Mohammad Hashim Mustehsan1, Cristina Sanina2, and Jose D. Tafur3 1 Division of Cardiology, Albert Einstein College of Medicine-Montefiore Medical Center, Bronx, NY, USA 2 Division of Cardiology, Department of Medicine, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA, USA 3 Department of Cardiovascular Diseases, John Ochsner Heart & Vascular Institute, The Ochsner Clinical School, University of Queensland School of Medicine, New Orleans, LA, USA Renal artery stenosis (RAS) is most frequently secondary to atherosclerotic renal artery stenosis (ARAS) (90%). Fibromuscular dysplasia (FMD) accounts for most of the remaining cases. Clinical manifestations include severe and refractory hypertension, ischemic nephropathy, and cardiac destabilizing syndromes (flash‐pulmonary edema, heart failure, acute coronary syndrome). Patients should be tested for RAS if they have: early (age ≤30 years) or late (age ≥55 years) onset of hypertension, resistant, accelerated, or malignant hypertension, acute renal failure after initiation of ACEi/ARB, renal atrophy, or sudden, unexplained pulmonary edema. Screening for RAS is performed using noninvasive imaging, namely renal artery Doppler ultrasound, computer tomographic angiography (CTA), or magnetic resonance angiography (MRA). Invasive testing with digital subtraction angiography is still considered the gold standard but carries the risk of procedural complications. Evidence from RCTs has failed to demonstrate a benefit for revascularization compared to medical therapy as an initial approach. However, revascularization for cases refractory to medical therapy is still indicated and appropriate patient selection is essential. Patients with recurrent flash‐pulmonary edema, hemodynamically significant RAS, refractory ACS, refractory hypertension resistant to optimal medical therapy, or progressively worsening renal insufficiency should be considered for RAS revascularization. The main goal of RAS revascularization is to prevent progression of, and potentially reverse, complications of RAS including hypertension, cardiac destabilizing syndromes, and ischemic nephropathy. Strategies to maximize results and prevent short‐ and long‐term complications include radial access, no‐touch techniques, and intravascular imaging. After intervention, all patients should be placed on at least single‐antiplatelet therapy with aspirin. Ensure close outpatient follow‐up, along with postprocedural renal Doppler ultrasound at 1, 6, and 12 months, and annually thereafter. Renal artery stenosis (RAS) is defined as an abnormal narrowing of one or both renal arteries. While there are several potential etiologies of RAS (Table 6.1), the overwhelming majority (~90%) of cases can be attributed to ARAS – with FMD accounting for most of the remaining cases (~10%), typically in younger females [1]. ARAS is common and its prevalence depends on the population being screened, with incidence increasing with age, affecting both men and women equally. ARAS is present in about 7% of patients over the age of 65 years and is more prevalent (~60%) in patients with hypertension, atherosclerotic arterial disease, and renal insufficiency [2]. Clinical manifestations of RAS include hypertension, ischemic nephropathy, and cardiac destabilizing syndromes. Table 6.1 Etiologies of renal artery stenosis. Hypertension: Both unilateral and bilateral RAS can lead to hypertension, but by slightly different mechanisms. It is posited that hemodynamically significant unilateral RAS results in the activation of the renin‐angiotensin‐aldosterone system (RAAS), leading to increased arterial tone and hypertension. Due to the preserved function of the contralateral kidney, appropriate natriuresis continues to occur, and no significant volume overload exists. Bilateral RAS similarly leads to RAAS activation; however, there is significant concomitant volume overload given that neither kidney can accommodate compensatory natriuresis. RAS‐related hypertension is the leading cause of secondary hypertension and may be difficult to control. Ischemic nephropathy: Hemodynamically significant RAS can result in ischemic nephropathy, which is characterized by loss of renal mass, reduction in glomerular filtration, and renal parenchymal fibrosis. Clinically this presents as progressive loss of renal function, proteinuria, and renal atrophy. Cardiac destabilizing syndromes: RAS‐related volume overload and hypertension can lead to flash‐pulmonary edema (particularly in the absence of valvular disease or heart failure), acute coronary syndrome, and refractory heart failure [3]. There are no existing guidelines on routine screening for RAS, and screening can be initiated by clinicians based on patient presentation and risk factors. Currently, Class I recommendations for screening by the ACC/AHA guidelines [4] include early (age ≤30 years) or late (age ≥55 years) onset of hypertension, resistant (hypertension with systolic blood pressure ≥140 ± diastolic blood pressure ≥90 despite use of three or more oral agents including a diuretic), accelerated (sudden worsening of previously controlled hypertension) or malignant (severe hypertension with evidence of end‐organ damage) hypertension, acute renal failure after initiation of ACEi/ARB, renal atrophy, asymmetric renal dimensions (discrepancy of >1.5 cm), and sudden, unexplained pulmonary edema. Other indications for screening include unexplained renal failure, new dialysis initiation, vascular disease (coronary disease or peripheral arterial disease), and unexplained heart failure [4] (Table 6.2). Renal doppler ultrasound (DUS): Renal DUS is an excellent initial test for the assessment of RAS, given that it is low cost and noninvasive nature. Peak systolic velocity (PSV) >200 cm/s by Doppler is 95% sensitive and 90% specific for identifying a renal artery lesion >50%, while an end‐diastolic velocity of >150 cm/s is highly predictive of a severe (>80%) lesion [5]
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Severe Renal Artery Stenosis: How to Intervene
Introduction
Background and Clinical Significance
Epidemiology
Clinical Manifestations
Atherosclerotic renal artery stenosis (ARAS) – 90% of cases
Fibromuscular dysplasia (FMD) – ~10% of cases
Trauma with resulting dissection
Renal artery dissection
Congenital
Williams syndrome (genetic condition, thought to involve deletion of the Elastin gene)
Patient Selection: Who to Screen for RAS
RAS Assessment
Noninvasive RAS Assessment
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