Atherosclerotic renovascular disease: beyond the renal artery stenosis

Atherosclerotic renovascular disease (ARVD) is a wellrecognized cause of arterial hypertension. However, the role of ARVD as an important contributor to renal failure remains a controversial issue. The original experiments of Goldblatt et al. [1] have demonstrated that arterial hypertension due to unilateral renal artery stenosis (RAS) can cause bilateral renal damages. Indeed, because of the reduced perfusion pressure beyond the clip, the tissue of the clipped kidney is exposed to chronic hypoxia, which leads to ischaemic kidney injury. In the unclipped kidney however, renal damage will progressively develop, due to the arterial hypertension caused by the activation of the renin– angiotensin–aldosterone system [1]. In recent years, attention to non-traditional mediators of ARVD such as inflammatory pathways and microvascular events has yielded new paradigms and avenues of research. Among other mechanisms, reactive oxygen species (ROS) production, ischaemia/ reperfusion damage and modulation of matrix turnover have been proposed to promote renal failure related to ARVD (Figure 1). The goal of this editorial is to review the potential role of these mediators in ARVD.