Glomerular Damage in Experimental Proliferative Glomerulonephritis Under Glomerular Capillary Hypertension
Background/Aims: Immunologically and hemodynamically mediated the destruction of glomerular architecture is thought to be the major causes of end-stage renal failure. The purpose of this study is to evaluate the effect of glomerular hypertension on glomerular injury and the progression of glomerular...
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| Veröffentlicht in: | Kidney & blood pressure research 2015-01, Vol.40 (2), p.188-199 |
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| description | Background/Aims: Immunologically and hemodynamically mediated the destruction of glomerular architecture is thought to be the major causes of end-stage renal failure. The purpose of this study is to evaluate the effect of glomerular hypertension on glomerular injury and the progression of glomerular sclerosis after Thy-1 nephritis was induced. Method: Thy-1 nephritis was induced in the stroke-prone spontaneously hypertensive rat strain (SHR-SP) (group SP) and in age-matched Wistar-Kyoto (WKY) (group WKY) rats, following unilateral nephrectomy (UNX), and a vehicle was injected alone in UNX SHR-SP as control (group SC). Result: The degree of glomerular damage in response to a single dose of anti-thy-1 antibody, and its functional consequences (eg. proteinuria, diminished GFR) are more pronounced in group SP than normotensive group WKY and hypertensive group SC without mesangial cell injury. While normotensive group WKY rats recovered completely from mesangial cell injury on day 28-42, glomeruli in group SP kept on persistent macrophage infiltration, α-SMA expression on day 42-56. In addition, glomerular capillary repair with the GECs was rarely seen in pronouncedly proliferative and sclerostic areas. The incidence of glomerular sclerosis and the level of proteinuria were markedly increased by day 56 in the group SP. Conclusions: Our results demonstrate that glomerular hypertension aggravate glomerular damage and glomerulosclerosis in this model of Thy 1 nephritis. |
| doi_str_mv | 10.1159/000368494 |
| format | Article |
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The purpose of this study is to evaluate the effect of glomerular hypertension on glomerular injury and the progression of glomerular sclerosis after Thy-1 nephritis was induced. Method: Thy-1 nephritis was induced in the stroke-prone spontaneously hypertensive rat strain (SHR-SP) (group SP) and in age-matched Wistar-Kyoto (WKY) (group WKY) rats, following unilateral nephrectomy (UNX), and a vehicle was injected alone in UNX SHR-SP as control (group SC). Result: The degree of glomerular damage in response to a single dose of anti-thy-1 antibody, and its functional consequences (eg. proteinuria, diminished GFR) are more pronounced in group SP than normotensive group WKY and hypertensive group SC without mesangial cell injury. While normotensive group WKY rats recovered completely from mesangial cell injury on day 28-42, glomeruli in group SP kept on persistent macrophage infiltration, α-SMA expression on day 42-56. In addition, glomerular capillary repair with the GECs was rarely seen in pronouncedly proliferative and sclerostic areas. The incidence of glomerular sclerosis and the level of proteinuria were markedly increased by day 56 in the group SP. Conclusions: Our results demonstrate that glomerular hypertension aggravate glomerular damage and glomerulosclerosis in this model of Thy 1 nephritis.</description><identifier>ISSN: 1420-4096</identifier><identifier>EISSN: 1423-0143</identifier><identifier>DOI: 10.1159/000368494</identifier><identifier>PMID: 25871528</identifier><identifier>CODEN: RPBIEL</identifier><language>eng</language><publisher>Basel, Switzerland: S. Karger AG</publisher><subject>Animals ; Capillaries - pathology ; Complications and side effects ; Development and progression ; Disease Progression ; Glomerular damage ; Glomerulonephritis ; Glomerulonephritis - pathology ; Hemodynamics - physiology ; Hypertension ; Hypertension, Renovascular - chemically induced ; Hypertension, Renovascular - pathology ; Isoantibodies ; Kidney - pathology ; Kidney Glomerulus - pathology ; Male ; Nephrectomy ; Original Paper ; Proteinuria - metabolism ; Rats ; Rats, Inbred SHR ; Rats, Inbred WKY ; Renal hypertension ; Sclerosis ; SHR-SP ; Thy-1 nephritis ; Unilateral nephrectomy</subject><ispartof>Kidney & blood pressure research, 2015-01, Vol.40 (2), p.188-199</ispartof><rights>2015 S. Karger AG, Basel</rights><rights>2015 S. Karger AG, Basel.</rights><rights>COPYRIGHT 2015 S. Karger AG</rights><rights>Copyright S. Karger AG Apr 2015</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c596t-835f8e3b2ab35889aa5f3fa014f70a49dc9229ce88914befafd9041f848dff043</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,778,782,862,2098,27618,27907,27908</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/25871528$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Wang, Pei-Rong</creatorcontrib><creatorcontrib>Kitamura, Hiroshi</creatorcontrib><creatorcontrib>Shimizu, Akira</creatorcontrib><creatorcontrib>Yamanaka, Nobuaki</creatorcontrib><title>Glomerular Damage in Experimental Proliferative Glomerulonephritis Under Glomerular Capillary Hypertension</title><title>Kidney & blood pressure research</title><addtitle>Kidney Blood Press Res</addtitle><description>Background/Aims: Immunologically and hemodynamically mediated the destruction of glomerular architecture is thought to be the major causes of end-stage renal failure. The purpose of this study is to evaluate the effect of glomerular hypertension on glomerular injury and the progression of glomerular sclerosis after Thy-1 nephritis was induced. Method: Thy-1 nephritis was induced in the stroke-prone spontaneously hypertensive rat strain (SHR-SP) (group SP) and in age-matched Wistar-Kyoto (WKY) (group WKY) rats, following unilateral nephrectomy (UNX), and a vehicle was injected alone in UNX SHR-SP as control (group SC). Result: The degree of glomerular damage in response to a single dose of anti-thy-1 antibody, and its functional consequences (eg. proteinuria, diminished GFR) are more pronounced in group SP than normotensive group WKY and hypertensive group SC without mesangial cell injury. While normotensive group WKY rats recovered completely from mesangial cell injury on day 28-42, glomeruli in group SP kept on persistent macrophage infiltration, α-SMA expression on day 42-56. In addition, glomerular capillary repair with the GECs was rarely seen in pronouncedly proliferative and sclerostic areas. The incidence of glomerular sclerosis and the level of proteinuria were markedly increased by day 56 in the group SP. Conclusions: Our results demonstrate that glomerular hypertension aggravate glomerular damage and glomerulosclerosis in this model of Thy 1 nephritis.</description><subject>Animals</subject><subject>Capillaries - pathology</subject><subject>Complications and side effects</subject><subject>Development and progression</subject><subject>Disease Progression</subject><subject>Glomerular damage</subject><subject>Glomerulonephritis</subject><subject>Glomerulonephritis - pathology</subject><subject>Hemodynamics - physiology</subject><subject>Hypertension</subject><subject>Hypertension, Renovascular - chemically induced</subject><subject>Hypertension, Renovascular - pathology</subject><subject>Isoantibodies</subject><subject>Kidney - pathology</subject><subject>Kidney Glomerulus - pathology</subject><subject>Male</subject><subject>Nephrectomy</subject><subject>Original Paper</subject><subject>Proteinuria - metabolism</subject><subject>Rats</subject><subject>Rats, Inbred SHR</subject><subject>Rats, Inbred WKY</subject><subject>Renal hypertension</subject><subject>Sclerosis</subject><subject>SHR-SP</subject><subject>Thy-1 nephritis</subject><subject>Unilateral nephrectomy</subject><issn>1420-4096</issn><issn>1423-0143</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2015</creationdate><recordtype>article</recordtype><sourceid>M--</sourceid><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DOA</sourceid><recordid>eNptkUFv1DAQhS0EomXhwB2hSFzgkGLHTmIfy1LaikogRM_WrDNevCRx6iSI_nuGZrsghHzwaPzNm3kexp4LfiJEad5yzmWllVEP2LFQhcy5UPLhXcxzxU11xJ6M446wkvPiMTsqSl2LstDHbHfexg7T3ELK3kMHW8xCn539HDCFDvsJ2uxzim3wmGAKPzC752OPw7cUpjBm132DKftLaA1DaCm4zS5uSWjCfgyxf8oeeWhHfLa_V-z6w9nX9UV-9en8cn16lbvSVFOuZek1yk0BG1lqbQBKLz2QJV9zUKZxpiiMQ3oSaoMefGO4El4r3XjPlVyxy0W3ibCzA_mgSWyEYO8SMW0tpCm4Fq0qjSRFU3tRq7Jx4GUtnNDGF6QFjrReL1pDijczjpPtwuiQzPUY59GKqq611kpIQl_9g-7inHpyakUtNReVodWs2MlCbYH6h97HKYGj02AXHH2qD5Q_rWRd0DGCCt4sBS7FcUzoD44Et7-3bw_bJ_blfoR502FzIO_X_WfG75C2mA7Ax3dfFgk7NJ6oF_-l9l1-AQN6v3k</recordid><startdate>20150101</startdate><enddate>20150101</enddate><creator>Wang, Pei-Rong</creator><creator>Kitamura, Hiroshi</creator><creator>Shimizu, Akira</creator><creator>Yamanaka, Nobuaki</creator><general>S. Karger AG</general><general>Karger Publishers</general><scope>M--</scope><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>IAO</scope><scope>3V.</scope><scope>7QL</scope><scope>7T7</scope><scope>7U9</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8FD</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>BENPR</scope><scope>C1K</scope><scope>CCPQU</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>H94</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>M7N</scope><scope>P64</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>S0X</scope><scope>7X8</scope><scope>DOA</scope></search><sort><creationdate>20150101</creationdate><title>Glomerular Damage in Experimental Proliferative Glomerulonephritis Under Glomerular Capillary Hypertension</title><author>Wang, Pei-Rong ; Kitamura, Hiroshi ; Shimizu, Akira ; Yamanaka, Nobuaki</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c596t-835f8e3b2ab35889aa5f3fa014f70a49dc9229ce88914befafd9041f848dff043</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2015</creationdate><topic>Animals</topic><topic>Capillaries - pathology</topic><topic>Complications and side effects</topic><topic>Development and progression</topic><topic>Disease Progression</topic><topic>Glomerular damage</topic><topic>Glomerulonephritis</topic><topic>Glomerulonephritis - pathology</topic><topic>Hemodynamics - physiology</topic><topic>Hypertension</topic><topic>Hypertension, Renovascular - chemically induced</topic><topic>Hypertension, Renovascular - pathology</topic><topic>Isoantibodies</topic><topic>Kidney - pathology</topic><topic>Kidney Glomerulus - pathology</topic><topic>Male</topic><topic>Nephrectomy</topic><topic>Original Paper</topic><topic>Proteinuria - metabolism</topic><topic>Rats</topic><topic>Rats, Inbred SHR</topic><topic>Rats, Inbred WKY</topic><topic>Renal hypertension</topic><topic>Sclerosis</topic><topic>SHR-SP</topic><topic>Thy-1 nephritis</topic><topic>Unilateral nephrectomy</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Wang, Pei-Rong</creatorcontrib><creatorcontrib>Kitamura, Hiroshi</creatorcontrib><creatorcontrib>Shimizu, Akira</creatorcontrib><creatorcontrib>Yamanaka, Nobuaki</creatorcontrib><collection>Karger Open Access</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Gale Academic OneFile</collection><collection>ProQuest Central (Corporate)</collection><collection>Bacteriology Abstracts (Microbiology B)</collection><collection>Industrial and Applied Microbiology Abstracts (Microbiology A)</collection><collection>Virology and AIDS Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Technology Research Database</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central</collection><collection>Environmental Sciences and Pollution Management</collection><collection>ProQuest One Community College</collection><collection>Engineering Research Database</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Algology Mycology and Protozoology Abstracts (Microbiology C)</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>SIRS Editorial</collection><collection>MEDLINE - Academic</collection><collection>DOAJ Directory of Open Access Journals</collection><jtitle>Kidney & blood pressure research</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Wang, Pei-Rong</au><au>Kitamura, Hiroshi</au><au>Shimizu, Akira</au><au>Yamanaka, Nobuaki</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Glomerular Damage in Experimental Proliferative Glomerulonephritis Under Glomerular Capillary Hypertension</atitle><jtitle>Kidney & blood pressure research</jtitle><addtitle>Kidney Blood Press Res</addtitle><date>2015-01-01</date><risdate>2015</risdate><volume>40</volume><issue>2</issue><spage>188</spage><epage>199</epage><pages>188-199</pages><issn>1420-4096</issn><eissn>1423-0143</eissn><coden>RPBIEL</coden><abstract>Background/Aims: Immunologically and hemodynamically mediated the destruction of glomerular architecture is thought to be the major causes of end-stage renal failure. The purpose of this study is to evaluate the effect of glomerular hypertension on glomerular injury and the progression of glomerular sclerosis after Thy-1 nephritis was induced. Method: Thy-1 nephritis was induced in the stroke-prone spontaneously hypertensive rat strain (SHR-SP) (group SP) and in age-matched Wistar-Kyoto (WKY) (group WKY) rats, following unilateral nephrectomy (UNX), and a vehicle was injected alone in UNX SHR-SP as control (group SC). Result: The degree of glomerular damage in response to a single dose of anti-thy-1 antibody, and its functional consequences (eg. proteinuria, diminished GFR) are more pronounced in group SP than normotensive group WKY and hypertensive group SC without mesangial cell injury. While normotensive group WKY rats recovered completely from mesangial cell injury on day 28-42, glomeruli in group SP kept on persistent macrophage infiltration, α-SMA expression on day 42-56. In addition, glomerular capillary repair with the GECs was rarely seen in pronouncedly proliferative and sclerostic areas. The incidence of glomerular sclerosis and the level of proteinuria were markedly increased by day 56 in the group SP. Conclusions: Our results demonstrate that glomerular hypertension aggravate glomerular damage and glomerulosclerosis in this model of Thy 1 nephritis.</abstract><cop>Basel, Switzerland</cop><pub>S. Karger AG</pub><pmid>25871528</pmid><doi>10.1159/000368494</doi><tpages>12</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Animals Capillaries - pathology Complications and side effects Development and progression Disease Progression Glomerular damage Glomerulonephritis Glomerulonephritis - pathology Hemodynamics - physiology Hypertension Hypertension, Renovascular - chemically induced Hypertension, Renovascular - pathology Isoantibodies Kidney - pathology Kidney Glomerulus - pathology Male Nephrectomy Original Paper Proteinuria - metabolism Rats Rats, Inbred SHR Rats, Inbred WKY Renal hypertension Sclerosis SHR-SP Thy-1 nephritis Unilateral nephrectomy |
| title | Glomerular Damage in Experimental Proliferative Glomerulonephritis Under Glomerular Capillary Hypertension |
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