A case of acute poststreptococcal glomerulonephritis complicated by interstitial nephritis related to streptococcal pyrogenic exotoxin B
This paper presents the case of a patient who developed acute kidney injury and nephrotic syndrome following streptococcal cutaneous infection. He presented with microhematuria, severe proteinuria and systemic edema 5 days after infection. Blood examination showed elevated creatinine level, hypocomp...
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| Veröffentlicht in: | Pathology international 2022-03, Vol.72 (3), p.200-206 |
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| creator | Kanazawa, Nobuhiro Iyoda, Masayuki Hayashi, Junichi Honda, Kazuho Oda, Takashi Honda, Hirokazu |
| description | This paper presents the case of a patient who developed acute kidney injury and nephrotic syndrome following streptococcal cutaneous infection. He presented with microhematuria, severe proteinuria and systemic edema 5 days after infection. Blood examination showed elevated creatinine level, hypocomplementemia, and elevated anti‐streptolysin O level. Renal biopsy revealed endocapillary proliferative glomerulonephritis with tubulointerstitial nephritis (TIN). Immunofluorescence revealed C3‐dominant glomerular staining, while electron microscopy showed hump‐shaped subepithelial deposits. The patient was therefore diagnosed with poststreptococcal glomerulonephritis. The unique histological feature was C3 deposition in the tubular basement membrane (TBM), in which we detected streptococcal pyrogenic exotoxin B (SpeB), a nephritogenic antigen produced by streptococci. No nephritis‐associated plasmin receptor or plasmin activity was evident in the TBM. These nephritogenic antigens and upregulation of plasmin activity were observed in glomeruli. This case suggests that TIN after poststreptococcal infection might be partially attributable to SpeB toxicity. |
| doi_str_mv | 10.1111/pin.13203 |
| format | Article |
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He presented with microhematuria, severe proteinuria and systemic edema 5 days after infection. Blood examination showed elevated creatinine level, hypocomplementemia, and elevated anti‐streptolysin O level. Renal biopsy revealed endocapillary proliferative glomerulonephritis with tubulointerstitial nephritis (TIN). Immunofluorescence revealed C3‐dominant glomerular staining, while electron microscopy showed hump‐shaped subepithelial deposits. The patient was therefore diagnosed with poststreptococcal glomerulonephritis. The unique histological feature was C3 deposition in the tubular basement membrane (TBM), in which we detected streptococcal pyrogenic exotoxin B (SpeB), a nephritogenic antigen produced by streptococci. No nephritis‐associated plasmin receptor or plasmin activity was evident in the TBM. These nephritogenic antigens and upregulation of plasmin activity were observed in glomeruli. This case suggests that TIN after poststreptococcal infection might be partially attributable to SpeB toxicity.</description><identifier>ISSN: 1320-5463</identifier><identifier>EISSN: 1440-1827</identifier><identifier>DOI: 10.1111/pin.13203</identifier><identifier>PMID: 35147256</identifier><language>eng</language><publisher>Australia: Wiley Subscription Services, Inc</publisher><subject>Acute Kidney Injury - etiology ; Adult ; Antigens ; Bacterial Proteins - adverse effects ; Bacterial Proteins - metabolism ; Biopsy ; Creatinine ; Edema ; Electron microscopy ; Exotoxins ; Exotoxins - adverse effects ; Exotoxins - metabolism ; Glomerulonephritis - etiology ; Glomerulonephritis - physiopathology ; Humans ; Hypocomplementemia ; Immunofluorescence ; Infections ; Male ; Nephritis ; Nephritis, Interstitial - etiology ; Nephritis, Interstitial - physiopathology ; nephritis‐associated plasmin receptor ; Nephrotic syndrome ; Nephrotic Syndrome - etiology ; Plasmin ; Poststreptococcal glomerulonephritis ; Proliferative kidney disease ; Proteinuria ; Streptococcal Infections - complications ; Streptococcal Infections - pathology ; streptococcal pyrogenic exotoxin B ; Streptococcus ; Toxicity ; Tubular basement membrane ; tubulointerstitial nephritis</subject><ispartof>Pathology international, 2022-03, Vol.72 (3), p.200-206</ispartof><rights>2022 Japanese Society of Pathology and John Wiley & Sons Australia, Ltd</rights><rights>2022 Japanese Society of Pathology and John Wiley & Sons Australia, Ltd.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c4103-b7a38549046c4f8a88a7bec5a56ab6b7205d157af0ef545ed2774ddeade923283</citedby><cites>FETCH-LOGICAL-c4103-b7a38549046c4f8a88a7bec5a56ab6b7205d157af0ef545ed2774ddeade923283</cites><orcidid>0000-0001-6111-8027</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1111%2Fpin.13203$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1111%2Fpin.13203$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>314,776,780,1411,27901,27902,45550,45551</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/35147256$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Kanazawa, Nobuhiro</creatorcontrib><creatorcontrib>Iyoda, Masayuki</creatorcontrib><creatorcontrib>Hayashi, Junichi</creatorcontrib><creatorcontrib>Honda, Kazuho</creatorcontrib><creatorcontrib>Oda, Takashi</creatorcontrib><creatorcontrib>Honda, Hirokazu</creatorcontrib><title>A case of acute poststreptococcal glomerulonephritis complicated by interstitial nephritis related to streptococcal pyrogenic exotoxin B</title><title>Pathology international</title><addtitle>Pathol Int</addtitle><description>This paper presents the case of a patient who developed acute kidney injury and nephrotic syndrome following streptococcal cutaneous infection. He presented with microhematuria, severe proteinuria and systemic edema 5 days after infection. Blood examination showed elevated creatinine level, hypocomplementemia, and elevated anti‐streptolysin O level. Renal biopsy revealed endocapillary proliferative glomerulonephritis with tubulointerstitial nephritis (TIN). Immunofluorescence revealed C3‐dominant glomerular staining, while electron microscopy showed hump‐shaped subepithelial deposits. The patient was therefore diagnosed with poststreptococcal glomerulonephritis. The unique histological feature was C3 deposition in the tubular basement membrane (TBM), in which we detected streptococcal pyrogenic exotoxin B (SpeB), a nephritogenic antigen produced by streptococci. No nephritis‐associated plasmin receptor or plasmin activity was evident in the TBM. These nephritogenic antigens and upregulation of plasmin activity were observed in glomeruli. This case suggests that TIN after poststreptococcal infection might be partially attributable to SpeB toxicity.</description><subject>Acute Kidney Injury - etiology</subject><subject>Adult</subject><subject>Antigens</subject><subject>Bacterial Proteins - adverse effects</subject><subject>Bacterial Proteins - metabolism</subject><subject>Biopsy</subject><subject>Creatinine</subject><subject>Edema</subject><subject>Electron microscopy</subject><subject>Exotoxins</subject><subject>Exotoxins - adverse effects</subject><subject>Exotoxins - metabolism</subject><subject>Glomerulonephritis - etiology</subject><subject>Glomerulonephritis - physiopathology</subject><subject>Humans</subject><subject>Hypocomplementemia</subject><subject>Immunofluorescence</subject><subject>Infections</subject><subject>Male</subject><subject>Nephritis</subject><subject>Nephritis, Interstitial - etiology</subject><subject>Nephritis, Interstitial - physiopathology</subject><subject>nephritis‐associated plasmin receptor</subject><subject>Nephrotic syndrome</subject><subject>Nephrotic Syndrome - etiology</subject><subject>Plasmin</subject><subject>Poststreptococcal glomerulonephritis</subject><subject>Proliferative kidney disease</subject><subject>Proteinuria</subject><subject>Streptococcal Infections - complications</subject><subject>Streptococcal Infections - pathology</subject><subject>streptococcal pyrogenic exotoxin B</subject><subject>Streptococcus</subject><subject>Toxicity</subject><subject>Tubular basement membrane</subject><subject>tubulointerstitial nephritis</subject><issn>1320-5463</issn><issn>1440-1827</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2022</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp1kE1LxDAQhoMofh_8AxLw5KGaNEnTHtfFj4VFPei5pOlUI21TkxR3_4E_2-iuigfnMsPMwzPwInREyRmNdT6Y_oyylLANtEs5JwnNU7kZ57hLBM_YDtrz_oUQKllGttEOE5TLVGS76H2CtfKAbYOVHgPgwfrgg4MhWG21Vi1-am0HbmxtD8OzM8F4rG03tEarADWultj0AZwP8RTxX8pB-0UEi_8ah6WzT9AbjWFhg12YHl8coK1GtR4O130fPV5dPkxvkvnd9Ww6mSeaU8KSSiqWC14Qnmne5CrPlaxACyUyVWWVTImoqZCqIdAILqBOpeR1DaqGImVpzvbRyco7OPs6gg_lix1dH1-WacZkwQqeyUidrijtrPcOmnJwplNuWVJSfmZexszLr8wje7w2jlUH9Q_5HXIEzlfAm2lh-b-pvJ_drpQfFNGPEg</recordid><startdate>202203</startdate><enddate>202203</enddate><creator>Kanazawa, Nobuhiro</creator><creator>Iyoda, Masayuki</creator><creator>Hayashi, Junichi</creator><creator>Honda, Kazuho</creator><creator>Oda, Takashi</creator><creator>Honda, Hirokazu</creator><general>Wiley Subscription Services, Inc</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7QO</scope><scope>7T5</scope><scope>7TO</scope><scope>7U9</scope><scope>8FD</scope><scope>FR3</scope><scope>H94</scope><scope>P64</scope><scope>RC3</scope><orcidid>https://orcid.org/0000-0001-6111-8027</orcidid></search><sort><creationdate>202203</creationdate><title>A case of acute poststreptococcal glomerulonephritis complicated by interstitial nephritis related to streptococcal pyrogenic exotoxin B</title><author>Kanazawa, Nobuhiro ; Iyoda, Masayuki ; Hayashi, Junichi ; Honda, Kazuho ; Oda, Takashi ; Honda, Hirokazu</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4103-b7a38549046c4f8a88a7bec5a56ab6b7205d157af0ef545ed2774ddeade923283</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2022</creationdate><topic>Acute Kidney Injury - etiology</topic><topic>Adult</topic><topic>Antigens</topic><topic>Bacterial Proteins - adverse effects</topic><topic>Bacterial Proteins - metabolism</topic><topic>Biopsy</topic><topic>Creatinine</topic><topic>Edema</topic><topic>Electron microscopy</topic><topic>Exotoxins</topic><topic>Exotoxins - adverse effects</topic><topic>Exotoxins - metabolism</topic><topic>Glomerulonephritis - etiology</topic><topic>Glomerulonephritis - physiopathology</topic><topic>Humans</topic><topic>Hypocomplementemia</topic><topic>Immunofluorescence</topic><topic>Infections</topic><topic>Male</topic><topic>Nephritis</topic><topic>Nephritis, Interstitial - etiology</topic><topic>Nephritis, Interstitial - physiopathology</topic><topic>nephritis‐associated plasmin receptor</topic><topic>Nephrotic syndrome</topic><topic>Nephrotic Syndrome - etiology</topic><topic>Plasmin</topic><topic>Poststreptococcal glomerulonephritis</topic><topic>Proliferative kidney disease</topic><topic>Proteinuria</topic><topic>Streptococcal Infections - complications</topic><topic>Streptococcal Infections - pathology</topic><topic>streptococcal pyrogenic exotoxin B</topic><topic>Streptococcus</topic><topic>Toxicity</topic><topic>Tubular basement membrane</topic><topic>tubulointerstitial nephritis</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Kanazawa, Nobuhiro</creatorcontrib><creatorcontrib>Iyoda, Masayuki</creatorcontrib><creatorcontrib>Hayashi, Junichi</creatorcontrib><creatorcontrib>Honda, Kazuho</creatorcontrib><creatorcontrib>Oda, Takashi</creatorcontrib><creatorcontrib>Honda, Hirokazu</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Biotechnology Research Abstracts</collection><collection>Immunology Abstracts</collection><collection>Oncogenes and Growth Factors Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>Technology Research Database</collection><collection>Engineering Research Database</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Genetics Abstracts</collection><jtitle>Pathology international</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Kanazawa, Nobuhiro</au><au>Iyoda, Masayuki</au><au>Hayashi, Junichi</au><au>Honda, Kazuho</au><au>Oda, Takashi</au><au>Honda, Hirokazu</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>A case of acute poststreptococcal glomerulonephritis complicated by interstitial nephritis related to streptococcal pyrogenic exotoxin B</atitle><jtitle>Pathology international</jtitle><addtitle>Pathol Int</addtitle><date>2022-03</date><risdate>2022</risdate><volume>72</volume><issue>3</issue><spage>200</spage><epage>206</epage><pages>200-206</pages><issn>1320-5463</issn><eissn>1440-1827</eissn><abstract>This paper presents the case of a patient who developed acute kidney injury and nephrotic syndrome following streptococcal cutaneous infection. He presented with microhematuria, severe proteinuria and systemic edema 5 days after infection. Blood examination showed elevated creatinine level, hypocomplementemia, and elevated anti‐streptolysin O level. Renal biopsy revealed endocapillary proliferative glomerulonephritis with tubulointerstitial nephritis (TIN). Immunofluorescence revealed C3‐dominant glomerular staining, while electron microscopy showed hump‐shaped subepithelial deposits. The patient was therefore diagnosed with poststreptococcal glomerulonephritis. The unique histological feature was C3 deposition in the tubular basement membrane (TBM), in which we detected streptococcal pyrogenic exotoxin B (SpeB), a nephritogenic antigen produced by streptococci. No nephritis‐associated plasmin receptor or plasmin activity was evident in the TBM. These nephritogenic antigens and upregulation of plasmin activity were observed in glomeruli. This case suggests that TIN after poststreptococcal infection might be partially attributable to SpeB toxicity.</abstract><cop>Australia</cop><pub>Wiley Subscription Services, Inc</pub><pmid>35147256</pmid><doi>10.1111/pin.13203</doi><tpages>7</tpages><orcidid>https://orcid.org/0000-0001-6111-8027</orcidid></addata></record> |
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| subjects | Acute Kidney Injury - etiology Adult Antigens Bacterial Proteins - adverse effects Bacterial Proteins - metabolism Biopsy Creatinine Edema Electron microscopy Exotoxins Exotoxins - adverse effects Exotoxins - metabolism Glomerulonephritis - etiology Glomerulonephritis - physiopathology Humans Hypocomplementemia Immunofluorescence Infections Male Nephritis Nephritis, Interstitial - etiology Nephritis, Interstitial - physiopathology nephritis‐associated plasmin receptor Nephrotic syndrome Nephrotic Syndrome - etiology Plasmin Poststreptococcal glomerulonephritis Proliferative kidney disease Proteinuria Streptococcal Infections - complications Streptococcal Infections - pathology streptococcal pyrogenic exotoxin B Streptococcus Toxicity Tubular basement membrane tubulointerstitial nephritis |
| title | A case of acute poststreptococcal glomerulonephritis complicated by interstitial nephritis related to streptococcal pyrogenic exotoxin B |
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