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Miguel Seco - One of the best experts on this subject based on the ideXlab platform.
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sequential development of pulmonary hemorrhage with mpo anca complicating anti glomerular Basement Membrane Antibody mediated glomerulonephritis
American Journal of Kidney Diseases, 2000Co-Authors: R Peces, Minerva Rodriguez, A Pobes, Miguel SecoAbstract:Abstract We report a case of rapidly progressive glomerulonephritis caused by anti–glomerular Basement Membrane (anti-GBM) antibodies that progressed to end-stage renal disease in a 67-year-old woman with diabetes. Intensive combined immunosuppressive therapy with methylprednisolone bolus, oral prednisone, and cyclophosphamide led to negativity of anti-GBM antibodies but was not able to restore renal function. After 28 months of hemodialysis, the patient suddenly presented with pulmonary hemorrhage. In this setting, high levels of myeloperoxidase (MPO)-antineutrophil cytoplasmic Antibody (ANCA) and negative anti-GBM antibodies were found. Therapy with oral prednisone and cyclophosphamide led to resolution of pulmonary hemorrhage and negativity of MPO-ANCA.
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antiglomerular Basement Membrane Antibody mediated glomerulonephritis after intranasal cocaine use
Nephron, 1999Co-Authors: R Peces, Rafael A Navascues, J Baltar, Miguel Seco, J AlvarezAbstract:We report a case of rapidly progressive glomerulonephritis due to antiglomerular Basement Membrane (anti-GBM) antibodies that progressed to end-stage renal disease in a 35-year-old man who used intranasal cocaine on an occasional basis. In contrast to many prior reports of acute renal failure occurring with cocaine-associated rhabdomyolysis, this patient did not have any evidence of acute muscle damage and myoglobin release. Circulating anti-GBM antibodies and renal biopsy with linear IgG and C3 deposits confirmed the diagnosis of anti-GBM disease. The possibility of anti-GBM must be considered in the differential diagnosis of acute renal failure in cocaine addicts. This unusual combination raises complex questions regarding the pathogenesis of this type of renal injury.
Chandra Mohan - One of the best experts on this subject based on the ideXlab platform.
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glutathione s transferase mu 2 transduced mesenchymal stem cells ameliorated anti glomerular Basement Membrane Antibody induced glomerulonephritis by inhibiting oxidation and inflammation
Stem Cell Research & Therapy, 2014Co-Authors: Mei Yan, Jichen Yang, Indu Raman, So Youn Min, Xiangdong Fang, Chandra MohanAbstract:Oxidative stress is implicated in tissue inflammation, and plays an important role in the pathogenesis of immune-mediated nephritis. Using the anti-glomerular Basement Membrane Antibody-induced glomerulonephritis (anti-GBM-GN) mouse model, we found that increased expression of glutathione S-transferase Mu 2 (GSTM2) was related to reduced renal damage caused by anti-GBM antibodies. Furthermore, mesenchymal stem cell (MSC)-based therapy has shed light on the treatment of immune-mediated kidney diseases. The aim of this study was to investigate if MSCs could be utilized as vehicles to deliver the GSTM2 gene product into the kidney and to evaluate its potential therapeutic effect on anti-GBM-GN. The human GSTM2 gene (hGSTM2) was transduced into mouse bone marrow-derived MSCs via a lentivirus vector to create a stable cell line (hGSTM2-MSC). The cultured hGSTM2-MSCs were treated with 0.5mM H2O2, and apoptotic cells were measured by terminal dUTP nick-end labeling (TUNEL) assay. The 129/svj mice, which were challenged with anti-GBM antibodies, were injected with 106 hGSTM2-MSCs via the tail vein. Expression of hGSTM2 and inflammatory cytokines in the kidney was assayed by quantitative PCR and western blotting. Renal function of mice was evaluated by monitoring proteinuria and levels of blood urea nitrogen (BUN), and renal pathological changes were analyzed by histochemistry. Immunohistochemical analysis was performed to measure inflammatory cell infiltration and renal cell apoptosis. MSCs transduced with hGSTM2 exhibited similar growth and differentiation properties to MSCs. hGSTM2-MSCs persistently expressed hGSTM2 and resisted H2O2-induced apoptosis. Upon injection into 129/svj mice, hGSTM2-MSCs migrated to the kidney and expressed hGSTM2. The anti-GBM-GN mice treated with hGSTM2-MSCs exhibited reduced proteinuria and BUN (58% and 59% reduction, respectively) and ameliorated renal pathological damage, compared with control mice. Mice injected with hGSTM2-MSCs showed alleviated renal inflammatory cell infiltration and reduced expression of chemokine (C-C motif) ligand 2 (CCL2), interleukin (IL)-1β and IL-6 (53%, 46% and 52% reduction, respectively), compared with controls. Moreover, hGSTM2-MSCs increased expression of renal superoxide dismutase and catalase, which may associate with detoxifying reactive oxygen species to prevent oxidative renal damage. Our data suggest that the enhanced protective effect of GSTM2-transduced MSCs against anti-GBM-GN might be associated with inhibition of oxidative stress-induced renal cell apoptosis and inflammation, through over-expression of hGSTM2 in mouse kidneys.
R Peces - One of the best experts on this subject based on the ideXlab platform.
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sequential development of pulmonary hemorrhage with mpo anca complicating anti glomerular Basement Membrane Antibody mediated glomerulonephritis
American Journal of Kidney Diseases, 2000Co-Authors: R Peces, Minerva Rodriguez, A Pobes, Miguel SecoAbstract:Abstract We report a case of rapidly progressive glomerulonephritis caused by anti–glomerular Basement Membrane (anti-GBM) antibodies that progressed to end-stage renal disease in a 67-year-old woman with diabetes. Intensive combined immunosuppressive therapy with methylprednisolone bolus, oral prednisone, and cyclophosphamide led to negativity of anti-GBM antibodies but was not able to restore renal function. After 28 months of hemodialysis, the patient suddenly presented with pulmonary hemorrhage. In this setting, high levels of myeloperoxidase (MPO)-antineutrophil cytoplasmic Antibody (ANCA) and negative anti-GBM antibodies were found. Therapy with oral prednisone and cyclophosphamide led to resolution of pulmonary hemorrhage and negativity of MPO-ANCA.
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antiglomerular Basement Membrane Antibody mediated glomerulonephritis after intranasal cocaine use
Nephron, 1999Co-Authors: R Peces, Rafael A Navascues, J Baltar, Miguel Seco, J AlvarezAbstract:We report a case of rapidly progressive glomerulonephritis due to antiglomerular Basement Membrane (anti-GBM) antibodies that progressed to end-stage renal disease in a 35-year-old man who used intranasal cocaine on an occasional basis. In contrast to many prior reports of acute renal failure occurring with cocaine-associated rhabdomyolysis, this patient did not have any evidence of acute muscle damage and myoglobin release. Circulating anti-GBM antibodies and renal biopsy with linear IgG and C3 deposits confirmed the diagnosis of anti-GBM disease. The possibility of anti-GBM must be considered in the differential diagnosis of acute renal failure in cocaine addicts. This unusual combination raises complex questions regarding the pathogenesis of this type of renal injury.
Raymond Nagle - One of the best experts on this subject based on the ideXlab platform.
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Kimura disease with advanced renal damage with anti-tubular Basement Membrane Antibody
Pediatric Nephrology, 2004Co-Authors: Mehul P. Dixit, Katherine M. Scott, Erika Bracamonte, Naznin M. Dixit, Michael J. Schumacher, John Hutter, Raymond NagleAbstract:Kimura disease (KD) is an autoimmune eosinophilic granulomatous disorder with generalized lymphadenopathy. A handful of pediatric patients with renal disease have been described, none of whom have been African-American (AA). We present an AA boy with KD and nephrotic syndrome (NS). Two months after stopping steroids, fever, asthma, eczema, and proteinuria recurred. His NS did not relapse but his platelet count decreased to 51,000/μl (×10^6/l). On restarting prednisone, his platelet count normalized. A kidney biopsy revealed 23 of 37 glomeruli obsolescent and advanced damage with over 50% of cortical tissue replaced by interstitial fibrosis and chronic inflammation. Glomerular immunofluorescence was largely negative; very intense linear anti-tubular Basement Membrane (TBM) deposits of IgA, IgG, C3, and C4 were noted. At present, 36 months from onset, serum creatinine is 1.2 mg/dl (106 µmol/l). We present a 4-year-old AA boy with KD, NS, relapsing thrombocytopenia, and renal damage with anti-TBM Antibody.
Lili Feng - One of the best experts on this subject based on the ideXlab platform.
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inhibition of cxcl16 attenuates inflammatory and progressive phases of anti glomerular Basement Membrane Antibody associated glomerulonephritis
American Journal of Pathology, 2007Co-Authors: Gabriela Garcia, Curtis B Wilson, Luan D Truong, Ping Zhang, Richard J Johnson, Lili FengAbstract:Chemokines recruit and activate leukocytes during inflammation. CXCL16 is a recently discovered chemokine that is expressed as a transMembrane protein that is cleaved to form the active, soluble chemokine. We analyzed the role of CXCL16 in the development of inflammation and in the progression of the anti-glomerular Basement Membrane (GBM) Antibody-induced experimental glomerulonephritis in Wistar-Kyoto rats. CXCL16 was expressed in glomerular endothelial cells and mediated adhesion of macrophages expressing CXCL16 and its cognate receptor, CXCR6. Glomerular infiltrates displayed a strong migratory response to soluble CXCL16. Soluble CXCL16 and its receptor CXCR6 were induced in nephri-tic glomeruli throughout the disease, and CXCL16 expression correlated with the up-regulation of ADAM10, suggesting that this disintegrin and metalloproteinase mediates the chemokine activity of CXCL16. Blocking CXCL16 in the acute inflammatory phase or progressive phase of established glomerulonephritis significantly attenuated monocyte/macrophage infil-tration and glomerular injury; proteinuria also improved. We conclude that CXCL16/CXCR6 plays a critical role in stimulating leukocyte influx, which causes glomerular damage during anti-GBM glomerulonephritis. Blocking CXCL16 actions limits the progression of anti-GBM glomerulonephritis even when the disease is established.
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in vivo inhibition of cc and cx3c chemokine induced leukocyte infiltration and attenuation of glomerulonephritis in wistar kyoto wky rats by vmip ii
Journal of Experimental Medicine, 1998Co-Authors: Shizhong Chen, Kevin B Bacon, Jeffrey K. Harrison, Yiyang Xia, Darren A. Thompson, Michael A. Siani, Tadashi Yamamoto, Gabriela Garcia, Lili FengAbstract:Chemokines play a central role in immune and inflammatory responses. It has been observed recently that certain viruses have evolved molecular piracy and mimicry mechanisms by encoding and synthesizing proteins that interfere with the normal host defense response. One such viral protein, vMIP-II, encoded by human herpesvirus 8, has been identified with in vitro antagonistic activities against CC and CXC chemokine receptors. We report here that vMIP-II has additional antagonistic activity against CX3CR1, the receptor for fractalkine. To investigate the potential therapeutic effect of this broad-spectrum chemokine antagonist, we studied the antiinflammatory activity of vMIP-II in a rat model of experimental glomerulonephritis induced by an antiglomerular Basement Membrane Antibody. vMIP-II potently inhibited monocyte chemoattractant protein 1–, macrophage inflammatory protein 1β–, RANTES (regulated on activation, normal T cell expressed and secreted)-, and fractalkine-induced chemotaxis of activated leukocytes isolated from nephritic glomeruli, significantly reduced leukocyte infiltration to the glomeruli, and markedly attenuated proteinuria. These results suggest that molecules encoded by some viruses may serve as useful templates for the development of antiinflammatory compounds.
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interleukin 1 receptor antagonist ameliorates experimental anti glomerular Basement Membrane Antibody associated glomerulonephritis
Journal of Clinical Investigation, 1994Co-Authors: Winson W Tang, Lili Feng, J L Vannice, C B WilsonAbstract:The contribution of IL-1 to leukocyte infiltration in anti-glomerular Basement Membrane (GBM) Antibody (Ab) glomerulonephritis (GN) was examined by the administration of a specific IL-1 receptor antagonist (IL-1ra). Lewis rats received anti-GBM Ab or normal rabbit serum and were treated with either 0.9% saline or 6 mg IL-1ra over a 24-h time period. Plasma IL-1ra concentration was 2,659 +/- 51 ng/ml 4 h after anti-GBM Ab and IL-1ra administration. PMN and monocyte/macrophage infiltration declined 39% (9.8 +/- 1.9 to 6.0 +/- 1.5 PMN/glomerulus, P < 0.001) and 29% (4.9 +/- 0.8 to 3.5 +/- 0.8 ED-1 cells/glomerulus, P = 0.002) with IL-1ra treatment at 4 h, respectively. Similarly, the number of glomerular cells staining for lymphocyte function-associated molecule-1 beta (CD18) declined 39% from 16.7 +/- 1.9 to 10.7 +/- 1.6 cells/glomerulus at 4 h (P = 0.0001). This was associated with a decrease in glomerular intracellular adhesion molecule-1 expression. The mean glomerular intracellular adhesion molecule-1 score in anti-GBM Ab GN rats treated with IL-1ra was less than that of rats administered anti-GBM Ab and 0.9% saline at 4 (2.0 +/- 0.2 vs 2.5 +/- 0.2, P < 0.05) and 24 (2.5 +/- 0.1 vs 3.1 +/- 0.2, P = 0.0001) h. These immunopathologic changes correlated with a 50% reduction in proteinuria from 147 +/- 34 to 75 +/- 25 mg/d (P < 0.002). Treatment with IL-1ra did not affect the steady state mRNA expression of either IL-1 beta or TNF alpha. An increase in the IL-1ra dose to 30 mg given within the initial 4 h provided no additional benefit. The decline in PMN and monocyte/macrophage infiltration of the glomerulus at 4 h was similar to that found in the initial study. Furthermore, the protective benefit of IL-1ra was abrogated by doubling the dose of the anti-GBM Ab GN, despite administering high dose IL-1ra (30 mg). In these studies, detectable IL-1ra was found in the serum of untreated anti-GBM Ab GN controls. These data suggest a positive yet limited role for IL-1ra in the therapeutic intervention of anti-GBM Ab GN.
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dysfunction of glomerular fibrinolysis in experimental antiglomerular Basement Membrane Antibody glomerulonephritis
Journal of The American Society of Nephrology, 1993Co-Authors: Lili Feng, Winson W Tang, David J Loskutoff, Curtis B WilsonAbstract:Glomerular plasminogen activator inhibitor-I (PAl-I) steady-state mRNA and bioactivity were increased after the induction of an augmented form of antiglomerular Basement Membrane (GBM) Antibody glomerulonephritis. PAl-I mRNA expression was noted at 6 h, peaking at I day, and although falling thereafter, remained higher than that of the control group through Day 17. PAl-I mRNA expression correlated with glomerular PAl-I bioactivity as determined by a functional tissue type plasminogen activator (t-PA) binding assay. Glomerular PAl- I bioactivity, not detected in controls, increased to I .4 ± 0.3 ng/mg of glomerular lysate at 6 h and then decreased to 0.7 ± 0.1 ng/mg of glomerular lysate by Day 6. The mRNA of the plasminogen activators (urokinase plasminogen activator, t-PA) either remained unchanged or declined through Day I , with a slight increase in t-PA mRNA at Day 6. InterleukinIfl mRNA expression was maximal at 6 h, declining by Day 3. Transforming growth factor fl� (TGF-fl1) mRNA began to increase at Day I, was maximal at Day 6, and fell only slightly by Day 17. Epidermal growth factor mRNA decreased. The increase in PAlI mRNA and bioactivity, possibly induced early by (+) (-) (+) (-) (+) (-) (+) (-) (+) (-) �‘ .,�, (+) (-) (+) (-) (+) (-) (+) (-) (+) (-)