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Atherosclerotic renal artery stenosis: there is no obvious reason to dilate.

It's narrow ± let's dilate it! Very often this seems to be the battle cry of our colleagues, be it the interventional cardiologist, radiologist or vascular surgeon, when facing a narrowed artery. Is this approach justified when the artery in question is an atherosclerotic renal artery? Atherosclerotic narrowing of one or both renal arteries is a common finding in an older population [1]. It may lead to renovascular hypertension and/or ischemic nephropathy, or both [2], but it may be an incidental finding with no clinical relevance in patients with essential hypertension and/or chronic kidney disease from a variety of other etiologies [3]. It might even be seen in normotensive subjects with no evidence of renal dysfunction [3±5]. Hundreds of papers were published in recent years regarding the diagnosis and treatment of this condition. Many articles report on renal artery stenosis, but use substantially different definitions. The most popular criterion for stenosis is reduction of luminal diameter. However, "significant" stenosis is 50% for some investigators [4,6], but 70% [7] and even 75% for others [8]. Moreover, the diagnosis of "significant" stenosis is made using diverse diagnostic modalities, like Doppler ultrasound, computed tomography angiography, magnetic resonance angiography, digital subtraction angiography and conventional arteriography, which are not interchangeable and difficult to compare [9,10], not to mention inter-observer differences [11] Any attempt to answer the above question should take into consideration the diverse clinical presentations and outcomes as well as the range of diagnostic criteria and tools. It should be noted that atherosclerosis is not the only cause of RAS; fibromuscular dysplasia accounts for about 10±30% of cases [2,12]. The results of angioplasty in RAS due to FMD (FMD-RAS) are much better than in atherosclerotic RAS [2,13]. Several reports in the literature include both ARAS and FMD-RAS, making the interpretation of the data even more complicated. As described above, the two main consequences of a narrowed renal artery are hypertension and ischemic nephropathy. For the purpose of this discussion these two clinical syndromes should be considered separately since the goal of treatment is different: to cure, or at least to control, hypertension vs. to save renal function and prevent end-stage renal failure. The diagnosis of renovascular hypertension should only be made when the stenosis of the renal artery is the only, or at least the main, cause of hypertension, usually via activation of the reninangiotensin system [2]. As such, renovascular hypertension is quite rare, accounting for 1±5% [5] of all cases of hypertension. However, hypertension on one hand and RAS on the other are common findings in the elderly population. The explanation of this apparent contradiction is that hypertension and ARAS coexist but there is no causal relationship between the two as most subjects actually suffer from essential hypertension, which is very common in the elderly population [2]. With the current armamentarium, it is possible to control hypertension with drug therapy alone in the vast majority of patients, including those with RAS [14]. While many publications addressed the issue of angioplasty vs. drug treatment alone in renovascular hypertension, very few are well-executed prospective randomized controlled trials. Van Jaarsveld et al. [3] reported the results of a randomized controlled trial of the Dutch Renal Artery Stenosis Intervention Cooperative Study group. The study included 106 patients with hypertension and RAS, randomly assigned to either percutaneous transluminal renal angioplasty or drug therapy. After 1 year of follow-up the conclusions are unequivocal: ` In the treatment of patients with hypertension and RAS angioplasty has little advantage over antihypertensive-drug therapy.'' The Scottish and Newcastle Renal Artery Stenosis Collaborative study included 135 patients of whom 55 were randomized to intervention or drug therapy alone; the other 80 were managed by the preferred local option but were assessed and followed by the same protocol as the randomized patients [16]. Again, the conclusions are unequivocal: "In hypertensive patients with atheromatous renal artery stenosis, percutaneous renal angioplasty results in a modest improvement in systolic BP compared with medical therapy alone. This benefit was confined to patients with bilateral disease....the use of angioplasty in hypertensive renovascular disease as a reserve procedure for patients whose BP cannot be controlled by medical therapy, or for those whose renal function is deteriorating despite medical therapy, rather than as a primary form of intervention." Plouin et al. [8] reported the results of the EMMA trial (Essai Multicentrique Medicaments vs Angioplastie). This randomized