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Anthony Chang - One of the best experts on this subject based on the ideXlab platform.
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Renal Vasculitis and Pauci-Immune Glomerulonephritis Associated With Immune Checkpoint Inhibitors.
American journal of kidney diseases : the official journal of the National Kidney Foundation, 2019Co-Authors: Alexander J. Gallan, Anthony Chang, Ellen Alexander, Pankti Reid, Fouad Kutuby, Kammi J HenriksenAbstract:Immune checkpoint inhibitors are increasingly used to treat a variety of solid-organ and hematologic cancers. However, overactivation of the immune system can lead to immune-related adverse events, which are increasingly recognized in the kidney. There have been only rare reported cases of checkpoint inhibitor–associated glomerulonephritis and renal vasculitis, although vasculitis in other organs has been well described. We report 4 cases of renal vasculitis or Pauci-Immune glomerulonephritis after checkpoint inhibitor therapy. Three patients had renal small- to medium-vessel vasculitis and 1 had focally crescentic Pauci-Immune glomerulonephritis. Three patients presented with acute kidney injury, and 1 presented with nephrotic syndrome and hematuria. Three patients were tested for antineutrophil cytoplasmic antibodies, which were negative. The time from checkpoint inhibitor initiation to immune-related adverse event presentation ranged from 2 weeks to 24 months. Three patients were treated with glucocorticoids, resulting in clinical resolution. Our series demonstrates that renal vasculitis and Pauci-Immune glomerulonephritis are important considerations in the differential diagnosis of checkpoint inhibitor–related reductions in kidney function.
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Pauci-Immune glomerulonephritis in children: a clinicopathologic study of 21 patients.
Pediatric nephrology (Berlin Germany), 2015Co-Authors: Mazdak A. Khalighi, Anthony Chang, Kammi J Henriksen, Shihtien Wang, Margret E. Bock, Mahima Keswani, Shane M. MeehanAbstract:Background Pauci-Immune glomerulonephritis (GN) represents a severe form of glomerular injury and is the most common cause of crescentic GN in adults. To date, the clinicopathologic features of Pauci-Immune GN are not well characterized in the pediatric population.
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M2 Macrophage Infiltrates in the Early Stages of ANCA-Associated Pauci-Immune Necrotizing GN
Clinical journal of the American Society of Nephrology : CJASN, 2014Co-Authors: Lei Zhao, Michael Z. David, Elizabeth Hyjek, Anthony Chang, Shane M. MeehanAbstract:Background and objectives This study examined kidney biopsies with focal segmental glomerular fibrinoid necrosis to identify early features of Pauci-Immune necrotizing GN and the primary effector cells mediating initial capillary injury. Design, setting, participants, & measurements Seventeen consecutive kidney biopsies with focal Pauci-Immune necrotizing GN, obtained over a 6-year period (2007–2012), were studied. Neutrophils and CD68 + , CD163 + , CD3 + , CD56 + , and CD20 + cells were scored in paraffin sections counterstained with periodic acid–Schiff. Electron microscopy was performed in 15 of 17 biopsies and additional examples of Pauci-Immune necrotizing GN ( n =25). Biopsies with thin basement membrane nephropathy ( n =5) served as immunohistologic normal controls. Results Biopsies with Pauci-Immune necrotizing GN had a mean of 10 (range=3–25) normal-appearing glomeruli, a mean of 2 (range=1–5) glomeruli with segmental fibrinoid necrosis, and a mean of 2 (range=1–11) glomeruli with cellular crescents. CD68 + and CD163 + macrophages predominated at sites of fibrinoid necrosis in Pauci-Immune necrotizing GN, exceeding the quantity of neutrophils and T cells (mean scores [SD]=2.5 [0.7] and 2.2 [0.75] versus 0.6 [0.5] and 0.1 [0.3], respectively; P + and CD163 + macrophages than the controls (CD68 + , 0.9 [0.3] versus 0.4 [0.3]; CD163 + , 1 [0.4] versus 0.4 [0.3]; P r =0.74 and r =0.71, respectively; P =0.001) but did not correlate with the extent of fibrinoid necrosis ( r =0.36). Macrophages were localized at minute perforations and attenuations of the capillary basement membrane by electron microscopy. Conclusions Early Pauci-Immune necrotizing GN is characterized by a selective localization of CD163 + M2 macrophages at sites of glomerular fibrinoid necrosis and in normal-appearing glomeruli. These observations indicate that alternatively activated macrophages are positioned as potential effectors of glomerular injury in the early stages of Pauci-Immune necrotizing GN and may be potential targets for therapeutic intervention.
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rare association of chronic lymphocytic leukemia small lymphocytic lymphoma ancas and pauci immune crescentic glomerulonephritis
American Journal of Kidney Diseases, 2011Co-Authors: Kammi J Henriksen, Richard Hong, Maria I Sobrero, Anthony ChangAbstract:We report a 69-year-old African American woman with hemoptysis and hematuria caused by a focally crescentic Pauci-Immune glomerular injury associated with the presence of antineutrophil cytoplasmic antibodies (ANCAs). An incidental diagnosis of chronic lymphocytic leukemia (CLL)/small lymphocytic lymphoma also was established based on the kidney biopsy. Given that a subset of patients with CLL can develop autoantibodies to red blood cells, platelets, or, rarely, neutrophils, the simultaneous presence of CLL, ANCA, and a Pauci-Immune crescentic glomerulonephritis may not be a coincidence. Recent advances in the pathogenic role of ANCAs in Pauci-Immune crescentic glomerulonephritis may link the underlying CLL to this patient's glomerular injury. Awareness of this possible association may be important for clinicians who manage patients with CLL, as well as for renal pathologists who diagnose Pauci-Immune crescentic glomerulonephritis.
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Rare association of chronic lymphocytic leukemia/small lymphocytic lymphoma, ANCAs, and Pauci-Immune crescentic glomerulonephritis.
American journal of kidney diseases : the official journal of the National Kidney Foundation, 2010Co-Authors: Kammi J Henriksen, Richard Hong, Maria I Sobrero, Anthony ChangAbstract:We report a 69-year-old African American woman with hemoptysis and hematuria caused by a focally crescentic Pauci-Immune glomerular injury associated with the presence of antineutrophil cytoplasmic antibodies (ANCAs). An incidental diagnosis of chronic lymphocytic leukemia (CLL)/small lymphocytic lymphoma also was established based on the kidney biopsy. Given that a subset of patients with CLL can develop autoantibodies to red blood cells, platelets, or, rarely, neutrophils, the simultaneous presence of CLL, ANCA, and a Pauci-Immune crescentic glomerulonephritis may not be a coincidence. Recent advances in the pathogenic role of ANCAs in Pauci-Immune crescentic glomerulonephritis may link the underlying CLL to this patient's glomerular injury. Awareness of this possible association may be important for clinicians who manage patients with CLL, as well as for renal pathologists who diagnose Pauci-Immune crescentic glomerulonephritis.
Kammi J Henriksen - One of the best experts on this subject based on the ideXlab platform.
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Renal Vasculitis and Pauci-Immune Glomerulonephritis Associated With Immune Checkpoint Inhibitors.
American journal of kidney diseases : the official journal of the National Kidney Foundation, 2019Co-Authors: Alexander J. Gallan, Anthony Chang, Ellen Alexander, Pankti Reid, Fouad Kutuby, Kammi J HenriksenAbstract:Immune checkpoint inhibitors are increasingly used to treat a variety of solid-organ and hematologic cancers. However, overactivation of the immune system can lead to immune-related adverse events, which are increasingly recognized in the kidney. There have been only rare reported cases of checkpoint inhibitor–associated glomerulonephritis and renal vasculitis, although vasculitis in other organs has been well described. We report 4 cases of renal vasculitis or Pauci-Immune glomerulonephritis after checkpoint inhibitor therapy. Three patients had renal small- to medium-vessel vasculitis and 1 had focally crescentic Pauci-Immune glomerulonephritis. Three patients presented with acute kidney injury, and 1 presented with nephrotic syndrome and hematuria. Three patients were tested for antineutrophil cytoplasmic antibodies, which were negative. The time from checkpoint inhibitor initiation to immune-related adverse event presentation ranged from 2 weeks to 24 months. Three patients were treated with glucocorticoids, resulting in clinical resolution. Our series demonstrates that renal vasculitis and Pauci-Immune glomerulonephritis are important considerations in the differential diagnosis of checkpoint inhibitor–related reductions in kidney function.
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Pauci-Immune glomerulonephritis in children: a clinicopathologic study of 21 patients.
Pediatric nephrology (Berlin Germany), 2015Co-Authors: Mazdak A. Khalighi, Anthony Chang, Kammi J Henriksen, Shihtien Wang, Margret E. Bock, Mahima Keswani, Shane M. MeehanAbstract:Background Pauci-Immune glomerulonephritis (GN) represents a severe form of glomerular injury and is the most common cause of crescentic GN in adults. To date, the clinicopathologic features of Pauci-Immune GN are not well characterized in the pediatric population.
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rare association of chronic lymphocytic leukemia small lymphocytic lymphoma ancas and pauci immune crescentic glomerulonephritis
American Journal of Kidney Diseases, 2011Co-Authors: Kammi J Henriksen, Richard Hong, Maria I Sobrero, Anthony ChangAbstract:We report a 69-year-old African American woman with hemoptysis and hematuria caused by a focally crescentic Pauci-Immune glomerular injury associated with the presence of antineutrophil cytoplasmic antibodies (ANCAs). An incidental diagnosis of chronic lymphocytic leukemia (CLL)/small lymphocytic lymphoma also was established based on the kidney biopsy. Given that a subset of patients with CLL can develop autoantibodies to red blood cells, platelets, or, rarely, neutrophils, the simultaneous presence of CLL, ANCA, and a Pauci-Immune crescentic glomerulonephritis may not be a coincidence. Recent advances in the pathogenic role of ANCAs in Pauci-Immune crescentic glomerulonephritis may link the underlying CLL to this patient's glomerular injury. Awareness of this possible association may be important for clinicians who manage patients with CLL, as well as for renal pathologists who diagnose Pauci-Immune crescentic glomerulonephritis.
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Rare association of chronic lymphocytic leukemia/small lymphocytic lymphoma, ANCAs, and Pauci-Immune crescentic glomerulonephritis.
American journal of kidney diseases : the official journal of the National Kidney Foundation, 2010Co-Authors: Kammi J Henriksen, Richard Hong, Maria I Sobrero, Anthony ChangAbstract:We report a 69-year-old African American woman with hemoptysis and hematuria caused by a focally crescentic Pauci-Immune glomerular injury associated with the presence of antineutrophil cytoplasmic antibodies (ANCAs). An incidental diagnosis of chronic lymphocytic leukemia (CLL)/small lymphocytic lymphoma also was established based on the kidney biopsy. Given that a subset of patients with CLL can develop autoantibodies to red blood cells, platelets, or, rarely, neutrophils, the simultaneous presence of CLL, ANCA, and a Pauci-Immune crescentic glomerulonephritis may not be a coincidence. Recent advances in the pathogenic role of ANCAs in Pauci-Immune crescentic glomerulonephritis may link the underlying CLL to this patient's glomerular injury. Awareness of this possible association may be important for clinicians who manage patients with CLL, as well as for renal pathologists who diagnose Pauci-Immune crescentic glomerulonephritis.
Ming-hui Zhao - One of the best experts on this subject based on the ideXlab platform.
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Renal Neutrophils Infiltration in Antineutrophil Cytoplasmic Antibodies-Negative Pauci-Immune Crescentic Glomerulonephritis
The American journal of the medical sciences, 2010Co-Authors: Guang-qun Xing, Min Chen, Su-xia Wang, Gang Liu, Ming-hui ZhaoAbstract:Abstract Introduction This study aims to investigate the evidence of neutrophil infiltration in renal tissue from patients with antineutrophil cytoplasmic antibodies (ANCA)-negative Pauci-Immune crescentic glomerulonephritis (CrGN), and a comparison with their ANCA-positive counterparts was performed. Methods Renal biopsy specimens from 31 patients with Pauci-Immune CrGN were collected. Twelve patients were ANCA negative, and 19 patients were ANCA positive. Neutrophil infiltration was investigated by staining of 2 markers, CD15 and myeloperoxidase (MPO), using immunohistochemistry. Results Positive-stained cells of CD15 (CD15 + ) and MPO (MPO+) were mainly located in glomeruli with cellular crescents and segmental fibrinoid necrotic lesions and in periglomerular area of cellular crescents, especially at the area of ruptured Bowman capsule. Scanty positive staining was found in normal renal tissue. The number of CD15 + cells in the glomeruli and periglomerular area was significantly higher in ANCA-negative group than in ANCA-positive group (in glomeruli: 2.70 ± 1.61 versus 1.38 ± 0.85, P = 0.019; in periglomerular area: 4.35 ± 4.36 versus 1.48 ± 1.67, P = 0.047). The number of MPO + cells in the periglomerular area was also significantly higher in ANCA-negative group than that in ANCA-positive group. Conclusions Renal neutrophil infiltration might play a pathogenic role in ANCA-negative Pauci-Immune CrGN, and the neutrophil infiltration might be more severe in ANCA-negative Pauci-Immune-CrGN than in ANCA-positive one.
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Differential deposition of C4d and MBL in glomeruli of patients with ANCA-negative Pauci-Immune crescentic glomerulonephritis.
Journal of clinical immunology, 2009Co-Authors: Guang-qun Xing, Min Chen, Gang Liu, Xin Zheng, Jie E, Ming-hui ZhaoAbstract:Objective Our previous study suggested involvement of alternative pathway activation of complement in ANCA-positive Pauci-Immune crescentic glomerulonephritis (CrGN). This study was to investigate the evidence of complement activation in renal biopsy specimens of patients with ANCA-negative Pauci-Immune CrGN.
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complement activation is involved in renal damage in human antineutrophil cytoplasmic autoantibody associated pauci immune vasculitis
Journal of Clinical Immunology, 2009Co-Authors: Guang-qun Xing, Min Chen, Jun-jun Zhang, Cees G. M. Kallenberg, Gang Liu, Xin Zheng, Peter Heeringa, E Jie, Ming-hui ZhaoAbstract:Objective This study was to investigate the evidence for complement activation in renal biopsy specimens of patients with myeloperoxidase (MPO)-antineutrophil cytoplasmic autoantibody (ANCA)-associated Pauci-Immune vasculitis.
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ANCA-negative Pauci-Immune crescentic glomerulonephritis
Nature reviews. Nephrology, 2009Co-Authors: Min Chen, Cees G. M. Kallenberg, Ming-hui ZhaoAbstract:Crescentic glomerulonephritis is a severe form of glomerular injury that is characterized by disruption of the glomerular basement membrane, cellular proliferation within Bowman space, and (often) fibrinoid necrosis. Pauci-Immune crescentic glomerulonephritis, so called because it involves little or no glomerular immunoglobulin deposition, is one of the most common causes of rapidly progressive glomerulonephritis. In the majority of patients, Pauci-Immune crescentic glomerulonephritis is a manifestation of antineutrophil cytoplasmic antibody (ANCA)-associated vasculitis. However, some patients with Pauci-Immune crescentic glomerulonephritis lack ANCAs. This Review compares the prevalence, clinical manifestations, histopathology, and outcomes of ANCA-negative Pauci-Immune crescentic glomerulonephritis with those of ANCA-positive disease. We also discuss the possible pathogenesis of ANCA-negative Pauci-Immune crescentic glomerulonephritis, paying particular attention to the mechanisms and role of neutrophil activation.
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Neutrophil degranulation in antineutrophil cytoplasmic antibody-negative Pauci-Immune crescentic glomerulonephritis.
Journal of nephrology, 2009Co-Authors: Fang Wang, Min Chen, Ming-hui ZhaoAbstract:BACKGROUND Patients with Pauci-Immune crescentic glomerulonephritis (CrGN) are frequently found to have antineutrophil cytoplasmic antibodies (ANCAs). It has been demonstrated that ANCAs can induce neutrophil activation and degranulation, which plays an important role in the pathogenesis of ANCA-associated vasculitis. However, the pathogenesis of ANCA-negative Pauci-Immune CrGN is not clear. This study aims to investigate the evidence for neutrophil activation and degranulation at disease presentation in patients with renal biopsy-proven ANCA-negative Pauci-Immune CrGN. METHODS Sera from 20 patients with ANCA-negative Pauci-Immune CrGN and 22 patients with ANCA-positive Pauci-Immune CrGN were collected at presentation. Serum neutrophil gelatinase-associated lipocalin (NGAL) and lactoferrin (LF) were measured using commercial ELISA kits. RESULTS Serum levels of NGAL in ANCA-negative patients were significantly higher than those of ANCA-positive patients (940.8 +/- 676.5 ng/mL vs. 569.3 +/- 287.2 ng/mL, p
Cees G. M. Kallenberg - One of the best experts on this subject based on the ideXlab platform.
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Pauci-Immune necrotizing glomerulonephritis
Rheumatic diseases clinics of North America, 2010Co-Authors: Abraham Rutgers, Jan S. F. Sanders, Coen A. Stegeman, Cees G. M. KallenbergAbstract:Pauci-Immune necrotizing glomerulonephritis is the most frequent cause of rapidly progressive glomerulonephritis and, in most cases, is associated with antineutrophil cytoplasmic antibodies (ANCA). It is either the renal manifestation of Wegener's granulomatosis, microscopic polyangiitis of Churg-Strauss syndrome, or a renal-limited vasculitis. In this review, the histopathologic changes seen in renal biopsies of patients with Pauci-Immune glomerulonephritis are described. The authors also describe why the disease is sometimes limited to the kidneys, the clinical course of renal disease, treatment issues, how to deal with disease relapses, and how to prevent them from occurring. Furthermore, the necessity of renal biopsy and rebiopsy, the usefulness of rapid ANCA detection at diagnosis, and serial measurement of ANCA during follow-up are discussed. The effect of dialysis on the disease process and the possibility of renal transplantation after disease remission are also debated.
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complement activation is involved in renal damage in human antineutrophil cytoplasmic autoantibody associated pauci immune vasculitis
Journal of Clinical Immunology, 2009Co-Authors: Guang-qun Xing, Min Chen, Jun-jun Zhang, Cees G. M. Kallenberg, Gang Liu, Xin Zheng, Peter Heeringa, E Jie, Ming-hui ZhaoAbstract:Objective This study was to investigate the evidence for complement activation in renal biopsy specimens of patients with myeloperoxidase (MPO)-antineutrophil cytoplasmic autoantibody (ANCA)-associated Pauci-Immune vasculitis.
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ANCA-negative Pauci-Immune crescentic glomerulonephritis
Nature reviews. Nephrology, 2009Co-Authors: Min Chen, Cees G. M. Kallenberg, Ming-hui ZhaoAbstract:Crescentic glomerulonephritis is a severe form of glomerular injury that is characterized by disruption of the glomerular basement membrane, cellular proliferation within Bowman space, and (often) fibrinoid necrosis. Pauci-Immune crescentic glomerulonephritis, so called because it involves little or no glomerular immunoglobulin deposition, is one of the most common causes of rapidly progressive glomerulonephritis. In the majority of patients, Pauci-Immune crescentic glomerulonephritis is a manifestation of antineutrophil cytoplasmic antibody (ANCA)-associated vasculitis. However, some patients with Pauci-Immune crescentic glomerulonephritis lack ANCAs. This Review compares the prevalence, clinical manifestations, histopathology, and outcomes of ANCA-negative Pauci-Immune crescentic glomerulonephritis with those of ANCA-positive disease. We also discuss the possible pathogenesis of ANCA-negative Pauci-Immune crescentic glomerulonephritis, paying particular attention to the mechanisms and role of neutrophil activation.
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Are antineutrophil cytoplasmic antibody-associated vasculitides Pauci-Immune?
Rheumatic diseases clinics of North America, 2001Co-Authors: Raoul H. Brons, Cees G. M. Kallenberg, Jan Willem Cohen TervaertAbstract:The role of immune complexes in antineutrophil cytoplasmic antibody (ANCA)-associated vasculitides remains controversial. The ANCA-associated vasculitides are described as being Pauci-Immune. The authors hypothesize that the absence of immune complexes is a result of an exaggerated inflammatory response due to the presence of ANCA. The authors present evidence indicating that immune complexes may play a role in the initiation or relapses of the disease.
Maria I Sobrero - One of the best experts on this subject based on the ideXlab platform.
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rare association of chronic lymphocytic leukemia small lymphocytic lymphoma ancas and pauci immune crescentic glomerulonephritis
American Journal of Kidney Diseases, 2011Co-Authors: Kammi J Henriksen, Richard Hong, Maria I Sobrero, Anthony ChangAbstract:We report a 69-year-old African American woman with hemoptysis and hematuria caused by a focally crescentic Pauci-Immune glomerular injury associated with the presence of antineutrophil cytoplasmic antibodies (ANCAs). An incidental diagnosis of chronic lymphocytic leukemia (CLL)/small lymphocytic lymphoma also was established based on the kidney biopsy. Given that a subset of patients with CLL can develop autoantibodies to red blood cells, platelets, or, rarely, neutrophils, the simultaneous presence of CLL, ANCA, and a Pauci-Immune crescentic glomerulonephritis may not be a coincidence. Recent advances in the pathogenic role of ANCAs in Pauci-Immune crescentic glomerulonephritis may link the underlying CLL to this patient's glomerular injury. Awareness of this possible association may be important for clinicians who manage patients with CLL, as well as for renal pathologists who diagnose Pauci-Immune crescentic glomerulonephritis.
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Rare association of chronic lymphocytic leukemia/small lymphocytic lymphoma, ANCAs, and Pauci-Immune crescentic glomerulonephritis.
American journal of kidney diseases : the official journal of the National Kidney Foundation, 2010Co-Authors: Kammi J Henriksen, Richard Hong, Maria I Sobrero, Anthony ChangAbstract:We report a 69-year-old African American woman with hemoptysis and hematuria caused by a focally crescentic Pauci-Immune glomerular injury associated with the presence of antineutrophil cytoplasmic antibodies (ANCAs). An incidental diagnosis of chronic lymphocytic leukemia (CLL)/small lymphocytic lymphoma also was established based on the kidney biopsy. Given that a subset of patients with CLL can develop autoantibodies to red blood cells, platelets, or, rarely, neutrophils, the simultaneous presence of CLL, ANCA, and a Pauci-Immune crescentic glomerulonephritis may not be a coincidence. Recent advances in the pathogenic role of ANCAs in Pauci-Immune crescentic glomerulonephritis may link the underlying CLL to this patient's glomerular injury. Awareness of this possible association may be important for clinicians who manage patients with CLL, as well as for renal pathologists who diagnose Pauci-Immune crescentic glomerulonephritis.