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NDT Advance Access originally published online on January 8, 2007
Nephrology Dialysis Transplantation 2007 22(4):1002-1006; doi:10.1093/ndt/gfl784
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© The Author [2007]. Published by Oxford University Press on behalf of ERA-EDTA. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org

Atherosclerotic renovascular disease: beyond the renal artery stenosis

Pascal Meier1, Jérôme Rossert2, Pierre-François Plouin3 and Michel Burnier1

1Service of Nephrology and Hypertension, Centre Hospitalier Universitaire Vaudois, 1011Lausanne, Switzerland, 2Service of Nephrology and Unité INSERM 652, Groupe Hospitalier HEGP/Broussais, Assistance Publique – Hôpitaux de Paris, Paris, France and 3Hypertension Unit, Groupe Hospitalier HEGP/Broussais, Assistance Publique – Hôpitaux de Paris, Paris, France

Correspondence and offprint requests to: Pascal Meier, MD, FASN, Service of Nephrology and Hypertension, Centre Hospitalier Universitaire Vaudois (CHUV), Rue de Bugnon, 1011 Lausanne, Switzerland. Email: pascal.meier@chuv.ch

Keywords: atherosclerosis; renal artery stenosis; ischemia/reperfusion; reactive oxygen species; fibrosis; inflammation

The first 150 words of the full text of this article appear below.



   Introduction
 
Atherosclerotic renovascular disease (ARVD) is a well-recognized cause of arterial hypertension. However, the role of ARVD as an important contributor to renal failure remains a controversial issue. The original experiments of Goldblatt et al. [1] have demonstrated that arterial hypertension due to unilateral renal artery stenosis (RAS) can cause bilateral renal damages. Indeed, because of the reduced perfusion pressure beyond the clip, the tissue of the clipped kidney is exposed to chronic hypoxia, which leads to ischaemic kidney injury. In the unclipped kidney however, renal damage will progressively develop, due to the arterial hypertension caused by the activation of the renin–angiotensin–aldosterone system [1].

In recent years, attention to non-traditional mediators of ARVD such as inflammatory pathways and microvascular events has yielded new paradigms and avenues of research. Among other mechanisms, reactive oxygen species (ROS) production, ischaemia/reperfusion damage and modulation of matrix turnover have been proposed . . . [Full Text of this Article]



   Reactive oxygen species and oxidative stress
 


   Ischaemia/reperfusion and renal damage
 


   Renal fibrosis and modulation of matrix turnover
 


   Clinical consequences
 


   Conclusions
 

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