PREVALENCE AND NATURAL HISTORY
Atherosclerotic renal artery stenosis (RAS) is the most common primary disease of the renal arteries, and it is associated with clinical syndromes such as ischemic renal disease and hypertension. It is a common cause of secondary hypertension and is found in 0.5% to 5% of all hypertensive patients (1
). Renovascular hypertension, ischemic nephropathy, and end-stage renal disease (ESRD) are the potential consequences of atherosclerotic RAS.
The prevalence of RAS has been well documented in patients affecting ˜7% of the population aged >65 years (1
). In patients with atherosclerotic coronary and peripheral artery disease (PAD), renal-arterial disease has been documented to be present in 30% of patients undergoing screening renal artery angiography at the time of cardiac catheterization. In these populations, significant obstructive RAS (>50%) has been reported in 11% to 19% of patients (2
). Prevalence studies have also demonstrated significant RAS in 22% to 59% of patients with PAD (5
), and bilateral RAS involvement is found in ˜44% with RAS (10
Atherosclerosis accounts for ∽90% of cases of stenosis within the renal arterial bed (11
). Atherosclerotic lesions usually involve the origin and proximal third of the main renal artery and also the perirenal aorta. Fibromuscular dysplasia (FMD) accounts for <10% of cases of RAS, and usually involves the distal two-thirds of the main renal artery or its branches. Medial fibroplasia, a subtype of medial FMD, is the histological finding in 75% to 80% of all cases of FMD. Microscopically there are alternating areas of thinned media and thickened fibromuscular ridges containing collagen. Some areas of the internal elastic membrane are lost (12
). A “string of beads” is used to describe its angiographic appearance, where the “bead” diameter is larger than the proximal vessel. The classification of FMD is demonstrated in Table 37-1
TABLE 37-1 Classifcation of Fibromuscular Dysplasia
Alternating areas of thinned media and thickened fbromuscular ridges containing collagen. Internal elastic membrane may be lost in some areas
Extensive collagen deposition in the outer half of the media
True smooth muscle cell hyperplasia without fbrosis
Circumferential or eccentric deposition of collagen in the intima. No lipid or infammatory component. Internal elastic lamina fragmented or duplicated
Adventitial (periarterial) fbroplasias
Dense collagen replaces the fbrous tissue of the adventitia and may extend into surrounding tissue
CLINICAL ENDPOINTS AND PHYSICAL EXAMINATION
Atherosclerotic RAS is a progressive disease. Progression to occlusion is more common in renal arteries with more severe stenosis. Over a 3-year period, Zierler and associates found that 48% of patients had progression of RAS from <60% to ≥60% stenosis. The renal arteries that progressed to occlusion were each characterized by a stenosis ≥60% at baseline. Progression of RAS occurred at an average rate of ∽7% per year (15
). Patients with atherosclerotic RAS who progress to dialysis-dependent ESRD have high mortality rates (16
). This may be because of systemic atherosclerotic disease and higher rates of cardiovascular ischemic events in these individuals. Although several retrospective studies have indicated that percutaneous renal artery revascularization improves blood pressure, and stabilizes or retards the deterioration in renal function, recent randomized prospective trials have not indicated the usefulness of such revascularization procedures. As a result, management of such patients is still not completely clear, and the relationship between RAS severity and the impact on renal function remains poorly understood.
Patients with atherosclerotic RAS who progress to ESRD and require dialysis have high mortality rates. The mean life expectancy of individuals older than 65 years with RAS who had ESRD is only ∽3 years (16
). This is thought to be because of the systemic atherosclerosis and higher rates of cardiovascular events in individuals with atherosclerotic RAS. The severity of renal impairment has been associated with reduced survival in patients with RAS. In patients with serum creatinine levels <1.4 mg/dL, 3-year survival was 92% (±4%). For serum creatinine levels of between 1.5 and 1.9 mg/dL, 3-year survival was 74% (±8%), and for creatinine ≥2.0 mg/dL, it was only 51% (±8%) (17
TABLE 37-2 Clinical Clues to the Diagnosis of Renal Artery Stenosis
Accelerated, resistant or malignant hypertension
Hypertension at early onset (<30 years) or severe hypertension at late onset (>55 years)
Development of new azotemia or worsening renal function after administration of ACE inhibitor or ARB
Sudden unexplained pulmonary edema
Unexplained renal dysfunction
Multivessel coronary artery disease
Unexplained congestive heart failure
Presence of an atrophic kidney (≥7-8 cm) or discrepancy in renal sizes (>1.5cm)
Several clinical features provide relative indications for application of more specific diagnostic testing strategies for RAS (Table 37-2
). One such indication is the presence of an atrophic kidney (≤7-8 cm) or discrepancy in renal sizes (>1.5cm) (18
). If the renal atrophy is unexplained by a prior history of pyelonephritis, reflux nephropathy, or trauma, then this is an indication for additional renal diagnostic tests to define RAS.
The physical examination of patients with RAS should focus on the assessment of blood pressure as RAS may be associated with sustained or labile hypertension. Assessment for fluid retention and history of flash pulmonary edema, unexplained congestive heart failure, and refractory angina are also useful. The patient should also have an evaluation for evidence of atherosclerosis in other vascular territories. The physical exam should include evaluation for a renal abdominal bruit. Epigastric renal bruits that are high pitched with a diastolic component tend to be more hemody-namically significant.
Patients at high risk for RAS should undergo a noninvasive screening test to rule out this condition. RAS is best diagnosed with an imaging modality (18
). Both the main and the accessory renal arteries should be assessed to identify the hemodynamic signifi-cance of lesions, the site and severity of the stenosis, and associated pathology, including the presence of an abdominal aortic aneurysm (AAA) or renal or adrenal masses.
TABLE 37-3 Screening Tests for Renal Artery Stenosis
Diffcult specifcity in obese patients
Magnetic resonance angiogram
Good sensitivity and specifcity
Increased false positives
Not useful if stents are present
Computed tomographic angiography
Good sensitivity and specifcity
Useful to visualize stents
Captopril renal artery scintigraphy
Poor sensitivity (#8764;10%-25% false negative)
Renal vein renin
Lateralizing renin predicts
Renal catheter-based angiography
High sensitivity and specifcity
Imaging modalities such as duplex ultrasound, magnetic resonance angiography (MRA), computed tomographic angiography (CTA), and MRA are the most effective diagnostic screening methods (Table 37-3
). The choice of imaging procedure will depend on patient characteristics, renal function, contrast allergy, and presence of prior stents or metallic objects (may be contraindications to MRA or CTA techniques). The American College of Cardiology (ACC) and American Heart Association (AHA) have given various recommendations as to diagnostic modalities that can be used to identify RAS. Captopril renal artery scintigraphy is a relatively specific but insensitive test to demonstrate unilateral RAS; however, the incidence of false negatives is substantial. Measurement of plasma renin levels is discouraged because it is neither a specific nor a sensitive indicator of renovascular hypertension.
RENAL ARTERY ANGIOGRAPHY IN THE CATH LAB
Catheter-based renal angiography remains the gold standard for imaging renal arteries, although the noninvasive testing methods mentioned above have superseded it as a screening exam. Angiography is required to establish the diagnosis of RAS in the case of ambiguous noninvasive imaging. It is also indicated in individuals in whom concomitant peripheral angiography or coronary angiography is to be performed (and who have consented and have prespecified clinical indications).
Catheter-based angiography has a low rate of complications; however, care must still be taken in order to reduce the risks of atheroembolization, contrast-related nephropathy, vascular complications/damage, bleeding, and contrast allergy. To avoid these complications, the following is recommended: