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(Circulation. 2007;115:263-270.)
© 2007 American Heart Association, Inc.

Controversies in Cardiovascular Medicine

Is renal artery stenting the correct treatment of renal artery stenosis? The Case for Renal Artery Stenting for Treatment of Renal Artery Stenosis

Christopher J. Cooper, MD; Timothy P. Murphy, MD

From the Department of Medicine, University of Toledo, Toledo (C.J.C.), and Department of Diagnostic Imaging, Brown University, Vascular Disease Research Center, Rhode Island Hospital, Providence (T.P.M.).

Correspondence to Christopher J. Cooper, MD, Department of Medicine, University of Toledo, 3000 Arlington Ave, Hospital Room No. 1192, Toledo, OH 43614–2598. E-mail ccooper@mco.edu

An extract of the first 250 words of the full text is provided, because this article has no abstract.

	Introduction

 
The case favoring renal artery stenting for individuals with renal artery hypertension is largely circumstantial. At best, the clinical evidence presented in this discussion is derived primarily from nonrandomized cohort studies. It would certainly be easier to argue that medical therapy is preferred for such individuals because there are 3 published randomized clinical trials that concluded just that and none that support renal artery intervention. Nonetheless, there is considerable evidence to support the role for revascularization in general, and stenting specifically, as an important adjunctive therapy to medical therapy in the care of patients with renal artery stenosis (RAS). The argument has 3 principal components: observations about the impact on cardiovascular physiology, end-organ effects, and natural history.

Response by Dworkin and Jamerson p 270

	RAS and Hypertension

 
RAS is associated with and is an important cause of secondary hypertension. RAS causes endocrine activation with release of renin from renal juxtaglomerular cells. Renin catalyzes the breakdown of angiotensinogen to angiotensin I. Angiotensin I is transformed by angiotensin-converting enzyme into angiotensin II, and angiotensin II promotes the release of aldosterone from the adrenal cortex.¹ Angiotensin II is a potent vasoconstrictor,² substantially more potent than epinephrine, and is implicated in end-organ damage in the heart³ and kidney.⁴ RAS is suggested to cause 2 types of hypertension. With unilateral RAS and a normally perfused and normally functioning contralateral kidney, blood pressure elevation is referred to as "renin dependent" and is characterized by increased peripheral resistance.^5,6 In this circumstance, renin and angiotensin levels remain elevated, but volume expansion . . . [Full Text of this Article]

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