Endothelial cell injury in acute and chronic glomerular lesions in patients with IgA nephropathy
Summary Endothelial cell injury may contribute to the progression of various glomerular diseases. In the present study, we examined glomerular capillary injury in acute and chronic glomerular lesions in patients with Immunoglobulin A nephropathy (IgAN). We selected renal biopsy samples of IgAN (n =...
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| Veröffentlicht in: | Human pathology 2016-03, Vol.49, p.135-144 |
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| creator | Kusano, Taiko, MD Takano, Hideki, MD, PhD Kang, Dedong, PhD Nagahama, Kiyotaka, MD, PhD Aoki, Michiko, MD Morita, Megumi, MD, PhD Kaneko, Tomohiro, MD, PhD Tsuruoka, Shuichi, MD, PhD Shimizu, Akira, MD, PhD |
| description | Summary Endothelial cell injury may contribute to the progression of various glomerular diseases. In the present study, we examined glomerular capillary injury in acute and chronic glomerular lesions in patients with Immunoglobulin A nephropathy (IgAN). We selected renal biopsy samples of IgAN (n = 200), and glomerular capillary injury in the acute and chronic glomerular lesions was assessed using immunohistochemistry for CD34 and electron microscopy. We examined the correlations between acute and chronic glomerular lesions and proteinuria, hematuria, and the renal function. The injured glomerular capillaries in the acute glomerular lesions were characterized morphologically by the separation of CD34+ endothelial cells from the glomerular basement membrane and the loss of glomerular endothelial cells and capillaries, together with inflammatory cell infiltration, fibrin exudation, rupture of the glomerular basement membrane, and/or crescent formation. In addition, the injured capillaries in the chronic glomerular lesions were characterized by the loss of CD34+ glomerular endothelial cells and capillaries exhibiting segmental and global glomerular sclerosis with or without fibrous crescents. In the acute glomerular lesions, the presence of endocapillary hypercellularity, fibrinoid necrosis, and cellular and fibrocellular crescents correlated significantly with hematuria, with or without proteinuria. In the chronic glomerular lesions, a significant relationship was evident between segmental or global sclerosis and proteinuria and/or the serum creatinine level. In conclusion, injuries of glomerular capillaries and the loss of endothelial cells occurred in the acute and chronic glomerular lesions in IgAN and may contribute to the development of hematuria, proteinuria, and renal dysfunction. |
| doi_str_mv | 10.1016/j.humpath.2015.10.013 |
| format | Article |
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In the present study, we examined glomerular capillary injury in acute and chronic glomerular lesions in patients with Immunoglobulin A nephropathy (IgAN). We selected renal biopsy samples of IgAN (n = 200), and glomerular capillary injury in the acute and chronic glomerular lesions was assessed using immunohistochemistry for CD34 and electron microscopy. We examined the correlations between acute and chronic glomerular lesions and proteinuria, hematuria, and the renal function. The injured glomerular capillaries in the acute glomerular lesions were characterized morphologically by the separation of CD34+ endothelial cells from the glomerular basement membrane and the loss of glomerular endothelial cells and capillaries, together with inflammatory cell infiltration, fibrin exudation, rupture of the glomerular basement membrane, and/or crescent formation. In addition, the injured capillaries in the chronic glomerular lesions were characterized by the loss of CD34+ glomerular endothelial cells and capillaries exhibiting segmental and global glomerular sclerosis with or without fibrous crescents. In the acute glomerular lesions, the presence of endocapillary hypercellularity, fibrinoid necrosis, and cellular and fibrocellular crescents correlated significantly with hematuria, with or without proteinuria. In the chronic glomerular lesions, a significant relationship was evident between segmental or global sclerosis and proteinuria and/or the serum creatinine level. In conclusion, injuries of glomerular capillaries and the loss of endothelial cells occurred in the acute and chronic glomerular lesions in IgAN and may contribute to the development of hematuria, proteinuria, and renal dysfunction.</description><identifier>ISSN: 0046-8177</identifier><identifier>EISSN: 1532-8392</identifier><identifier>DOI: 10.1016/j.humpath.2015.10.013</identifier><identifier>PMID: 26826420</identifier><language>eng</language><publisher>United States: Elsevier Inc</publisher><subject>Acute Disease ; Acute glomerular lesion ; Adolescent ; Adult ; Aged ; Antigens, CD34 - analysis ; Biomarkers - analysis ; Biopsy ; Blood ; Capillaries - chemistry ; Capillaries - pathology ; Capillaries - ultrastructure ; CD34 ; Child ; Child, Preschool ; Chronic Disease ; Chronic glomerular lesion ; Classification ; Endothelial cell injury ; Endothelial Cells - chemistry ; Endothelial Cells - pathology ; Endothelial Cells - ultrastructure ; Female ; Gangrene ; Glomerular capillary injury ; Glomerulonephritis - metabolism ; Glomerulonephritis - pathology ; Glomerulonephritis, IGA - metabolism ; Glomerulonephritis, IGA - pathology ; Humans ; IgA nephropathy ; Immunohistochemistry ; Kidney Glomerulus - blood supply ; Kidneys ; Male ; Microscopy, Electron ; Middle Aged ; Nephrology ; Pathology ; Retrospective Studies ; Rodents ; Statistical analysis ; Variance analysis ; Young Adult</subject><ispartof>Human pathology, 2016-03, Vol.49, p.135-144</ispartof><rights>Elsevier Inc.</rights><rights>2015 Elsevier Inc.</rights><rights>Copyright © 2015 Elsevier Inc. All rights reserved.</rights><rights>Copyright Elsevier Limited Mar 2016</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c481t-fdfb09fc9a6afac6e79a1abd614d30274b2a6a2bf22d2cdeb3723fda816f87b13</citedby><cites>FETCH-LOGICAL-c481t-fdfb09fc9a6afac6e79a1abd614d30274b2a6a2bf22d2cdeb3723fda816f87b13</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1016/j.humpath.2015.10.013$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,780,784,3548,27923,27924,45994</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/26826420$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Kusano, Taiko, MD</creatorcontrib><creatorcontrib>Takano, Hideki, MD, PhD</creatorcontrib><creatorcontrib>Kang, Dedong, PhD</creatorcontrib><creatorcontrib>Nagahama, Kiyotaka, MD, PhD</creatorcontrib><creatorcontrib>Aoki, Michiko, MD</creatorcontrib><creatorcontrib>Morita, Megumi, MD, PhD</creatorcontrib><creatorcontrib>Kaneko, Tomohiro, MD, PhD</creatorcontrib><creatorcontrib>Tsuruoka, Shuichi, MD, PhD</creatorcontrib><creatorcontrib>Shimizu, Akira, MD, PhD</creatorcontrib><title>Endothelial cell injury in acute and chronic glomerular lesions in patients with IgA nephropathy</title><title>Human pathology</title><addtitle>Hum Pathol</addtitle><description>Summary Endothelial cell injury may contribute to the progression of various glomerular diseases. In the present study, we examined glomerular capillary injury in acute and chronic glomerular lesions in patients with Immunoglobulin A nephropathy (IgAN). We selected renal biopsy samples of IgAN (n = 200), and glomerular capillary injury in the acute and chronic glomerular lesions was assessed using immunohistochemistry for CD34 and electron microscopy. We examined the correlations between acute and chronic glomerular lesions and proteinuria, hematuria, and the renal function. The injured glomerular capillaries in the acute glomerular lesions were characterized morphologically by the separation of CD34+ endothelial cells from the glomerular basement membrane and the loss of glomerular endothelial cells and capillaries, together with inflammatory cell infiltration, fibrin exudation, rupture of the glomerular basement membrane, and/or crescent formation. In addition, the injured capillaries in the chronic glomerular lesions were characterized by the loss of CD34+ glomerular endothelial cells and capillaries exhibiting segmental and global glomerular sclerosis with or without fibrous crescents. In the acute glomerular lesions, the presence of endocapillary hypercellularity, fibrinoid necrosis, and cellular and fibrocellular crescents correlated significantly with hematuria, with or without proteinuria. In the chronic glomerular lesions, a significant relationship was evident between segmental or global sclerosis and proteinuria and/or the serum creatinine level. In conclusion, injuries of glomerular capillaries and the loss of endothelial cells occurred in the acute and chronic glomerular lesions in IgAN and may contribute to the development of hematuria, proteinuria, and renal dysfunction.</description><subject>Acute Disease</subject><subject>Acute glomerular lesion</subject><subject>Adolescent</subject><subject>Adult</subject><subject>Aged</subject><subject>Antigens, CD34 - analysis</subject><subject>Biomarkers - analysis</subject><subject>Biopsy</subject><subject>Blood</subject><subject>Capillaries - chemistry</subject><subject>Capillaries - pathology</subject><subject>Capillaries - ultrastructure</subject><subject>CD34</subject><subject>Child</subject><subject>Child, Preschool</subject><subject>Chronic Disease</subject><subject>Chronic glomerular lesion</subject><subject>Classification</subject><subject>Endothelial cell injury</subject><subject>Endothelial Cells - chemistry</subject><subject>Endothelial Cells - pathology</subject><subject>Endothelial Cells - ultrastructure</subject><subject>Female</subject><subject>Gangrene</subject><subject>Glomerular capillary injury</subject><subject>Glomerulonephritis - metabolism</subject><subject>Glomerulonephritis - pathology</subject><subject>Glomerulonephritis, IGA - metabolism</subject><subject>Glomerulonephritis, IGA - pathology</subject><subject>Humans</subject><subject>IgA nephropathy</subject><subject>Immunohistochemistry</subject><subject>Kidney Glomerulus - blood supply</subject><subject>Kidneys</subject><subject>Male</subject><subject>Microscopy, Electron</subject><subject>Middle Aged</subject><subject>Nephrology</subject><subject>Pathology</subject><subject>Retrospective Studies</subject><subject>Rodents</subject><subject>Statistical analysis</subject><subject>Variance analysis</subject><subject>Young Adult</subject><issn>0046-8177</issn><issn>1532-8392</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2016</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkk1v1DAQhi0EotvCTwBZ4sIli8d2vi6gqmqhUiUOwNk49qRx8CaLnYD232NrF5B66Wms8TOf7xDyCtgWGFTvxu2w7vZ6GbacQZl8WwbiCdlAKXjRiJY_JRvGZFU0UNdn5DzGkTGAUpbPyRmvGl5Jzjbk-_Vk52VA77SnBr2nbhrXcEiGarMuSPVkqRnCPDlD7_28w7B6HajH6OYpZi514XBaIv3tloHe3l_SCfcpInd3eEGe9dpHfHmyF-TbzfXXq0_F3eePt1eXd4WRDSxFb_uOtb1pdaV7bSqsWw26sxVIKxivZcfTD-96zi03FjtRc9Fb3UDVN3UH4oK8Pebdh_nninFROxfzQHrCeY0KmrKVDW-BP47WFdSC1cAS-uYBOs5rmNIgmeISpGhz7fJImTDHGLBX--B2OhwUMJXVUqM6qaWyWtmd1Epxr0_Z126H9l_UX3kS8OEIYNrcL4dBRZNWbdC6gGZRdnaPlnj_IIPxLkmp_Q88YPw_jYpcMfUln0y-GCjTS4pG_AFrHb47</recordid><startdate>20160301</startdate><enddate>20160301</enddate><creator>Kusano, Taiko, MD</creator><creator>Takano, Hideki, MD, PhD</creator><creator>Kang, Dedong, PhD</creator><creator>Nagahama, Kiyotaka, MD, PhD</creator><creator>Aoki, Michiko, MD</creator><creator>Morita, Megumi, MD, PhD</creator><creator>Kaneko, Tomohiro, MD, PhD</creator><creator>Tsuruoka, Shuichi, MD, PhD</creator><creator>Shimizu, Akira, MD, PhD</creator><general>Elsevier Inc</general><general>Elsevier Limited</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>K9.</scope><scope>7X8</scope><scope>7U7</scope><scope>C1K</scope></search><sort><creationdate>20160301</creationdate><title>Endothelial cell injury in acute and chronic glomerular lesions in patients with IgA nephropathy</title><author>Kusano, Taiko, MD ; Takano, Hideki, MD, PhD ; Kang, Dedong, PhD ; Nagahama, Kiyotaka, MD, PhD ; Aoki, Michiko, MD ; Morita, Megumi, MD, PhD ; Kaneko, Tomohiro, MD, PhD ; Tsuruoka, Shuichi, MD, PhD ; Shimizu, Akira, MD, PhD</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c481t-fdfb09fc9a6afac6e79a1abd614d30274b2a6a2bf22d2cdeb3723fda816f87b13</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2016</creationdate><topic>Acute Disease</topic><topic>Acute glomerular lesion</topic><topic>Adolescent</topic><topic>Adult</topic><topic>Aged</topic><topic>Antigens, CD34 - analysis</topic><topic>Biomarkers - analysis</topic><topic>Biopsy</topic><topic>Blood</topic><topic>Capillaries - chemistry</topic><topic>Capillaries - pathology</topic><topic>Capillaries - ultrastructure</topic><topic>CD34</topic><topic>Child</topic><topic>Child, Preschool</topic><topic>Chronic Disease</topic><topic>Chronic glomerular lesion</topic><topic>Classification</topic><topic>Endothelial cell injury</topic><topic>Endothelial Cells - chemistry</topic><topic>Endothelial Cells - pathology</topic><topic>Endothelial Cells - ultrastructure</topic><topic>Female</topic><topic>Gangrene</topic><topic>Glomerular capillary injury</topic><topic>Glomerulonephritis - metabolism</topic><topic>Glomerulonephritis - pathology</topic><topic>Glomerulonephritis, IGA - metabolism</topic><topic>Glomerulonephritis, IGA - pathology</topic><topic>Humans</topic><topic>IgA nephropathy</topic><topic>Immunohistochemistry</topic><topic>Kidney Glomerulus - blood supply</topic><topic>Kidneys</topic><topic>Male</topic><topic>Microscopy, Electron</topic><topic>Middle Aged</topic><topic>Nephrology</topic><topic>Pathology</topic><topic>Retrospective Studies</topic><topic>Rodents</topic><topic>Statistical analysis</topic><topic>Variance analysis</topic><topic>Young Adult</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Kusano, Taiko, MD</creatorcontrib><creatorcontrib>Takano, Hideki, MD, PhD</creatorcontrib><creatorcontrib>Kang, Dedong, PhD</creatorcontrib><creatorcontrib>Nagahama, Kiyotaka, MD, PhD</creatorcontrib><creatorcontrib>Aoki, Michiko, MD</creatorcontrib><creatorcontrib>Morita, Megumi, MD, PhD</creatorcontrib><creatorcontrib>Kaneko, Tomohiro, MD, PhD</creatorcontrib><creatorcontrib>Tsuruoka, Shuichi, MD, PhD</creatorcontrib><creatorcontrib>Shimizu, Akira, MD, PhD</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>MEDLINE - Academic</collection><collection>Toxicology Abstracts</collection><collection>Environmental Sciences and Pollution Management</collection><jtitle>Human pathology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Kusano, Taiko, MD</au><au>Takano, Hideki, MD, PhD</au><au>Kang, Dedong, PhD</au><au>Nagahama, Kiyotaka, MD, PhD</au><au>Aoki, Michiko, MD</au><au>Morita, Megumi, MD, PhD</au><au>Kaneko, Tomohiro, MD, PhD</au><au>Tsuruoka, Shuichi, MD, PhD</au><au>Shimizu, Akira, MD, PhD</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Endothelial cell injury in acute and chronic glomerular lesions in patients with IgA nephropathy</atitle><jtitle>Human pathology</jtitle><addtitle>Hum Pathol</addtitle><date>2016-03-01</date><risdate>2016</risdate><volume>49</volume><spage>135</spage><epage>144</epage><pages>135-144</pages><issn>0046-8177</issn><eissn>1532-8392</eissn><abstract>Summary Endothelial cell injury may contribute to the progression of various glomerular diseases. In the present study, we examined glomerular capillary injury in acute and chronic glomerular lesions in patients with Immunoglobulin A nephropathy (IgAN). We selected renal biopsy samples of IgAN (n = 200), and glomerular capillary injury in the acute and chronic glomerular lesions was assessed using immunohistochemistry for CD34 and electron microscopy. We examined the correlations between acute and chronic glomerular lesions and proteinuria, hematuria, and the renal function. The injured glomerular capillaries in the acute glomerular lesions were characterized morphologically by the separation of CD34+ endothelial cells from the glomerular basement membrane and the loss of glomerular endothelial cells and capillaries, together with inflammatory cell infiltration, fibrin exudation, rupture of the glomerular basement membrane, and/or crescent formation. In addition, the injured capillaries in the chronic glomerular lesions were characterized by the loss of CD34+ glomerular endothelial cells and capillaries exhibiting segmental and global glomerular sclerosis with or without fibrous crescents. In the acute glomerular lesions, the presence of endocapillary hypercellularity, fibrinoid necrosis, and cellular and fibrocellular crescents correlated significantly with hematuria, with or without proteinuria. In the chronic glomerular lesions, a significant relationship was evident between segmental or global sclerosis and proteinuria and/or the serum creatinine level. In conclusion, injuries of glomerular capillaries and the loss of endothelial cells occurred in the acute and chronic glomerular lesions in IgAN and may contribute to the development of hematuria, proteinuria, and renal dysfunction.</abstract><cop>United States</cop><pub>Elsevier Inc</pub><pmid>26826420</pmid><doi>10.1016/j.humpath.2015.10.013</doi><tpages>10</tpages></addata></record> |
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| subjects | Acute Disease Acute glomerular lesion Adolescent Adult Aged Antigens, CD34 - analysis Biomarkers - analysis Biopsy Blood Capillaries - chemistry Capillaries - pathology Capillaries - ultrastructure CD34 Child Child, Preschool Chronic Disease Chronic glomerular lesion Classification Endothelial cell injury Endothelial Cells - chemistry Endothelial Cells - pathology Endothelial Cells - ultrastructure Female Gangrene Glomerular capillary injury Glomerulonephritis - metabolism Glomerulonephritis - pathology Glomerulonephritis, IGA - metabolism Glomerulonephritis, IGA - pathology Humans IgA nephropathy Immunohistochemistry Kidney Glomerulus - blood supply Kidneys Male Microscopy, Electron Middle Aged Nephrology Pathology Retrospective Studies Rodents Statistical analysis Variance analysis Young Adult |
| title | Endothelial cell injury in acute and chronic glomerular lesions in patients with IgA nephropathy |
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