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Narrowing of the lumen of the renal artery is termed renal artery stenosis (RAS) and can be a cause of hypertension and chronic kidney disease (CKD).1 When hypertension is caused by RAS the term renovascular hypertension is used, but the only way to be certain of the diagnosis is to demonstrate that relief of the renal artery narrowing results in a return to a normal blood pressure. This is because essential hypertension is considerably more common than, and a risk factor for, RAS so the coexistence of RAS and hypertension in a patient does not infer causality. In addition, even where clinically significant RAS is the initial cause of hypertension, reversal of the stenosis may not result in a normal blood pressure or renal function if longstanding hypertension has produced irreversible contralateral renal injury.2
RAS is most commonly due to atherosclerotic renal artery stenosis (ARAS) and has been reported to be present in around 30% of patients having routine coronary angiography and up to 50% of patients undergoing peripheral angiography.2 The presence and anatomical location of RAS can be confirmed by non‐invasive imaging with duplex ultrasound, computed tomographic or magnetic resonance angiography or by invasive imaging with catheter‐based angiography.2 Isotope renography combined with administration of the ACE inhibitor captopril can be used to assess the functional severity of the stenosis, and comparison of the renin activity in the two renal veins is sometimes useful to confirm the diagnosis.2 However, none of these investigations can reliably indicate which patients will respond to percutaneous or surgical intervention and which are best managed with antihypertensive drugs.
The medical management of ARAS centres on effective blood pressure control, lipid‐lowering treatment, smoking cessation and antiplatelet treatment.1,2 Restoration of near‐normal blood flow to the kidney by angioplasty or surgery (revascularisation) holds an intuitive appeal, but a recent systematic review found no clear evidence to suggest that revascularisation was better than medical treatment.3 There may be modest improvements in hypertension control but cure of hypertension is unlikely, and no firm conclusions can be drawn about the impact of renal artery revascularisation on the development of ischaemic heart disease, stroke and death.3,4 In contrast, medical management of hypertension is well established and has a large evidence base.5 Also, there is no good evidence to support an improvement in kidney function after renal artery revascularisation.3 On the other hand, angioplasty can produce serious complications such as renal artery occlusion and cholesterol embolisation2 and, with a lack of robust evidence demonstrating benefit, its role is still unclear.
With this management uncertainty as a background, the American College of Cardiology and the American Heart Association (ACC/AHA) recently produced guidelines for when renal arteriography should be performed at the time of coronary arteriography (so called “drive‐by” renal arteriography).6 These brief drive‐by arteriography guidelines are based on the considerably more substantial guidelines for the management of peripheral vascular disease (including ARAS)7 and state that it is reasonable to screen for ARAS in at‐risk patients who are candidates for revascularisation.6 The definitions of at‐risk patients and recommendations for revascularisation are presented in table 11.
Within the guidelines the following is suggested: “Percutaneous revascularisation is reasonable for patients with haemodynamically significant RAS and unstable angina”. Haemodynamically significant renal artery stenosis is defined as (a) a 50–70% diameter stenosis by visual estimation with a peak translesional gradient (measured with a 5F or smaller catheter or pressure wire) of at least 20 mm Hg or a mean gradient of at least 10 mm Hg; (b) any stenosis of at least 70% diameter; or (c) 70% diameter stenosis by intravascular ultrasound measurement.7 The authors acknowledge that this guidance for patients with unstable angina is based on small case series of selected patients because larger, more robust, studies have yet to be performed. Given that unstable angina is a common indication for coronary arteriography, a large number of patients will also be candidates for renal artery imaging. This is in addition to the significant number of patients who will be candidates for renal artery imaging based on a history of hypertension or CKD. In America, percutaneous renal artery revascularisation is increasingly being performed by cardiologists,8 so a by‐product of increased renovascular imaging is likely to be an increase in renal artery revascularisation at the time of coronary arteriography. In the UK fewer cardiologists routinely perform renal artery angioplasty at present. However, because coronary angioplasty requires similar skills there is considerable potential for the number of renal artery revascularisation procedures to increase.
The new ACC/AHA guidelines for when renal arteriography should be performed in patients undergoing coronary arteriography amount to the introduction of a new and unproved screening programme. However, the guidelines fail to meet the screening criteria adopted by the World Health Organisation9 (box 1) because haemodynamically significant ARAS will be diagnosed without a strong evidence base for management. We would strongly discourage renal artery revascularisation at the time of coronary arteriography until a considerably more robust evidence base is available.
ACC/AHA - American College of Cardiology and the American Heart Association
ARAS - atherosclerotic renal artery stenosis
CKD - chronic kidney disease
RAS - renal artery stenosis
Competing interests: None.