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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Gespeichert in:

Autor*in:	Pei-Rong Wang [verfasserIn] Hiroshi Kitamura [verfasserIn] Akira Shimizu [verfasserIn] Nobuaki Yamanaka [verfasserIn]

Format:	E-Artikel
Sprache:	Englisch

Erschienen:	2015

Schlagwörter:	SHR-SP Unilateral nephrectomy Thy-1 nephritis Hypertension Glomerular damage

Übergeordnetes Werk:	In: Kidney & Blood Pressure Research - Karger Publishers, 2002, 40(2015), 2, Seite 188-199
Übergeordnetes Werk:	volume:40 ; year:2015 ; number:2 ; pages:188-199

Links:	Link aufrufen Link aufrufen Link aufrufen Journal toc Journal toc

DOI / URN:	10.1159/000368494

Katalog-ID:	DOAJ009815317

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520			\|a 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.
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653		0	\|a Diseases of the genitourinary system. Urology
700	0		\|a Hiroshi Kitamura \|e verfasserin \|4 aut
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spelling	10.1159/000368494 doi (DE-627)DOAJ009815317 (DE-599)DOAJ459349d97f1745dcaf371c189f2dffac DE-627 ger DE-627 rakwb eng RL1-803 RC666-701 RC870-923 Pei-Rong Wang verfasserin aut Glomerular Damage in Experimental Proliferative Glomerulonephritis Under Glomerular Capillary Hypertension 2015 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier 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. SHR-SP Unilateral nephrectomy Thy-1 nephritis Hypertension Glomerular damage Dermatology Diseases of the circulatory (Cardiovascular) system Diseases of the genitourinary system. Urology Hiroshi Kitamura verfasserin aut Akira Shimizu verfasserin aut Nobuaki Yamanaka verfasserin aut In Kidney & Blood Pressure Research Karger Publishers, 2002 40(2015), 2, Seite 188-199 (DE-627)300593767 (DE-600)1482922-8 14230143 nnns volume:40 year:2015 number:2 pages:188-199 https://doi.org/10.1159/000368494 kostenfrei https://doaj.org/article/459349d97f1745dcaf371c189f2dffac kostenfrei http://www.karger.com/Article/FullText/368494 kostenfrei https://doaj.org/toc/1420-4096 Journal toc kostenfrei https://doaj.org/toc/1423-0143 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_374 GBV_ILN_602 GBV_ILN_2014 GBV_ILN_2018 GBV_ILN_2153 GBV_ILN_2885 GBV_ILN_2886 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 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_4338 GBV_ILN_4367 GBV_ILN_4700 AR 40 2015 2 188-199
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allfieldsSound	10.1159/000368494 doi (DE-627)DOAJ009815317 (DE-599)DOAJ459349d97f1745dcaf371c189f2dffac DE-627 ger DE-627 rakwb eng RL1-803 RC666-701 RC870-923 Pei-Rong Wang verfasserin aut Glomerular Damage in Experimental Proliferative Glomerulonephritis Under Glomerular Capillary Hypertension 2015 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier 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. SHR-SP Unilateral nephrectomy Thy-1 nephritis Hypertension Glomerular damage Dermatology Diseases of the circulatory (Cardiovascular) system Diseases of the genitourinary system. Urology Hiroshi Kitamura verfasserin aut Akira Shimizu verfasserin aut Nobuaki Yamanaka verfasserin aut In Kidney & Blood Pressure Research Karger Publishers, 2002 40(2015), 2, Seite 188-199 (DE-627)300593767 (DE-600)1482922-8 14230143 nnns volume:40 year:2015 number:2 pages:188-199 https://doi.org/10.1159/000368494 kostenfrei https://doaj.org/article/459349d97f1745dcaf371c189f2dffac kostenfrei http://www.karger.com/Article/FullText/368494 kostenfrei https://doaj.org/toc/1420-4096 Journal toc kostenfrei https://doaj.org/toc/1423-0143 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_374 GBV_ILN_602 GBV_ILN_2014 GBV_ILN_2018 GBV_ILN_2153 GBV_ILN_2885 GBV_ILN_2886 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 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_4338 GBV_ILN_4367 GBV_ILN_4700 AR 40 2015 2 188-199
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callnumber-first	R - Medicine
author	Pei-Rong Wang
spellingShingle	Pei-Rong Wang misc RL1-803 misc RC666-701 misc RC870-923 misc SHR-SP misc Unilateral nephrectomy misc Thy-1 nephritis misc Hypertension misc Glomerular damage misc Dermatology misc Diseases of the circulatory (Cardiovascular) system misc Diseases of the genitourinary system. Urology Glomerular Damage in Experimental Proliferative Glomerulonephritis Under Glomerular Capillary Hypertension
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topic_title	RL1-803 RC666-701 RC870-923 Glomerular Damage in Experimental Proliferative Glomerulonephritis Under Glomerular Capillary Hypertension SHR-SP Unilateral nephrectomy Thy-1 nephritis Hypertension Glomerular damage
topic	misc RL1-803 misc RC666-701 misc RC870-923 misc SHR-SP misc Unilateral nephrectomy misc Thy-1 nephritis misc Hypertension misc Glomerular damage misc Dermatology misc Diseases of the circulatory (Cardiovascular) system misc Diseases of the genitourinary system. Urology
topic_unstemmed	misc RL1-803 misc RC666-701 misc RC870-923 misc SHR-SP misc Unilateral nephrectomy misc Thy-1 nephritis misc Hypertension misc Glomerular damage misc Dermatology misc Diseases of the circulatory (Cardiovascular) system misc Diseases of the genitourinary system. Urology
topic_browse	misc RL1-803 misc RC666-701 misc RC870-923 misc SHR-SP misc Unilateral nephrectomy misc Thy-1 nephritis misc Hypertension misc Glomerular damage misc Dermatology misc Diseases of the circulatory (Cardiovascular) system misc Diseases of the genitourinary system. Urology
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title	Glomerular Damage in Experimental Proliferative Glomerulonephritis Under Glomerular Capillary Hypertension
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title_full	Glomerular Damage in Experimental Proliferative Glomerulonephritis Under Glomerular Capillary Hypertension
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title_sort	glomerular damage in experimental proliferative glomerulonephritis under glomerular capillary hypertension
callnumber	RL1-803
title_auth	Glomerular Damage in Experimental Proliferative Glomerulonephritis Under Glomerular Capillary Hypertension
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.
abstractGer	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_unstemmed	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.
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title_short	Glomerular Damage in Experimental Proliferative Glomerulonephritis Under Glomerular Capillary Hypertension
url	https://doi.org/10.1159/000368494 https://doaj.org/article/459349d97f1745dcaf371c189f2dffac http://www.karger.com/Article/FullText/368494 https://doaj.org/toc/1420-4096 https://doaj.org/toc/1423-0143
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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. 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Glomerular Damage in Experimental Proliferative Glomerulonephritis Under Glomerular Capillary Hypertension

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