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.

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  ARAS is prevalent with advancing age and has been found to affect 6.8% of patients in a population-based study of elderly people.

  
  
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  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

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  ARAS is anatomically in the artery ostium as a continuation of plaque from the abdominal aorta.²

  
  
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  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.

  
  
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  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.

  
  
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  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.

Clinical Features

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  ARAS has been implicated as a cause for HTN, deteriorating renal function, and cardiac disturbance syndromes (recurrent unexplained congestive heart failure, refractory angina, and flash pulmonary edema).

  
  
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  HTN related to underlying ARAS should be suspected in the following patients: patients older than 55 years at the time of onset, persons with resistant HTN (the inability to achieve goal blood pressure of 140/90 mm Hg or lower despite the use of three antihypertensive medications at maximum tolerable doses used in appropriate combinations), or in patients who experience exacerbation of previously well-controlled HTN.

  
  
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  ARAS should be suspected when there is deterioration in renal function following initiation of angiotensin-converting enzyme inhibitors or angiotensin receptor antagonists, unexplained azotemia, and an unexplained discrepancy in renal size.

Noninvasive Imaging Studies

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  Renal artery duplex ultrasonography is accurate, inexpensive, and painless, and thus is an ideal noninvasive option for confirming or refuting the diagnosis of renal artery stenosis.³

  
  
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  Duplex ultrasound criteria for the diagnosis of renal artery stenosis combines peak systolic velocities within the renal artery as well as the ratio of the peak systolic velocity as measured in the aorta at the level of the superior mesenteric artery and the peak systolic velocity at the level of the renal artery origin, known as the renal-to-aortic ratio.

  
  
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  Acceptable duplex criteria for the diagnosis of renal artery stenosis are presented in Table 43-1.

  
  
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  Computed tomography angiography (CTA) and magnetic resonance angiography (MRA) accurately assess ARAS, while providing excellent three-dimensional images of the renal arteries. Advantages include the ability to visualize accessory (polar) renal arteries and the abdominal aorta and kidneys, as well as other important pathologies such as aneurysms. Disadvantages of CTA include exposure to radiation, the need for iodinated contrast agents, and the inability to differentiate completely between calcification and the renal artery lumen. Disadvantages of MRA include the need for contrast agents (ie, gadolinium), a tendency to overestimate the severity of arterial stenosis, inability to visualize within metallic stents, and the rare occurrence of nephrogenic systemic fibrosis.

  
  
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  Other than the degree of stenosis, other noninvasive measurements and laboratory findings have been proposed to suggest which patients will respond to renal artery revascularization: cortical thinning, resistive index,⁴ and preprocedural proteinuria. The utility of resistive index has not been reproduced by all.