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Atherosclerotic renal artery stenosis (ARAS) is a growing dilemma. The condition is increasingly common and can promulgate hypertension and result in renal failure. However, patients with ARAS generally die owing to their coronaries or cerebral vessels. Intervention, by stenting or angioplasty is beloved and believed, but not proved. The American Heart Association has recently published guidelines regarding patients at high risk for ARAS who are potential candidates for revascularisation. Since this phraseology includes practically every patient with atherosclerosis, these guidelines appear ill advised.
In this issue of Heart, Dear, Padfield and Webb1 take umbrage at recent (2006) recommendations published by the American Heart Association (AHA) regarding new guidelines for “drive‐by” renal arteriography during interventions for atherosclerotic lesions elsewhere in the body.2 This Practice Guideline was followed by a multispecialty consensus document stating basically the same thing.3 The multispecialty pundits concluded that renal angiography should be “selectively applied to patients at high risk for atherosclerotic renal artery stenosis (ARAS) who are potential candidates for revascularisation”. Dear et al draw attention to the fact that the guidelines recommend screening for ARAS in all patients at risk who are candidates for revascularisation.1 “At risk” was defined according to hypertension, age of onset, accelerated course, kidney size discrepancy, “flash” pulmonary oedema, worsening renal function and multivessel atherosclerosis elsewhere. Since the “unstentable” patient is yet to be encountered, Dear et al suggest that the number of patients subjected to renal artery stenting is bound to increase. They point out that the AHA recommends a generalised “screening programme” for an entity that has no sound basis for management. A recent meta‐analysis by Balk et al underlines their view.4 Have Dear et al indeed caught old Auntie AHA with her pantaloons at half mast?
The issues are complex. ARAS is a moving target in an ever‐aging, ever‐more diabetic population. Furthermore, the options offered by medical treatments, such as optimal blood pressure reduction, cholesterol lowering, antiplatelet drugs, and renin–angiotensin–aldosterone system blockade, have improved substantially in recent years.5 In parallel, the invasive crowd has also steadily done its homework. Percutaneous interventions have improved dramatically and complications have (probably) decreased.6
The risk of renal artery stenting is low but not trivial. Figure 11 shows an angiogram from a middle‐aged hypertensive woman with ARAS in her left renal artery (fig1A). Stenting was uneventful with an excellent visual result (not shown). However, flank pain and an increase in her serum creatinine concentration prompted the second study (fig 1B1B)) showing a stent thrombosis. Additional intervention, coupled with abciximab treatment, resolved the problem (fig 1C1C),), albeit not without morbidity to the patient and soul searching by the authors. Another example is shown in fig 1D1D.. This hypertensive 79‐year‐old woman with three‐vessel coronary disease (raised troponin T), an aortic aneurysm (>5.5 cm), and ARAS underwent intervention. An interesting discussion was, “who goes first here”? The interventionalists put her on the list as requiring fixing of her coronary arteries, placement of an aortic endoprosthesis and stenting of her renal arteries. The three teams reached consensus and the befuddled patient gave her consent to everything. The ARAS was first and easily stented. Her creatinine doubled and a localised livido reticularis developed on her back, far from the expected arterial run‐off. The skin biopsy shows obvious clefts from cholesterol emboli in a small skin artery. Cholesterol embolisation is not a trivial problem and not necessarily a “downstream” event.7 We have no reason to believe that her brain arterioles looked any different from those on her back.
“There ain't substitutes for data!” Herein lies our dilemma. Fortunately, there are efforts to get some. One example is the Cardiovascular Outcomes in Renal Atherosclerotic Lesions (CORAL) study. The end points of CORAL are cardiovascular or renal death, stroke, myocardial infarction, admission to hospital for heart failure, doubling of serum creatinine concentration and dialysis dependency. Auntie AHA did at least publish a “pro” and “con” by the CORAL co‐principal investigators. Cooper (a “dyed‐in‐the‐wool” and superb interventionalist) presented the arguments for stenting.8 Dworkin, a nephrologist (we need say no more), defended the “optimal medical therapy” line.9
Our group applied for CORAL membership and was accepted. Our referring colleagues are enthusiastic, but only up to a point. “I think it is great that you are doing this, but not with my patient!” Herein lies the rub. Faith is an incredibly strong force, but no substitute for data. In our view, only those patients should undergo interventions of their renal arteries that are included in a randomised, controlled, trial of ARAS such as CORAL. Dear and colleagues have done us a service in drawing attention to “Guideline Mayhem”.1
AHA - American Heart Association
ARAS - atherosclerotic renal artery stenosis
CORAL - Cardiovascular Outcomes in Renal Atherosclerotic Lesions
Competing interests: None declared.