A 67-year-old man treated for hypertension (HTN) for the past 25 years is now having difficulty with his blood pressure control. His medical history is notable for long-standing hypercholesterolemia and former tobacco abuse (25 pack-years) until 1 month ago when he was hospitalized for chest pain. At that time his blood pressure was 195/110 mm Hg. He has noted that blood pressure control has been gradually worsening over the past several years. Most recently, his blood pressure measurements have not been below 160/95 mm Hg. He has eliminated salt from his diet, has been watching his weight, and has been compliant with his three antihypertensive medications, all of which have been prescribed at maximal doses (hydrochlorothiazide 25 mg/d, lisinopril 40 mg/d, and amlodipine 10 mg/d). On physical examination he has a midline systolic bruit just above the umbilicus radiating to his right flank. Figures 43-1,43-2, and 43-3 demonstrate the typical appearance of atherosclerotic renal artery stenosis (ARAS) by duplex ultrasonography, computed tomography (CT), and contrast angiography.
Duplex ultrasound of right renal artery ostial stenosis.
Three-dimensional reconstructed computed tomography angiography (CTA) image of right renal artery stenosis (arrow).
Angiography of left renal artery ostial stenosis in a renal artery and an accessory renal artery (arrowheads).
ARAS is prevalent with advancing age and has been found to affect 6.8% of patients in a population-based study of elderly people.
ARAS is most prevalent in at-risk populations, including patients with systemic atherosclerosis, patients with coronary artery disease (18%-20%), or patients with peripheral artery disease, where it was found in up to 59% of patients.1
ARAS is anatomically in the artery ostium as a continuation of plaque from the abdominal aorta.2
HTN in ARAS results from activation of the renin-angiotensin-aldosterone pathway. The kidney ipsilateral to the stenosis responds by secreting renin, which promotes sodium retention and vasoconstriction via the renin-angiotensin-aldosterone pathway. The nonstenotic contralateral kidney responds by natriuresis that promotes intravascular volume depletion. The stenotic kidney excretes more renin as its perfusion pressure has been reduced. At some point natriuresis is overpowered by the renin-angiotensin-aldosterone pathway, resulting in HTN.
Renal failure in patients with ARAS results from multiple potential etiologies: long-standing systemic HTN, renal ischemia, recurrent atheromatous embolization from an atherosclerotic aorta, and contrast nephropathy following multiple imaging studies.
While ARAS is more prevalent in patients with end-stage renal failure than those without it, there is no linear relationship between the degree of ARAS and HTN or renal dysfunction.