Management of Renal Artery Stenosis - an Update

The role of the renal vasculature in eliciting renovascular hypertension (RVH) was established in 1934, when Goldblatt et al. [1] in a classical experimental study demonstrated that partial obstruction of the renal artery increased mean arterial blood pressure (BP). The pathophysiology of renal artery stenosis (RAS) is incompletely understood but has been postulated to be related to increased afterload from neurohormonal activation and cytokine release [2]. Atherosclerotic RAS (ARAS) is increasingly diagnosed in the expanding elderly population, which also has a high prevalence of arterial hypertension. There is still considerable uncertainty concerning the optimal management of patients with RAS. Many hypertensive patients with RAS have co-existing essential hypertension and furthermore, it is often difficult to determine to what degree the RAS is responsible for the impairment of renal function. There are three possible treatment strategies: medical management, surgery, or percutaneous transluminal renal angioplasty (PTRA) with or without stent implantation. The use of stents has improved the technical success rate of PTRA and also led to lower risk of restenosis, in particular for ostial RAS. PTRA with stenting has therefore replaced surgical revascularisation for most patients with RAS and has led to a lower threshold for intervention. The treatment of choice to control hypertension in fibromuscular dysplasia (FMD) is generally accepted to be PTRA [3]. In ARAS, on the other hand, the benefits with PTRA are less clear [4] and the challenge to identify which patients are likely to benefit from revascularisation remains unknown.