The Experts below are selected from a list of 9339 Experts worldwide ranked by ideXlab platform
Shinya Nagasaka - One of the best experts on this subject based on the ideXlab platform.
-
Proliferative Glomerulonephritis with monoclonal immunoglobulin G3κ deposits in association with parvovirus B19 infection
Human Pathology, 2012Co-Authors: Emiko Fujita, Tomohiro Kaneko, Yukinari Masuda, Chikara Ishihara, Seiichiro Higo, Yusuke Kajimoto, Go Kanzaki, Akira Shimizu, Shinya NagasakaAbstract:Summary Proliferative Glomerulonephritis with monoclonal immunoglobulin G deposits is a recently described disease entity, characterized by nonorganized electron-dense deposits in glomeruli and immunofluorescence findings indicating monoclonal immunoglobulin G deposits. The pathogenesis of many cases of Proliferative Glomerulonephritis with monoclonal immunoglobulin G deposits remains unknown. We herein report 2 patients with parvovirus B19 infection who developed acute nephritic syndrome with hypocomplementemia (patient 1) or persistent proteinuria and congestive heart failure (patient 2); however, neither patient had detectable levels of serum monoclonal immunoglobulin G. Renal biopsy in both patients showed diffuse endocapillary Proliferative Glomerulonephritis with monoclonal immunoglobulin G3 κ deposits, and electron microscopy showed nonorganized electron-dense deposits mainly in the subendothelial and mesangial areas. Clinical symptoms, abnormal laboratory findings, and urinary abnormalities recovered spontaneously in both cases within 4 weeks. Our 2 cases may be the first reported patients with Proliferative Glomerulonephritis with monoclonal immunoglobulin G deposits possibly associated with parvovirus B19 infection. Virus infection–associated immune disorders could be implicated in the pathogenesis of Proliferative Glomerulonephritis with monoclonal immunoglobulin G deposits.
Y Ville - One of the best experts on this subject based on the ideXlab platform.
-
Lupus erythematosus Proliferative Glomerulonephritis in fetus.
Lupus, 2005Co-Authors: F. Daikha-dahmane, J P Bault, D Molina-gomes, D Hillion, Y VilleAbstract:We report the case of a fetus with Proliferative Glomerulonephritis in the context of maternal systemic lupus erythematosus (SLE). The pattern of the renal lesions correspond to the class III of revisited WHO classification of Glomerulonephritis in SLE. Amniotic fluid analysis showed a high level of albumin and the presence of anti-Ro and anti-DNA antibodies that were possibly responsible for the renal injury.
Emiko Fujita - One of the best experts on this subject based on the ideXlab platform.
-
Proliferative Glomerulonephritis with monoclonal immunoglobulin G3κ deposits in association with parvovirus B19 infection
Human Pathology, 2012Co-Authors: Emiko Fujita, Tomohiro Kaneko, Yukinari Masuda, Chikara Ishihara, Seiichiro Higo, Yusuke Kajimoto, Go Kanzaki, Akira Shimizu, Shinya NagasakaAbstract:Summary Proliferative Glomerulonephritis with monoclonal immunoglobulin G deposits is a recently described disease entity, characterized by nonorganized electron-dense deposits in glomeruli and immunofluorescence findings indicating monoclonal immunoglobulin G deposits. The pathogenesis of many cases of Proliferative Glomerulonephritis with monoclonal immunoglobulin G deposits remains unknown. We herein report 2 patients with parvovirus B19 infection who developed acute nephritic syndrome with hypocomplementemia (patient 1) or persistent proteinuria and congestive heart failure (patient 2); however, neither patient had detectable levels of serum monoclonal immunoglobulin G. Renal biopsy in both patients showed diffuse endocapillary Proliferative Glomerulonephritis with monoclonal immunoglobulin G3 κ deposits, and electron microscopy showed nonorganized electron-dense deposits mainly in the subendothelial and mesangial areas. Clinical symptoms, abnormal laboratory findings, and urinary abnormalities recovered spontaneously in both cases within 4 weeks. Our 2 cases may be the first reported patients with Proliferative Glomerulonephritis with monoclonal immunoglobulin G deposits possibly associated with parvovirus B19 infection. Virus infection–associated immune disorders could be implicated in the pathogenesis of Proliferative Glomerulonephritis with monoclonal immunoglobulin G deposits.
Yukinari Masuda - One of the best experts on this subject based on the ideXlab platform.
-
Proliferative Glomerulonephritis with monoclonal immunoglobulin G3κ deposits in association with parvovirus B19 infection
Human Pathology, 2012Co-Authors: Emiko Fujita, Tomohiro Kaneko, Yukinari Masuda, Chikara Ishihara, Seiichiro Higo, Yusuke Kajimoto, Go Kanzaki, Akira Shimizu, Shinya NagasakaAbstract:Summary Proliferative Glomerulonephritis with monoclonal immunoglobulin G deposits is a recently described disease entity, characterized by nonorganized electron-dense deposits in glomeruli and immunofluorescence findings indicating monoclonal immunoglobulin G deposits. The pathogenesis of many cases of Proliferative Glomerulonephritis with monoclonal immunoglobulin G deposits remains unknown. We herein report 2 patients with parvovirus B19 infection who developed acute nephritic syndrome with hypocomplementemia (patient 1) or persistent proteinuria and congestive heart failure (patient 2); however, neither patient had detectable levels of serum monoclonal immunoglobulin G. Renal biopsy in both patients showed diffuse endocapillary Proliferative Glomerulonephritis with monoclonal immunoglobulin G3 κ deposits, and electron microscopy showed nonorganized electron-dense deposits mainly in the subendothelial and mesangial areas. Clinical symptoms, abnormal laboratory findings, and urinary abnormalities recovered spontaneously in both cases within 4 weeks. Our 2 cases may be the first reported patients with Proliferative Glomerulonephritis with monoclonal immunoglobulin G deposits possibly associated with parvovirus B19 infection. Virus infection–associated immune disorders could be implicated in the pathogenesis of Proliferative Glomerulonephritis with monoclonal immunoglobulin G deposits.
-
Apoptosis in the repair process of experimental Proliferative Glomerulonephritis.
Kidney international, 1995Co-Authors: Akira Shimizu, Yukinari Masuda, Hiroshi Kitamura, Masamichi Ishizaki, Yuichi Sugisaki, Nobuaki YamanakaAbstract:Apoptosis in the repair process of experimental Proliferative Glomerulonephritis. The recovery from the Proliferative Glomerulonephritis (GN) with reduction of hypercellularity is known in various experimental and human GN. To elucidate the participation of apoptosis in GN, we studied the experimental Thy-1.1 GN for six weeks. Apoptosis was recognized by both light and electron microscopy, and the biochemical expression of apoptosis was morphologically confirmed by in situ end-labeling method of fragmented DNA, using terminal deoxy-transferase. MesangioProliferative GN was induced by a single administration of anti-Thy-1.1 monoclonal antibody in a rat. Mesangial cell proliferation started early in the process and the number of glomerular cells peaked from day 7 to day 10. Subsequently, the degree of Proliferative lesion diminished with obvious reconstruction of the capillary structure, as well as decrease in the number of glomerular cells. During this period, proliferated mesangial cells returned to their original level of cellularity and apoptosis apparently increased in number among the glomeruli. Apoptosis was significantly noted from day 7 to week 4 and was in its maximum at day 10 to week 2. Following this period, by week 6 most of the glomeruli reverted to their original structure. The number of infiltrated neutrophils and macrophages in the glomeruli slowly decreased during the course of the disease, and a few apoptosis were also observed. It is concluded that proliferated glomerular cells regress by apoptosis in the repairing process of GN. Apoptosis plays an essential role in the recovery to the original glomerular structure in GN.
Akira Shimizu - One of the best experts on this subject based on the ideXlab platform.
-
Proliferative Glomerulonephritis with monoclonal immunoglobulin G3κ deposits in association with parvovirus B19 infection
Human Pathology, 2012Co-Authors: Emiko Fujita, Tomohiro Kaneko, Yukinari Masuda, Chikara Ishihara, Seiichiro Higo, Yusuke Kajimoto, Go Kanzaki, Akira Shimizu, Shinya NagasakaAbstract:Summary Proliferative Glomerulonephritis with monoclonal immunoglobulin G deposits is a recently described disease entity, characterized by nonorganized electron-dense deposits in glomeruli and immunofluorescence findings indicating monoclonal immunoglobulin G deposits. The pathogenesis of many cases of Proliferative Glomerulonephritis with monoclonal immunoglobulin G deposits remains unknown. We herein report 2 patients with parvovirus B19 infection who developed acute nephritic syndrome with hypocomplementemia (patient 1) or persistent proteinuria and congestive heart failure (patient 2); however, neither patient had detectable levels of serum monoclonal immunoglobulin G. Renal biopsy in both patients showed diffuse endocapillary Proliferative Glomerulonephritis with monoclonal immunoglobulin G3 κ deposits, and electron microscopy showed nonorganized electron-dense deposits mainly in the subendothelial and mesangial areas. Clinical symptoms, abnormal laboratory findings, and urinary abnormalities recovered spontaneously in both cases within 4 weeks. Our 2 cases may be the first reported patients with Proliferative Glomerulonephritis with monoclonal immunoglobulin G deposits possibly associated with parvovirus B19 infection. Virus infection–associated immune disorders could be implicated in the pathogenesis of Proliferative Glomerulonephritis with monoclonal immunoglobulin G deposits.
-
Apoptosis in the repair process of experimental Proliferative Glomerulonephritis.
Kidney international, 1995Co-Authors: Akira Shimizu, Yukinari Masuda, Hiroshi Kitamura, Masamichi Ishizaki, Yuichi Sugisaki, Nobuaki YamanakaAbstract:Apoptosis in the repair process of experimental Proliferative Glomerulonephritis. The recovery from the Proliferative Glomerulonephritis (GN) with reduction of hypercellularity is known in various experimental and human GN. To elucidate the participation of apoptosis in GN, we studied the experimental Thy-1.1 GN for six weeks. Apoptosis was recognized by both light and electron microscopy, and the biochemical expression of apoptosis was morphologically confirmed by in situ end-labeling method of fragmented DNA, using terminal deoxy-transferase. MesangioProliferative GN was induced by a single administration of anti-Thy-1.1 monoclonal antibody in a rat. Mesangial cell proliferation started early in the process and the number of glomerular cells peaked from day 7 to day 10. Subsequently, the degree of Proliferative lesion diminished with obvious reconstruction of the capillary structure, as well as decrease in the number of glomerular cells. During this period, proliferated mesangial cells returned to their original level of cellularity and apoptosis apparently increased in number among the glomeruli. Apoptosis was significantly noted from day 7 to week 4 and was in its maximum at day 10 to week 2. Following this period, by week 6 most of the glomeruli reverted to their original structure. The number of infiltrated neutrophils and macrophages in the glomeruli slowly decreased during the course of the disease, and a few apoptosis were also observed. It is concluded that proliferated glomerular cells regress by apoptosis in the repairing process of GN. Apoptosis plays an essential role in the recovery to the original glomerular structure in GN.
