Steroid-sensitive recurrent mesangial proliferative glomerulonephritis with monoclonal IgG deposits
Abstract Proliferative glomerulonephritis with monoclonal immunoglobulin G (IgG) deposits (PGNMID) is a rare kidney disease. The predominant pathological finding of PGNMID is the presence of monoclonal Ig deposits on the glomerular basement membrane (GBM). However, there is some variation in deposit...
Ausführliche Beschreibung
Gespeichert in:
| Autor*in: |
Nomura, Kazutoshi [verfasserIn] Miyatake, Nobuhiko [verfasserIn] Okada, Keiichiro [verfasserIn] Hayashi, Norifumi [verfasserIn] Fujimoto, Keiji [verfasserIn] Adachi, Hiroki [verfasserIn] Furuichi, Kengo [verfasserIn] Shimizu, Akira [verfasserIn] Yokoyama, Hitoshi [verfasserIn] |
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| Format: |
E-Artikel |
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| Sprache: |
Englisch |
| Erschienen: |
2021 |
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| Schlagwörter: |
Proliferative glomerulonephritis with monoclonal immunoglobulin G deposits (PGNMID) |
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| Übergeordnetes Werk: |
Enthalten in: CEN Case Reports - Tokyo : Springer Japan, 2012, 10(2021), 2 vom: 04. Jan., Seite 308-313 |
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| Übergeordnetes Werk: |
volume:10 ; year:2021 ; number:2 ; day:04 ; month:01 ; pages:308-313 |
| Links: |
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| DOI / URN: |
10.1007/s13730-020-00562-x |
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| Katalog-ID: |
SPR043693784 |
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| 520 | |a Abstract Proliferative glomerulonephritis with monoclonal immunoglobulin G (IgG) deposits (PGNMID) is a rare kidney disease. The predominant pathological finding of PGNMID is the presence of monoclonal Ig deposits on the glomerular basement membrane (GBM). However, there is some variation in deposition pattern in this kidney disease. We report a case of steroid-sensitive recurrent mesangial proliferative type of PGNMID. A 40-year-old female noticed lower leg pitting edema and polyuria. Approximately 10 days prior to the first clinic visit, she was diagnosed with nephrotic syndrome based on the laboratory data of urine and blood. Immunological and hematological examination revealed no abnormality. However, kidney biopsy specimens showed mild mesangial cell proliferation and mesangial matrix accumulation on light microscopic findings. Regarding immunofluorescence staining, granular deposits of IgG, C1q, and β1c were observed on GBM and mesangial area. Granular deposits of IgG3 and λ were also observed on GBM and mesangial area. Moreover, negative results were obtained for the phospholipase A2 receptor antibody and thrombospondin type-1 domain-containing 7A. Electron microscopy revealed highly electron dense deposits mainly in the mesangial region. Kidney biopsy showed mesangial proliferative glomerulonephritis characterized by monoclonal Ig deposition of IgG3/λ. Steroid therapy was initiated, and complete remission was achieved on day 36. After the discontinuation of steroid therapy, proteinuria recurred and second kidney biopsy findings were almost similar to the first biopsy. However, complete remission was achieved with steroid therapy. This is a rare recurrent case of steroid-sensitive PGNMID. The pathological feature of this case was mesangial proliferative glomerulonephritis with Ig deposition of IgG3/λ. | ||
| 650 | 4 | |a Proliferative glomerulonephritis with monoclonal immunoglobulin G deposits (PGNMID) |7 (dpeaa)DE-He213 | |
| 650 | 4 | |a Steroid sensitive |7 (dpeaa)DE-He213 | |
| 650 | 4 | |a Kidney biopsy |7 (dpeaa)DE-He213 | |
| 650 | 4 | |a IgG3/λ |7 (dpeaa)DE-He213 | |
| 700 | 1 | |a Miyatake, Nobuhiko |e verfasserin |4 aut | |
| 700 | 1 | |a Okada, Keiichiro |e verfasserin |4 aut | |
| 700 | 1 | |a Hayashi, Norifumi |e verfasserin |4 aut | |
| 700 | 1 | |a Fujimoto, Keiji |e verfasserin |4 aut | |
| 700 | 1 | |a Adachi, Hiroki |e verfasserin |4 aut | |
| 700 | 1 | |a Furuichi, Kengo |e verfasserin |4 aut | |
| 700 | 1 | |a Shimizu, Akira |e verfasserin |4 aut | |
| 700 | 1 | |a Yokoyama, Hitoshi |e verfasserin |4 aut | |
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10.1007/s13730-020-00562-x doi (DE-627)SPR043693784 (DE-599)SPRs13730-020-00562-x-e (SPR)s13730-020-00562-x-e DE-627 ger DE-627 rakwb eng 610 ASE Nomura, Kazutoshi verfasserin aut Steroid-sensitive recurrent mesangial proliferative glomerulonephritis with monoclonal IgG deposits 2021 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract Proliferative glomerulonephritis with monoclonal immunoglobulin G (IgG) deposits (PGNMID) is a rare kidney disease. The predominant pathological finding of PGNMID is the presence of monoclonal Ig deposits on the glomerular basement membrane (GBM). However, there is some variation in deposition pattern in this kidney disease. We report a case of steroid-sensitive recurrent mesangial proliferative type of PGNMID. A 40-year-old female noticed lower leg pitting edema and polyuria. Approximately 10 days prior to the first clinic visit, she was diagnosed with nephrotic syndrome based on the laboratory data of urine and blood. Immunological and hematological examination revealed no abnormality. However, kidney biopsy specimens showed mild mesangial cell proliferation and mesangial matrix accumulation on light microscopic findings. Regarding immunofluorescence staining, granular deposits of IgG, C1q, and β1c were observed on GBM and mesangial area. Granular deposits of IgG3 and λ were also observed on GBM and mesangial area. Moreover, negative results were obtained for the phospholipase A2 receptor antibody and thrombospondin type-1 domain-containing 7A. Electron microscopy revealed highly electron dense deposits mainly in the mesangial region. Kidney biopsy showed mesangial proliferative glomerulonephritis characterized by monoclonal Ig deposition of IgG3/λ. Steroid therapy was initiated, and complete remission was achieved on day 36. After the discontinuation of steroid therapy, proteinuria recurred and second kidney biopsy findings were almost similar to the first biopsy. However, complete remission was achieved with steroid therapy. This is a rare recurrent case of steroid-sensitive PGNMID. The pathological feature of this case was mesangial proliferative glomerulonephritis with Ig deposition of IgG3/λ. Proliferative glomerulonephritis with monoclonal immunoglobulin G deposits (PGNMID) (dpeaa)DE-He213 Steroid sensitive (dpeaa)DE-He213 Kidney biopsy (dpeaa)DE-He213 IgG3/λ (dpeaa)DE-He213 Miyatake, Nobuhiko verfasserin aut Okada, Keiichiro verfasserin aut Hayashi, Norifumi verfasserin aut Fujimoto, Keiji verfasserin aut Adachi, Hiroki verfasserin aut Furuichi, Kengo verfasserin aut Shimizu, Akira verfasserin aut Yokoyama, Hitoshi verfasserin aut Enthalten in CEN Case Reports Tokyo : Springer Japan, 2012 10(2021), 2 vom: 04. Jan., Seite 308-313 (DE-627)718611055 (DE-600)2660492-9 2192-4449 nnns volume:10 year:2021 number:2 day:04 month:01 pages:308-313 https://dx.doi.org/10.1007/s13730-020-00562-x lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_152 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_206 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2118 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4328 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4393 GBV_ILN_4700 AR 10 2021 2 04 01 308-313 |
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10.1007/s13730-020-00562-x doi (DE-627)SPR043693784 (DE-599)SPRs13730-020-00562-x-e (SPR)s13730-020-00562-x-e DE-627 ger DE-627 rakwb eng 610 ASE Nomura, Kazutoshi verfasserin aut Steroid-sensitive recurrent mesangial proliferative glomerulonephritis with monoclonal IgG deposits 2021 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract Proliferative glomerulonephritis with monoclonal immunoglobulin G (IgG) deposits (PGNMID) is a rare kidney disease. The predominant pathological finding of PGNMID is the presence of monoclonal Ig deposits on the glomerular basement membrane (GBM). However, there is some variation in deposition pattern in this kidney disease. We report a case of steroid-sensitive recurrent mesangial proliferative type of PGNMID. A 40-year-old female noticed lower leg pitting edema and polyuria. Approximately 10 days prior to the first clinic visit, she was diagnosed with nephrotic syndrome based on the laboratory data of urine and blood. Immunological and hematological examination revealed no abnormality. However, kidney biopsy specimens showed mild mesangial cell proliferation and mesangial matrix accumulation on light microscopic findings. Regarding immunofluorescence staining, granular deposits of IgG, C1q, and β1c were observed on GBM and mesangial area. Granular deposits of IgG3 and λ were also observed on GBM and mesangial area. Moreover, negative results were obtained for the phospholipase A2 receptor antibody and thrombospondin type-1 domain-containing 7A. Electron microscopy revealed highly electron dense deposits mainly in the mesangial region. Kidney biopsy showed mesangial proliferative glomerulonephritis characterized by monoclonal Ig deposition of IgG3/λ. Steroid therapy was initiated, and complete remission was achieved on day 36. After the discontinuation of steroid therapy, proteinuria recurred and second kidney biopsy findings were almost similar to the first biopsy. However, complete remission was achieved with steroid therapy. This is a rare recurrent case of steroid-sensitive PGNMID. The pathological feature of this case was mesangial proliferative glomerulonephritis with Ig deposition of IgG3/λ. Proliferative glomerulonephritis with monoclonal immunoglobulin G deposits (PGNMID) (dpeaa)DE-He213 Steroid sensitive (dpeaa)DE-He213 Kidney biopsy (dpeaa)DE-He213 IgG3/λ (dpeaa)DE-He213 Miyatake, Nobuhiko verfasserin aut Okada, Keiichiro verfasserin aut Hayashi, Norifumi verfasserin aut Fujimoto, Keiji verfasserin aut Adachi, Hiroki verfasserin aut Furuichi, Kengo verfasserin aut Shimizu, Akira verfasserin aut Yokoyama, Hitoshi verfasserin aut Enthalten in CEN Case Reports Tokyo : Springer Japan, 2012 10(2021), 2 vom: 04. Jan., Seite 308-313 (DE-627)718611055 (DE-600)2660492-9 2192-4449 nnns volume:10 year:2021 number:2 day:04 month:01 pages:308-313 https://dx.doi.org/10.1007/s13730-020-00562-x lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_152 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_206 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2118 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4328 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4393 GBV_ILN_4700 AR 10 2021 2 04 01 308-313 |
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10.1007/s13730-020-00562-x doi (DE-627)SPR043693784 (DE-599)SPRs13730-020-00562-x-e (SPR)s13730-020-00562-x-e DE-627 ger DE-627 rakwb eng 610 ASE Nomura, Kazutoshi verfasserin aut Steroid-sensitive recurrent mesangial proliferative glomerulonephritis with monoclonal IgG deposits 2021 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract Proliferative glomerulonephritis with monoclonal immunoglobulin G (IgG) deposits (PGNMID) is a rare kidney disease. The predominant pathological finding of PGNMID is the presence of monoclonal Ig deposits on the glomerular basement membrane (GBM). However, there is some variation in deposition pattern in this kidney disease. We report a case of steroid-sensitive recurrent mesangial proliferative type of PGNMID. A 40-year-old female noticed lower leg pitting edema and polyuria. Approximately 10 days prior to the first clinic visit, she was diagnosed with nephrotic syndrome based on the laboratory data of urine and blood. Immunological and hematological examination revealed no abnormality. However, kidney biopsy specimens showed mild mesangial cell proliferation and mesangial matrix accumulation on light microscopic findings. Regarding immunofluorescence staining, granular deposits of IgG, C1q, and β1c were observed on GBM and mesangial area. Granular deposits of IgG3 and λ were also observed on GBM and mesangial area. Moreover, negative results were obtained for the phospholipase A2 receptor antibody and thrombospondin type-1 domain-containing 7A. Electron microscopy revealed highly electron dense deposits mainly in the mesangial region. Kidney biopsy showed mesangial proliferative glomerulonephritis characterized by monoclonal Ig deposition of IgG3/λ. Steroid therapy was initiated, and complete remission was achieved on day 36. After the discontinuation of steroid therapy, proteinuria recurred and second kidney biopsy findings were almost similar to the first biopsy. However, complete remission was achieved with steroid therapy. This is a rare recurrent case of steroid-sensitive PGNMID. The pathological feature of this case was mesangial proliferative glomerulonephritis with Ig deposition of IgG3/λ. Proliferative glomerulonephritis with monoclonal immunoglobulin G deposits (PGNMID) (dpeaa)DE-He213 Steroid sensitive (dpeaa)DE-He213 Kidney biopsy (dpeaa)DE-He213 IgG3/λ (dpeaa)DE-He213 Miyatake, Nobuhiko verfasserin aut Okada, Keiichiro verfasserin aut Hayashi, Norifumi verfasserin aut Fujimoto, Keiji verfasserin aut Adachi, Hiroki verfasserin aut Furuichi, Kengo verfasserin aut Shimizu, Akira verfasserin aut Yokoyama, Hitoshi verfasserin aut Enthalten in CEN Case Reports Tokyo : Springer Japan, 2012 10(2021), 2 vom: 04. Jan., Seite 308-313 (DE-627)718611055 (DE-600)2660492-9 2192-4449 nnns volume:10 year:2021 number:2 day:04 month:01 pages:308-313 https://dx.doi.org/10.1007/s13730-020-00562-x lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_152 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_206 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2118 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4328 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4393 GBV_ILN_4700 AR 10 2021 2 04 01 308-313 |
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10.1007/s13730-020-00562-x doi (DE-627)SPR043693784 (DE-599)SPRs13730-020-00562-x-e (SPR)s13730-020-00562-x-e DE-627 ger DE-627 rakwb eng 610 ASE Nomura, Kazutoshi verfasserin aut Steroid-sensitive recurrent mesangial proliferative glomerulonephritis with monoclonal IgG deposits 2021 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract Proliferative glomerulonephritis with monoclonal immunoglobulin G (IgG) deposits (PGNMID) is a rare kidney disease. The predominant pathological finding of PGNMID is the presence of monoclonal Ig deposits on the glomerular basement membrane (GBM). However, there is some variation in deposition pattern in this kidney disease. We report a case of steroid-sensitive recurrent mesangial proliferative type of PGNMID. A 40-year-old female noticed lower leg pitting edema and polyuria. Approximately 10 days prior to the first clinic visit, she was diagnosed with nephrotic syndrome based on the laboratory data of urine and blood. Immunological and hematological examination revealed no abnormality. However, kidney biopsy specimens showed mild mesangial cell proliferation and mesangial matrix accumulation on light microscopic findings. Regarding immunofluorescence staining, granular deposits of IgG, C1q, and β1c were observed on GBM and mesangial area. Granular deposits of IgG3 and λ were also observed on GBM and mesangial area. Moreover, negative results were obtained for the phospholipase A2 receptor antibody and thrombospondin type-1 domain-containing 7A. Electron microscopy revealed highly electron dense deposits mainly in the mesangial region. Kidney biopsy showed mesangial proliferative glomerulonephritis characterized by monoclonal Ig deposition of IgG3/λ. Steroid therapy was initiated, and complete remission was achieved on day 36. After the discontinuation of steroid therapy, proteinuria recurred and second kidney biopsy findings were almost similar to the first biopsy. However, complete remission was achieved with steroid therapy. This is a rare recurrent case of steroid-sensitive PGNMID. The pathological feature of this case was mesangial proliferative glomerulonephritis with Ig deposition of IgG3/λ. Proliferative glomerulonephritis with monoclonal immunoglobulin G deposits (PGNMID) (dpeaa)DE-He213 Steroid sensitive (dpeaa)DE-He213 Kidney biopsy (dpeaa)DE-He213 IgG3/λ (dpeaa)DE-He213 Miyatake, Nobuhiko verfasserin aut Okada, Keiichiro verfasserin aut Hayashi, Norifumi verfasserin aut Fujimoto, Keiji verfasserin aut Adachi, Hiroki verfasserin aut Furuichi, Kengo verfasserin aut Shimizu, Akira verfasserin aut Yokoyama, Hitoshi verfasserin aut Enthalten in CEN Case Reports Tokyo : Springer Japan, 2012 10(2021), 2 vom: 04. Jan., Seite 308-313 (DE-627)718611055 (DE-600)2660492-9 2192-4449 nnns volume:10 year:2021 number:2 day:04 month:01 pages:308-313 https://dx.doi.org/10.1007/s13730-020-00562-x lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_152 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_206 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2118 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4328 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4393 GBV_ILN_4700 AR 10 2021 2 04 01 308-313 |
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10.1007/s13730-020-00562-x doi (DE-627)SPR043693784 (DE-599)SPRs13730-020-00562-x-e (SPR)s13730-020-00562-x-e DE-627 ger DE-627 rakwb eng 610 ASE Nomura, Kazutoshi verfasserin aut Steroid-sensitive recurrent mesangial proliferative glomerulonephritis with monoclonal IgG deposits 2021 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract Proliferative glomerulonephritis with monoclonal immunoglobulin G (IgG) deposits (PGNMID) is a rare kidney disease. The predominant pathological finding of PGNMID is the presence of monoclonal Ig deposits on the glomerular basement membrane (GBM). However, there is some variation in deposition pattern in this kidney disease. We report a case of steroid-sensitive recurrent mesangial proliferative type of PGNMID. A 40-year-old female noticed lower leg pitting edema and polyuria. Approximately 10 days prior to the first clinic visit, she was diagnosed with nephrotic syndrome based on the laboratory data of urine and blood. Immunological and hematological examination revealed no abnormality. However, kidney biopsy specimens showed mild mesangial cell proliferation and mesangial matrix accumulation on light microscopic findings. Regarding immunofluorescence staining, granular deposits of IgG, C1q, and β1c were observed on GBM and mesangial area. Granular deposits of IgG3 and λ were also observed on GBM and mesangial area. Moreover, negative results were obtained for the phospholipase A2 receptor antibody and thrombospondin type-1 domain-containing 7A. Electron microscopy revealed highly electron dense deposits mainly in the mesangial region. Kidney biopsy showed mesangial proliferative glomerulonephritis characterized by monoclonal Ig deposition of IgG3/λ. Steroid therapy was initiated, and complete remission was achieved on day 36. After the discontinuation of steroid therapy, proteinuria recurred and second kidney biopsy findings were almost similar to the first biopsy. However, complete remission was achieved with steroid therapy. This is a rare recurrent case of steroid-sensitive PGNMID. The pathological feature of this case was mesangial proliferative glomerulonephritis with Ig deposition of IgG3/λ. Proliferative glomerulonephritis with monoclonal immunoglobulin G deposits (PGNMID) (dpeaa)DE-He213 Steroid sensitive (dpeaa)DE-He213 Kidney biopsy (dpeaa)DE-He213 IgG3/λ (dpeaa)DE-He213 Miyatake, Nobuhiko verfasserin aut Okada, Keiichiro verfasserin aut Hayashi, Norifumi verfasserin aut Fujimoto, Keiji verfasserin aut Adachi, Hiroki verfasserin aut Furuichi, Kengo verfasserin aut Shimizu, Akira verfasserin aut Yokoyama, Hitoshi verfasserin aut Enthalten in CEN Case Reports Tokyo : Springer Japan, 2012 10(2021), 2 vom: 04. Jan., Seite 308-313 (DE-627)718611055 (DE-600)2660492-9 2192-4449 nnns volume:10 year:2021 number:2 day:04 month:01 pages:308-313 https://dx.doi.org/10.1007/s13730-020-00562-x lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_152 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_206 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2118 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4328 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4393 GBV_ILN_4700 AR 10 2021 2 04 01 308-313 |
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Enthalten in CEN Case Reports 10(2021), 2 vom: 04. Jan., Seite 308-313 volume:10 year:2021 number:2 day:04 month:01 pages:308-313 |
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Proliferative glomerulonephritis with monoclonal immunoglobulin G deposits (PGNMID) Steroid sensitive Kidney biopsy IgG3/λ |
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Nomura, Kazutoshi @@aut@@ Miyatake, Nobuhiko @@aut@@ Okada, Keiichiro @@aut@@ Hayashi, Norifumi @@aut@@ Fujimoto, Keiji @@aut@@ Adachi, Hiroki @@aut@@ Furuichi, Kengo @@aut@@ Shimizu, Akira @@aut@@ Yokoyama, Hitoshi @@aut@@ |
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The predominant pathological finding of PGNMID is the presence of monoclonal Ig deposits on the glomerular basement membrane (GBM). However, there is some variation in deposition pattern in this kidney disease. We report a case of steroid-sensitive recurrent mesangial proliferative type of PGNMID. A 40-year-old female noticed lower leg pitting edema and polyuria. Approximately 10 days prior to the first clinic visit, she was diagnosed with nephrotic syndrome based on the laboratory data of urine and blood. Immunological and hematological examination revealed no abnormality. However, kidney biopsy specimens showed mild mesangial cell proliferation and mesangial matrix accumulation on light microscopic findings. Regarding immunofluorescence staining, granular deposits of IgG, C1q, and β1c were observed on GBM and mesangial area. Granular deposits of IgG3 and λ were also observed on GBM and mesangial area. Moreover, negative results were obtained for the phospholipase A2 receptor antibody and thrombospondin type-1 domain-containing 7A. Electron microscopy revealed highly electron dense deposits mainly in the mesangial region. Kidney biopsy showed mesangial proliferative glomerulonephritis characterized by monoclonal Ig deposition of IgG3/λ. Steroid therapy was initiated, and complete remission was achieved on day 36. After the discontinuation of steroid therapy, proteinuria recurred and second kidney biopsy findings were almost similar to the first biopsy. However, complete remission was achieved with steroid therapy. This is a rare recurrent case of steroid-sensitive PGNMID. 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|
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Nomura, Kazutoshi |
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Nomura, Kazutoshi ddc 610 misc Proliferative glomerulonephritis with monoclonal immunoglobulin G deposits (PGNMID) misc Steroid sensitive misc Kidney biopsy misc IgG3/λ Steroid-sensitive recurrent mesangial proliferative glomerulonephritis with monoclonal IgG deposits |
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610 ASE Steroid-sensitive recurrent mesangial proliferative glomerulonephritis with monoclonal IgG deposits Proliferative glomerulonephritis with monoclonal immunoglobulin G deposits (PGNMID) (dpeaa)DE-He213 Steroid sensitive (dpeaa)DE-He213 Kidney biopsy (dpeaa)DE-He213 IgG3/λ (dpeaa)DE-He213 |
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ddc 610 misc Proliferative glomerulonephritis with monoclonal immunoglobulin G deposits (PGNMID) misc Steroid sensitive misc Kidney biopsy misc IgG3/λ |
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Nomura, Kazutoshi Miyatake, Nobuhiko Okada, Keiichiro Hayashi, Norifumi Fujimoto, Keiji Adachi, Hiroki Furuichi, Kengo Shimizu, Akira Yokoyama, Hitoshi |
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Nomura, Kazutoshi |
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steroid-sensitive recurrent mesangial proliferative glomerulonephritis with monoclonal igg deposits |
| title_auth |
Steroid-sensitive recurrent mesangial proliferative glomerulonephritis with monoclonal IgG deposits |
| abstract |
Abstract Proliferative glomerulonephritis with monoclonal immunoglobulin G (IgG) deposits (PGNMID) is a rare kidney disease. The predominant pathological finding of PGNMID is the presence of monoclonal Ig deposits on the glomerular basement membrane (GBM). However, there is some variation in deposition pattern in this kidney disease. We report a case of steroid-sensitive recurrent mesangial proliferative type of PGNMID. A 40-year-old female noticed lower leg pitting edema and polyuria. Approximately 10 days prior to the first clinic visit, she was diagnosed with nephrotic syndrome based on the laboratory data of urine and blood. Immunological and hematological examination revealed no abnormality. However, kidney biopsy specimens showed mild mesangial cell proliferation and mesangial matrix accumulation on light microscopic findings. Regarding immunofluorescence staining, granular deposits of IgG, C1q, and β1c were observed on GBM and mesangial area. Granular deposits of IgG3 and λ were also observed on GBM and mesangial area. Moreover, negative results were obtained for the phospholipase A2 receptor antibody and thrombospondin type-1 domain-containing 7A. Electron microscopy revealed highly electron dense deposits mainly in the mesangial region. Kidney biopsy showed mesangial proliferative glomerulonephritis characterized by monoclonal Ig deposition of IgG3/λ. Steroid therapy was initiated, and complete remission was achieved on day 36. After the discontinuation of steroid therapy, proteinuria recurred and second kidney biopsy findings were almost similar to the first biopsy. However, complete remission was achieved with steroid therapy. This is a rare recurrent case of steroid-sensitive PGNMID. The pathological feature of this case was mesangial proliferative glomerulonephritis with Ig deposition of IgG3/λ. |
| abstractGer |
Abstract Proliferative glomerulonephritis with monoclonal immunoglobulin G (IgG) deposits (PGNMID) is a rare kidney disease. The predominant pathological finding of PGNMID is the presence of monoclonal Ig deposits on the glomerular basement membrane (GBM). However, there is some variation in deposition pattern in this kidney disease. We report a case of steroid-sensitive recurrent mesangial proliferative type of PGNMID. A 40-year-old female noticed lower leg pitting edema and polyuria. Approximately 10 days prior to the first clinic visit, she was diagnosed with nephrotic syndrome based on the laboratory data of urine and blood. Immunological and hematological examination revealed no abnormality. However, kidney biopsy specimens showed mild mesangial cell proliferation and mesangial matrix accumulation on light microscopic findings. Regarding immunofluorescence staining, granular deposits of IgG, C1q, and β1c were observed on GBM and mesangial area. Granular deposits of IgG3 and λ were also observed on GBM and mesangial area. Moreover, negative results were obtained for the phospholipase A2 receptor antibody and thrombospondin type-1 domain-containing 7A. Electron microscopy revealed highly electron dense deposits mainly in the mesangial region. Kidney biopsy showed mesangial proliferative glomerulonephritis characterized by monoclonal Ig deposition of IgG3/λ. Steroid therapy was initiated, and complete remission was achieved on day 36. After the discontinuation of steroid therapy, proteinuria recurred and second kidney biopsy findings were almost similar to the first biopsy. However, complete remission was achieved with steroid therapy. This is a rare recurrent case of steroid-sensitive PGNMID. The pathological feature of this case was mesangial proliferative glomerulonephritis with Ig deposition of IgG3/λ. |
| abstract_unstemmed |
Abstract Proliferative glomerulonephritis with monoclonal immunoglobulin G (IgG) deposits (PGNMID) is a rare kidney disease. The predominant pathological finding of PGNMID is the presence of monoclonal Ig deposits on the glomerular basement membrane (GBM). However, there is some variation in deposition pattern in this kidney disease. We report a case of steroid-sensitive recurrent mesangial proliferative type of PGNMID. A 40-year-old female noticed lower leg pitting edema and polyuria. Approximately 10 days prior to the first clinic visit, she was diagnosed with nephrotic syndrome based on the laboratory data of urine and blood. Immunological and hematological examination revealed no abnormality. However, kidney biopsy specimens showed mild mesangial cell proliferation and mesangial matrix accumulation on light microscopic findings. Regarding immunofluorescence staining, granular deposits of IgG, C1q, and β1c were observed on GBM and mesangial area. Granular deposits of IgG3 and λ were also observed on GBM and mesangial area. Moreover, negative results were obtained for the phospholipase A2 receptor antibody and thrombospondin type-1 domain-containing 7A. Electron microscopy revealed highly electron dense deposits mainly in the mesangial region. Kidney biopsy showed mesangial proliferative glomerulonephritis characterized by monoclonal Ig deposition of IgG3/λ. Steroid therapy was initiated, and complete remission was achieved on day 36. After the discontinuation of steroid therapy, proteinuria recurred and second kidney biopsy findings were almost similar to the first biopsy. However, complete remission was achieved with steroid therapy. This is a rare recurrent case of steroid-sensitive PGNMID. The pathological feature of this case was mesangial proliferative glomerulonephritis with Ig deposition of IgG3/λ. |
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Steroid-sensitive recurrent mesangial proliferative glomerulonephritis with monoclonal IgG deposits |
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| score |
7.4015245 |