scholarly journals N-Acetyl-Seryl-Aspartyl-Lysyl-Proline Ameliorates the Progression of Renal Dysfunction and Fibrosis in WKY Rats with Established Anti–Glomerular Basement Membrane Nephritis

2006 ◽  
Vol 17 (3) ◽  
pp. 674-685 ◽  
Author(s):  
Mitsugu Omata ◽  
Hajime Taniguchi ◽  
Daisuke Koya ◽  
Keizo Kanasaki ◽  
Rumiko Sho ◽  
...  
Keyword(s):  
Basement Membrane ◽  
Renal Dysfunction ◽  
Glomerular Basement Membrane ◽  
Wky Rats

scholarly journals Myeloproliferative neoplasm related nephropathy

2021 ◽  
Vol 6 (4) ◽  
pp. 331-333
Author(s):  
Biji K Aravind ◽  
Dhanya P G ◽  
Jojo Pullockara ◽  
Deepak Charles
Keyword(s):  
Basement Membrane ◽  
Renal Dysfunction ◽  
Focal Segmental Glomerulosclerosis ◽  
Glomerular Basement Membrane ◽  
Kidney Biopsy ◽  
Myeloproliferative Neoplasm ◽  
Primary Myelofibrosis ◽  
Review Of The Literature ◽  
Detailed Review ◽  
Marrow Space

Primary Myelofibrosis associated Nephropathy is a recently described entity. Primary Myelofibrosis (PMF) is a Myeloproliferative Neoplasm (MPN) where the marrow space shows fibrosis with megakaryocyte dysplasia. We present a case of a 32 year old patient who was detected to have proteinuria, renal dysfunction and anemia ,on a routine health check up. Primary Myelofibrosis was confirmed by positive Jak 2 expression. Kidney biopsy showed focal segmental glomerulosclerosis along with thickened glomerular basement membrane. The histomorphological features of renal and bonemarrow biopsies are analysed and a detailed review of the literature is done.

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.

scholarly journals A Possible Clue for the Production of Anti-Glomerular Basement Membrane Antibody Associated with Ureteral Obstruction and Hydronephrosis

2015 ◽  
Vol 5 (1) ◽  
pp. 87-95
Author(s):  
Yasuo Takeuchi ◽  
Emiko Takeuchi ◽  
Kouju Kamata
Keyword(s):  
Risk Factors ◽  
Basement Membrane ◽  
Renal Dysfunction ◽  
Glomerular Basement Membrane ◽  
Ureteral Obstruction ◽  
Rapidly Progressive Glomerulonephritis ◽  
Urinary Sediment ◽  
Biopsy Specimens ◽  
History Of ◽  
Medical Histories

Background: Anti-glomerular basement membrane (anti-GBM) antibody-mediated glomerulonephritis (anti-GBM GN) is an autoimmune disease with rapidly progressive glomerulonephritis. Based on a case report of anti-GBM GN following hydronephrosis, we hypothesized that hydronephrosis may act as a trigger for the development of anti-GBM antibodies. Patients and Methods: We evaluated 11 patients who were diagnosed with hydronephrosis. It was measured with serum anti-GBM antibody. These patients' medical histories as well as risk factors for the development of anti-GBM antibodies and causes of hydronephrosis were reviewed. Renal function and hematuria were also considered. The serum anti-GBM antibody was measured with enzyme-linked immunosorbent assays (ELISA) or chemiluminescent enzyme immunoassays (CLEIA). Histopathological findings of renal biopsy specimens were also evaluated. Results: No patient had a medical history of renal disease. Five patients had a history of smoking. Ten of the 11 patients had renal dysfunction as evidenced by serum creatinine levels of 0.85-13.8 mg/dl, while 8 patients had RBCs in their urinary sediment at the time of diagnosis for hydronephrosis. Two of the patients assessed by ELISA and CLEIA were positive for anti-GBM antibodies. In 1 of these 3 patients, anti-GBM antibodies and renal dysfunction improved upon treatment for hydronephrosis. Another of the 3 patients developed anti-GBM GN, but anti-GBM antibodies and renal dysfunction improved dramatically upon treatment. In the 3rd patient without improved hydronephrosis, anti-GBM antibodies and renal dysfunction remained unchanged. Conclusion: Our results provide insights into the development of anti-GBM antibodies in patients with ureteral obstruction and hydronephrosis.

scholarly journals Suppression of anti-glomerular basement membrane nephritis by administration of anti-monocyte chemoattractant protein-1 antibody in WKY rats.

1997 ◽  
Vol 8 (7) ◽  
pp. 1174-1178
Author(s):  
H Fujinaka ◽  
T Yamamoto ◽  
M Takeya ◽  
L Feng ◽  
K Kawasaki ◽  
...  
Keyword(s):  
Basement Membrane ◽  
Cross Section ◽  
Glomerular Basement Membrane ◽  
Suppressive Effect ◽  
Glomerular Injury ◽  
Crescent Formation ◽  
Monocyte Chemoattractant Protein 1 ◽  
Monocyte Chemoattractant ◽  
Monocyte Chemoattractant Protein ◽  
Wky Rats

Anti-glomerular basement membrane (GBM) nephritis in WKY rats is characterized by an accumulation of CD8-positive lymphocytes (CD8+ lym) and monocytes/macrophages (Mo/M psi) in the glomeruli and crescent formation. In the study presented here, the involvement of a chemokine for Mo/M psi, monocyte chemoattractant protein-1 (MCP-1), was examined in this model. An intense induction of mRNA for MCP-1 in the glomeruli and a suppressive effect of anti-MCP-1 antibody administration on the glomerular Mo/M psi accumulation and proteinuria were found. MCP-1 mRNA was expressed intensely in the glomeruli 4 d after the anti-GBM antibody injection. When MCP-1 was neutralized with anti-MCP-1 antibody administration, the number of Mo/M psi infiltrating in the glomeruli decreased by 34.7% (19.6 +/- 7.1 versus 30.0 +/- 6.0 per glomerular cross-section, P < 0.01) and proteinuria by 66.2% (15.6 +/- 9.3 versus 46.1 +/- 15.1 mg/d, P < 0.01) at day 4. In contrast, the number of CD8+ lym accumulating in the glomeruli was not affected significantly (6.6 +/- 2.7 versus 6.0 +/- 3.0 per glomerular cross-section, P > 0.05). However, the treatment with the anti-MCP-1 antibody did not reduce Mo/M psi infiltration, urinary protein excretion, and crescent formation at day 8. These data suggest that MCP-1 plays a role in the glomerular accumulation of Mo/M psi, and that the infiltrating Mo/M psi cause glomerular injury and increased excretion of protein in the urine.

Implication of the complement system in the induction of anti-glomerular basement membrane glomerulonephritis in WKY rats

2003 ◽  
Vol 53 (11) ◽  
pp. 757-761 ◽  
Author(s):  
Tatsuhiko Shike ◽  
Masato Isome ◽  
Masashi Mizuno ◽  
Junzo Suzuki ◽  
Seiichi Matsuo ◽  
...  
Keyword(s):  
Basement Membrane ◽  
Glomerular Basement Membrane ◽  
Complement System ◽  
Wky Rats ◽  
The Complement System

Electron microscopic radioautographic studies on the incorporation of 3H proline in the glomerular basement membrane (GBM) in antistreptococcal-cell-membrane (SCM) injected mice

1984 ◽  
Vol 42 ◽  
pp. 188-189
Author(s):  
R.P. Nayyar ◽  
C.F. Lange ◽  
J. L. Borke
Keyword(s):  
Body Weight ◽  
Cell Membrane ◽  
Basement Membrane ◽  
Glomerular Basement Membrane ◽  
Mesangial Matrix ◽  
Electron Microscopic ◽  
Group A ◽  
Injection Protocol

Streptococcal cell membrane (SCM) antiserum injected mice show a significant thickening of glomerular basement membrane (GBM) and an increase in mesangial matrix within 4 to 24 hours of antiserum administration (1,2,3). This study was undertaken to evaluate the incorporation of 3H proline into glomerular cells and GBM under normal and anti-SCM induced conditions. Mice were administered, intraperitoneally, 0.1 ml of normal or anti-SCM serum followed by a 10 µC/g body weight injection of 3H proline. Details of the preparation of anti-SCM (Group A type 12 streptococcal pyogenes) and other sera and injection protocol have been described elsewhere (2). After 15 minutes of isotope injection a chase of cold proline was given and animal sacrificed at 20 minutes, 1,2,4,8,24 and 48 hours. One of the removed kidneys was processed for immunofluorescence, light and electron microscopic radioautographic studies; second kidney was used for GBM isolation and aminoacid analysis.

Fibronectin binding to glomerular basement membrane is altered in diabetes

Diabetes ◽  
1987 ◽  
Vol 36 (6) ◽  
pp. 758-763 ◽  
Author(s):  
M. P. Cohen ◽  
R. Saini ◽  
H. Klepser ◽  
L. G. Vasanthi
Keyword(s):  
Basement Membrane ◽  
Glomerular Basement Membrane ◽  
Fibronectin Binding
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