Article Text

Download PDFPDF
Atherosclerotic renal artery stenosis, ACE inhibitors, and avoiding cardiovascular death
  1. John Main
  1. Correspondence to:
    Dr John Main
    Renal Unit, James Cook University Hospital, Marton Road, Middlesbrough TS4 3BW, UK;

Statistics from

Request Permissions

If you wish to reuse any or all of this article please use the link below which will take you to the Copyright Clearance Center’s RightsLink service. You will be able to get a quick price and instant permission to reuse the content in many different ways.

Atherosclerotic renal artery stenosis (ARAS) has become topical since the development of percutaneous angioplasty and stenting. Studies defining the place for intervention have been difficult to perform and inconclusive. However, it is becoming clear that intervention makes only a modest contribution to blood pressure control. Furthermore, although ARAS is often present in elderly patients with renal impairment, the contribution of intervention to preventing progression of renal failure has been disappointing. The increasingly widespread use of angiotensin converting enzyme (ACE) inhibitors and angiotensin II receptor blockers (ARBs) has increased the clinical relevance of ARAS, and may be altering the indications for intervention. ARAS is more likely to end in cardiovascular death than renal failure, suggesting that it may be more rewarding to focus on the heart than the kidneys in this condition.


There is a stark difference in our understanding of the benefits of intervention in coronary artery disease (CAD) as opposed to ARAS. There are three principal reasons for this: the non-specific nature of the clinical sequelae of ARAS, all of which have more common causes (table 1); a lack of understanding of the link between ARAS and renal damage; and the relative rarity of pathologically significant ARAS, which precludes intervention trials of the size which have informed the management of CAD.

View this table:
Table 1

 Clinical presentations of ARAS and alternative causes

The relation between CAD and its clinical sequelae is relatively clear cut. Coronary artery narrowing produces angina, and angina in the presence of coronary artery narrowing is almost invariable caused by that narrowing. Coronary artery narrowing increases the risk of arterial thrombosis and myocardial infarction, and myocardial infarction has no other common cause. The relation between ARAS and clinical disease is much more complex.

Renal artery narrowing may activate the renin–angiotensin–aldosterone system (RAAS) and raise blood pressure, but the vast majority …

View Full Text