developed glomerular inflammation and albuminuria upon immunization. Quantitative analysis showed that the number and composition of inflammatory cells in glomeruli of immunized LEWWKY chimeras were similar to those in immunized WKY rats at their inflammatory peak. Thus, glomerular inflammation was controlled by BM-derived non-T cell populations. However, unlike WKY rats, LEWWKY rats did not develop fibrosis until the end of experiments (84 days) in spite of persistent inflammation and albuminuria. Conclusion: Inflammation alone was not sufficient to trigger fibrosis, suggesting a critical role of glomerular cells in the fibrotic process. As LEWWKY chimera allows us to separate glomerular inflammation from fibrosis, this model provides a useful tool to study how fibrosis is initiated following inflammation.

Ovine Mesangiocapillary Glomerulonephritis Type I and Crescent Formation

1990 ◽  
Vol 27 (1) ◽  
pp. 26-34 ◽  
Author(s):  
P. F. Frelier ◽  
D. L. Armstrong ◽  
J. Pritchard
Keyword(s):  
Basement Membrane ◽  
Glomerular Basement Membrane ◽  
Inflammatory Cells ◽  
Suitable Model ◽  
Type I ◽  
Human Beings ◽  
Crescent Formation ◽  
Mesangiocapillary Glomerulonephritis ◽  
Bowman's Capsule

Morphologic examination of four Finnish Landrace mixed-breed lambs, 27 to 35 days of age, affected with mesangiocapillary glomerulonephritis type 1, demonstrated a progressive glomerulonephritis. By 27 days of age, three lambs had crescents in 58 to 93% of glomeruli. These three lambs were also uremic. The accelerated rate of crescent formation was attributed to infiltrating polymorphonuclear leukocytes and monocytes, the result of discontinuities (gaps) in the glomerular basement membrane, and to the loss of the integrity of Bowman's capsule. In the three lambs, platelets were identified adjacent to the endothelium or denuded glomerular basement membrane. Two distinctly different types of crescents were noted, apparently dependent on the integrity of Bowman's capsule. One type resulted from the influx of inflammatory cells and dissociation of parietal epithelial cells from Bowman's capsule. The other type was more extensive and contained collagen and was associated with damage to Bowman's capsule resulting in cellular infiltration from the interstitium and sclerosis. Based on morphologic similarities, ovine mesangiocapillary glomerulonephritis is a suitable model for studying the pathogenesis and treatment of mesangiocapillary glomerulonephritis type 1 in human beings.

Isolation and characterization of nephritogenic antigen from bovine glomerular basement membrane

1984 ◽  
Vol 798 (1) ◽  
pp. 96-102 ◽  
Author(s):  
Yoshikazu Sado ◽  
Kiyohiro Watanabe ◽  
Tohru Okigaki ◽  
Haruo Takamiya ◽  
Satimaru Seno
Keyword(s):  
Basement Membrane ◽  
Glomerular Basement Membrane ◽  
Isolation And Characterization

scholarly journals Mesangiocapillary glomerulonephritis.

1992 ◽  
Vol 2 (10) ◽  
pp. S159
Author(s):  
G D'Amico ◽  
F Ferrario
Keyword(s):  
Basement Membrane ◽  
Glomerular Basement Membrane ◽  
Inflammatory Cells ◽  
Type I ◽  
Mesangiocapillary Glomerulonephritis ◽  
Dense Deposits ◽  
Table Analysis ◽  
System Activation ◽  
Morphological Variants

The clinical and histological features of idiopathic mesangiocapillary glomerulonephritis (MCGN) have been reviewed, with a survey of the most recent literature, including the retrospective analysis of the data of the Italian Study Group of Renal Immunopathology on 368 patients. In both major types of MCGN, six morphological variants have been characterized (classical MCGN, nodular MCGN, exudative MCGN, focal segmental MCGN, MCGN with massive deposits, and crescentic MCGN) that have different etiologic, pathogenetic, or clinical outcome correlates. Actuarial renal survival 10 yr after renal biopsy has been calculated with life-table analysis to be 60 to 65% in type I MCGN, without significant differences between treated and untreated patients; none of the therapeutic regimens tested up to now for this disease have been independently demonstrated to be efficacious. As for the pathogenesis, the interrelationships between the three mechanisms that contribute to the development of the morphological features of the disease (accumulation of electron-dense deposits on the subendothelial side of the glomerular basement membrane or within the glomerular basement membrane; mesangial proliferation and peripheral interposition; and inflow of inflammatory cells, mainly monocytes) have been discussed, and the role of hypocomplementemia and circulating nephritic factors (NFa and NFt) has been analyzed. Available evidence suggests that MCGN is an immunocomplex-mediated disease, the deposition of immune deposits being the initiating phenomenon, whereas the morphologic changes and complement system activation are secondary events.

Mechanisms of glomerular injury

2015 ◽  
Author(s):  
Neil Turner
Keyword(s):  
Basement Membrane ◽  
Glomerular Basement Membrane ◽  
Inflammatory Diseases ◽  
Calcineurin Inhibitors ◽  
Inflammatory Cells ◽  
Renal Diseases ◽  
Direct Effects ◽  
Glomerular Injury ◽  
Wide Range

Proteinuric diseases, historically termed ‘nephrosis’, are characterized by subtle abnormalities in podocytes or by abnormal glomerular matrix, including the scarring laid down by inflammatory diseases. Angiotensin blockers, corticosteroids, calcineurin inhibitors, and a wide range of other drugs known or believed to be effective in different renal diseases, appear to have direct effects on podocytes that reduce proteinuria that may be important to their effectiveness. Several of these have previously been assumed to work via haemodynamic, immune or other modes. Haematuric diseases are characterized by inflammatory disruption of the glomerular basement membrane (GBM) (‘nephritis’), or less commonly by fragile GBM without inflammation. The majority of haematuric conditions are slowly or rapidly destructive diseases associated with infiltration of inflammatory cells, and proliferation of endogenous cells of the glomerulus, probably in attempts at repair. With time, many haematuric diseases are associated with the development of proteinuria, possibly as a consequence of scarring and its effects on podocyte function.

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