• 文献检索
  • 文档翻译
  • 深度研究
  • 学术资讯
  • Suppr Zotero 插件Zotero 插件
  • 邀请有礼
  • 套餐&价格
  • 历史记录
应用&插件
Suppr Zotero 插件Zotero 插件浏览器插件Mac 客户端Windows 客户端微信小程序
定价
高级版会员购买积分包购买API积分包
服务
文献检索文档翻译深度研究API 文档MCP 服务
关于我们
关于 Suppr公司介绍联系我们用户协议隐私条款
关注我们

Suppr 超能文献

核心技术专利:CN118964589B侵权必究
粤ICP备2023148730 号-1Suppr @ 2026

文献检索

告别复杂PubMed语法,用中文像聊天一样搜索,搜遍4000万医学文献。AI智能推荐,让科研检索更轻松。

立即免费搜索

文件翻译

保留排版,准确专业,支持PDF/Word/PPT等文件格式,支持 12+语言互译。

免费翻译文档

深度研究

AI帮你快速写综述,25分钟生成高质量综述,智能提取关键信息,辅助科研写作。

立即免费体验

肾小管间质病变介导阿霉素肾病中的肾损伤。

Tubulo-interstitial lesions mediate renal damage in adriamycin glomerulopathy.

作者信息

Bertani T, Cutillo F, Zoja C, Broggini M, Remuzzi G

出版信息

Kidney Int. 1986 Oct;30(4):488-96. doi: 10.1038/ki.1986.212.

DOI:10.1038/ki.1986.212
PMID:3784288
Abstract

The present study was designed to investigate the relationship between proteinuria, focal sclerosis, and tubulo-interstitial changes in the evolution of renal damage in experimental nephrosis. We utilized an accelerated unilateral model of adriamycin (ADR) nephrosis characterized by morphological changes more severe than in the classical model. The first events in ADR-induced glomerulopathy were epithelial cell damage and proteinuria. Subsequently, tubular casts were formed at the distal level. The cast formation preceded the development of interstitial damage, which was determined by tubular obstruction and breaking of tubular basement membrane (TBM), which in turn promoted an interstitial inflammatory reaction. Despite the severity of tubulo-interstitial damage observed after a long period of heavy proteinuria, the incidence of focal segmental glomerulosclerosis (FSG) was very low. The results of the present study indicate that chronic proteinuria is not necessarily accompanied by the development of focal sclerosis. Tubulo-interstitial lesions appear to be the most important determinant for the progression of renal damage in this model.

摘要

本研究旨在探讨实验性肾病肾损伤进展过程中蛋白尿、局灶性硬化和肾小管间质变化之间的关系。我们采用了阿霉素(ADR)肾病的加速单侧模型,其特征是形态学变化比经典模型更为严重。ADR诱导的肾小球病的最初事件是上皮细胞损伤和蛋白尿。随后,在远端形成肾小管管型。管型形成先于间质损伤的发展,间质损伤是由肾小管梗阻和肾小管基底膜(TBM)破裂所决定的,而这反过来又促进了间质炎症反应。尽管在长期大量蛋白尿后观察到肾小管间质损伤严重,但局灶节段性肾小球硬化(FSG)的发生率非常低。本研究结果表明,慢性蛋白尿不一定伴有局灶性硬化的发展。在该模型中,肾小管间质病变似乎是肾损伤进展的最重要决定因素。

相似文献

1
Tubulo-interstitial lesions mediate renal damage in adriamycin glomerulopathy.肾小管间质病变介导阿霉素肾病中的肾损伤。
Kidney Int. 1986 Oct;30(4):488-96. doi: 10.1038/ki.1986.212.
2
Adriamycin-induced glomerulosclerosis in the rat.
Am J Kidney Dis. 1986 Jan;7(1):12-9. doi: 10.1016/s0272-6386(86)80051-8.
3
Age-related nephropathy and proteinuria in rats with intact kidneys exposed to diets with different protein content.不同蛋白质含量饮食对完整肾脏大鼠年龄相关性肾病及蛋白尿的影响
Lab Invest. 1989 Feb;60(2):196-204.
4
Increased glomerular thromboxane synthesis as a possible cause of proteinuria in experimental nephrosis.肾小球血栓素合成增加可能是实验性肾病蛋白尿的一个原因。
J Clin Invest. 1985 Jan;75(1):94-101. doi: 10.1172/JCI111703.
5
Lysosomal iron accumulation and tubular damage in rat puromycin nephrosis and ageing.大鼠嘌呤霉素肾病及衰老过程中的溶酶体铁蓄积与肾小管损伤
Clin Exp Pharmacol Physiol. 1994 Feb;21(2):73-81. doi: 10.1111/j.1440-1681.1994.tb02472.x.
6
Dendrin location in podocytes is associated with disease progression in animal and human glomerulopathy.足细胞中 Dendrin 的位置与动物和人类肾小球病的疾病进展有关。
Am J Nephrol. 2011;33(6):537-49. doi: 10.1159/000327995. Epub 2011 May 23.
7
Phenotypic changes and cell cycle activation in early tubulointerstitial injury of rat adriamycin nephrosis.
Pathol Int. 2002 Mar;52(3):214-23. doi: 10.1046/j.1440-1827.2002.01339.x.
8
[The status of negative charge of the RBC and glomeruli and its relation to proteinuria in adriamycin nephrosis in rats].[大鼠阿霉素肾病中红细胞和肾小球的负电荷状态及其与蛋白尿的关系]
Zhonghua Yi Xue Za Zhi. 1990 Feb;70(2):91-3, 8.
9
Involvement of renal ACE activity in proteinuria-associated renal damage in untreated and treated adriamycin nephrotic rats.未治疗及已治疗的阿霉素肾病大鼠中肾血管紧张素转换酶(ACE)活性与蛋白尿相关肾损伤的关系
J Renin Angiotensin Aldosterone Syst. 2003 Jun;4(2):106-12. doi: 10.3317/jraas.2003.010.
10
Involvement of tumor necrosis factor and platelet-activating factor in the pathogenesis of experimental nephrosis in rats.肿瘤坏死因子和血小板活化因子在大鼠实验性肾病发病机制中的作用。
Lab Invest. 1994 Apr;70(4):449-59.

引用本文的文献

1
Proteinuria and proximal tubular epithelial cells: correlation between immunofluorescence, histology, and degree of proteinuria.蛋白尿与近端肾小管上皮细胞:免疫荧光、组织学及蛋白尿程度之间的相关性
Front Nephrol. 2024 Oct 31;4:1469388. doi: 10.3389/fneph.2024.1469388. eCollection 2024.
2
Effects of chronic kidney disease on cognitive function and α-klotho expression in hippocampus.慢性肾脏病对认知功能及海马体中α-klotho表达的影响。
Transl Androl Urol. 2022 Aug;11(8):1157-1168. doi: 10.21037/tau-22-465.
3
An impaired hepatic clock system effects lipid metabolism in rats with nephropathy.
肝时钟系统受损会影响肾病大鼠的脂质代谢。
Int J Mol Med. 2018 Nov;42(5):2720-2736. doi: 10.3892/ijmm.2018.3833. Epub 2018 Aug 22.
4
Nephrotic syndrome in acute promyelocytic leukemia.急性早幼粒细胞白血病中的肾病综合征
Clin Kidney J. 2014 Aug;7(4):424-5. doi: 10.1093/ckj/sfu062. Epub 2014 Jun 23.
5
The experimental model of nephrotic syndrome induced by Doxorubicin in rodents: an update.阿霉素诱导啮齿动物肾病综合征的实验模型:最新进展
Inflamm Res. 2015 May;64(5):287-301. doi: 10.1007/s00011-015-0813-1. Epub 2015 Mar 19.
6
A comparison of the long-term effects of lanthanum carbonate and calcium carbonate on the course of chronic renal failure in rats with adriamycin-induced nephropathy.碳酸镧和碳酸钙对阿霉素诱导的肾病大鼠慢性肾衰竭病程的长期影响比较。
PLoS One. 2014 May 20;9(5):e97859. doi: 10.1371/journal.pone.0097859. eCollection 2014.
7
Urinary vitamin D binding protein: a potential novel marker of renal interstitial inflammation and fibrosis.尿维生素 D 结合蛋白:一种潜在的新型肾间质炎症和纤维化标志物。
PLoS One. 2013;8(2):e55887. doi: 10.1371/journal.pone.0055887. Epub 2013 Feb 11.
8
Proteinuria triggers renal lymphangiogenesis prior to the development of interstitial fibrosis.蛋白尿在间质纤维化发生之前引发肾脏淋巴管生成。
PLoS One. 2012;7(11):e50209. doi: 10.1371/journal.pone.0050209. Epub 2012 Nov 26.
9
Protective effects of thymoquinone on streptozotocin-induced diabetic nephropathy.百里醌对链脲佐菌素诱导的糖尿病肾病的保护作用。
J Mol Histol. 2009 Apr;40(2):107-15. doi: 10.1007/s10735-009-9220-7. Epub 2009 May 31.
10
Reduction of proteinuria in adriamycin-induced nephropathy is associated with reduction of renal kidney injury molecule (Kim-1) over time.随着时间的推移,阿霉素诱导的肾病中蛋白尿的减少与肾损伤分子(Kim-1)的减少有关。
Am J Physiol Renal Physiol. 2009 May;296(5):F1136-45. doi: 10.1152/ajprenal.00541.2007. Epub 2009 Feb 18.