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Stenting and medical therapy for atherosclerotic renal-artery stenosis.经皮腔内血管成形术及药物治疗动脉粥样硬化性肾动脉狭窄
N Engl J Med. 2014 Jan 2;370(1):13-22. doi: 10.1056/NEJMoa1310753. Epub 2013 Nov 18.
2
Redox signaling is an early event in the pathogenesis of renovascular hypertension.氧化还原信号是血管性高血压发病机制中的早期事件。
Int J Mol Sci. 2013 Sep 10;14(9):18640-56. doi: 10.3390/ijms140918640.
3
Inhibition of p38 MAPK attenuates renal atrophy and fibrosis in a murine renal artery stenosis model.p38 MAPK 的抑制可减轻小鼠肾动脉狭窄模型中的肾萎缩和纤维化。
Am J Physiol Renal Physiol. 2013 Apr 1;304(7):F938-47. doi: 10.1152/ajprenal.00706.2012. Epub 2013 Jan 30.
4
TGF expression and macrophage accumulation in atherosclerotic renal artery stenosis.TGF 的表达与巨噬细胞在动脉粥样硬化性肾动脉狭窄中的聚集。
Clin J Am Soc Nephrol. 2013 Apr;8(4):546-53. doi: 10.2215/CJN.06460612. Epub 2012 Dec 20.
5
Inflammatory and injury signals released from the post-stenotic human kidney.人狭窄后肾脏释放的炎症和损伤信号。
Eur Heart J. 2013 Feb;34(7):540-548a. doi: 10.1093/eurheartj/ehs197. Epub 2012 Jul 6.
6
Genetic deficiency of Smad3 protects the kidneys from atrophy and interstitial fibrosis in 2K1C hypertension.Smad3 基因缺失可保护肾脏免于 2K1C 高血压引起的萎缩和间质纤维化。
Am J Physiol Renal Physiol. 2012 Jun 1;302(11):F1455-64. doi: 10.1152/ajprenal.00645.2011. Epub 2012 Feb 29.
7
Atherosclerotic renal artery stenosis: flaws in estimated glomerular filtration rate and the problem of progressive kidney injury.动脉粥样硬化性肾动脉狭窄:估算肾小球滤过率的缺陷与进行性肾损伤问题
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8
Genetic deficiency of Smad3 protects against murine ischemic acute kidney injury.Smad3 基因缺失可预防小鼠缺血性急性肾损伤。
Am J Physiol Renal Physiol. 2011 Aug;301(2):F436-42. doi: 10.1152/ajprenal.00162.2011. Epub 2011 Apr 27.
9
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Hypertension. 2011 Feb;57(2):132-40. doi: 10.1161/HYPERTENSIONAHA.110.163576. Epub 2010 Dec 13.
10
Unilateral renal artery stenosis causes a chronic vascular inflammatory response in ApoE-/- mice.单侧肾动脉狭窄在载脂蛋白E基因敲除(ApoE-/-)小鼠中引发慢性血管炎症反应。
Trans Am Clin Climatol Assoc. 2010;121:252-64; 264-6.

肾动脉狭窄的管理:实验证据告诉了我们什么?

Management of renal artery stenosis: What does the experimental evidence tell us?

作者信息

Al-Suraih Mohammed, Grande Joseph Peter

机构信息

Mohammed Al-Suraih, Joseph Peter Grande, Department of Laboratory Medicine and Pathology, Mayo Clinic, Rochester, MN 55905, United States.

出版信息

World J Cardiol. 2014 Aug 26;6(8):855-60. doi: 10.4330/wjc.v6.i8.855.

DOI:10.4330/wjc.v6.i8.855
PMID:25228964
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4163714/
Abstract

Optimal management of patients with renal artery stenosis (RAS) is a subject of considerable controversy. There is incontrovertible evidence that renal artery stenosis has profound effects on the heart and cardiovascular system in addition to the kidney. Recent evidence indicates that restoration of blood flow alone does not improve renal or cardiovascular outcomes in patients with renal artery stenosis. A number of human and experimental studies have documented the clinical, hemodynamic, and histopathologic features in renal artery stenosis. New approaches to the treatment of renovascular hypertension due to RAS depend on better understanding of basic mechanisms underlying the development of chronic renal disease in these patients. Several groups have employed the two kidney one clip model of renovascular hypertension to define basic signaling mechanisms responsible for the development of chronic renal disease. Recent studies have underscored the importance of inflammation in the development and progression of renal damage in renal artery stenosis. In particular, interactions between the renin-angiotensin system, oxidative stress, and inflammation appear to play a critical role in this process. In this overview, results of recent studies to define basic pathways responsible for renal disease progression will be highlighted. These studies may provide the rationale for novel therapeutic approaches to treat patients with renovascular hypertension.

摘要

肾动脉狭窄(RAS)患者的最佳管理是一个颇具争议的话题。有确凿证据表明,肾动脉狭窄除了对肾脏有影响外,还对心脏和心血管系统有深远影响。最近的证据表明,仅恢复血流并不能改善肾动脉狭窄患者的肾脏或心血管预后。多项人体和实验研究记录了肾动脉狭窄的临床、血流动力学和组织病理学特征。治疗由RAS引起的肾血管性高血压的新方法取决于对这些患者慢性肾病发展的基本机制有更好的理解。几个研究小组采用肾血管性高血压的两肾一夹模型来确定导致慢性肾病发展的基本信号传导机制。最近的研究强调了炎症在肾动脉狭窄肾损伤发展和进展中的重要性。特别是,肾素-血管紧张素系统、氧化应激和炎症之间的相互作用似乎在这个过程中起关键作用。在本综述中,将重点介绍最近确定肾病进展基本途径的研究结果。这些研究可能为治疗肾血管性高血压患者的新治疗方法提供理论依据。