Renovascuclar Disease: Mechanisms of its Poor Cardiovascular response to Revascularization

Renal artery stenosis (RAS) is caused by narrowing of the renal artery which supplies the downstream kidney. The etiologies of RAS vary with atherosclerosis being the most common, accounting for approximately 90% of the lesions that obstruct blood flow to the renal arteries [1]. Atherosclerotic RAS (ARAS) typically involves the ostium and/or proximal one-third of the renal artery and often the adjacent aorta. It could affect one or both kidneys. The prevalence of ARAS, like coronary artery disease and other atherosclerotic vascular lesions, increases with advancing age and with the presence of traditional cardiovascular risk factors such as age, hyperlipidemia, smoking, diabetes, and overweight/obesity. The degree of obstruction deteriorates over time, compromising post-stenotic kidney function. Indeed, a prospective study revealed that ARAS accounts for 14% of patients with end-stage renal disease in whom dialysis was newly initiated [2]. Importantly, patients with ARAS develop renovascular hypertension, which not only accelerates renal injury, but also strongly associates with cardiovascular complications. Due to subsequent and persistent activation of renin-angiotensin-aldosterone system, the blood pressure is elevated and can affect the heart, leading to myocardial infarction, left ventricular hypertrophy, heart failure, and even pulmonary edema [3]. Indeed, the presence of ARAS is known to predict adverse coronary events and mortality [4,5]. It can also affect the peripheral vasculature causing blood vessel remodeling and atherosclerosis, as well as the brain causing stroke [3].