Medical therapy for atherosclerotic renal artery stenosis

Abstract

Atherosclerotic renal artery stenosis (ARAS) is a common manifestation of generalized atherosclerosis (ATS) and is the most common disorder of the renal arterial circulation [1–3]. Furthermore, ARAS typically occurs in patients at high risk of cardiovascular disease with coexistent vascular disease at nonrenal sites. Indeed, the prevalence of ARAS in a population-based study of people aged 65 years or over is 7%. Prevalence rates for ARAS is 18% in patients with hypertension, 20% in patients with diabetes mellitus and hypertension, 25% in patients with peripheral vascular disease and 33% in those with abdominal aortic aneurysm [4]. Patients affected by ARAS are likely to have more complications and more extensive target-organ damage than patients without ARAS. Indeed, hemodynamically significant ARAS (stenosis >70%) leads to a fall in poststenosis pressure, and if perfusion pressure falls below the limit of renal autoregulation, the glomerular filtration rate decreases. The renin–angiotensin–aldosterone system (RAAS) is activated by the decrease in renal perfusion with increased production of angiotensin II, whose action led to an increase in hemodynamic resistance and systemic blood pressure. Its other nonhemodynamic effects play an important role in structural changes in the ischemic kidney [5]. Recent experimental evidence suggests that ARAS is associated with the activation of intrarenal fibrogenic and inflammatory pathways, oxidative stress and microvascular remodeling, and blocking these mechanisms can improve renal hemodynamics and function. As recent evidence indicates, the relationship between renal artery stenosis and ATS is complex, and mediators implicated in the pathophysiology of atherosclerotic renovascular disease may also contribute to the progression of cardiovascular damage. The therapeutic options to date include revascularization usually by percutaneous transluminal renal angioplasty (PTRA) with or without stenting and/or medical treatment. However, although the angiographic results after PTRA are often remarkable, clinical results are rarely satisfactory regarding hypertension, renal function and survival [6–11]. It is of note that these studies usually concern patients with stable clinical conditions and, in many cases, only moderate ARAS lesions. Recognizing these limitations, the conclusions drawn from these trials are that, compared with best medical management, PTRA with stenting has a very small role in the management of ARAS. Most importantly, there was no difference in the change in renal function and overall cardiovascular mortality. However, these results do not affect patients with ARAS associated to acute kidney injury, flash pulmonary edema or with malignant or treatment-resistant hypertension. Other patients are in great risk for acute kidney injury namely those with critical ARAS and rapid deterioration of renal function on RAAS inhibitors.