Portal de Periódicos da CAPES

Atherosclerotic Renal Artery Stenosis—Diagnosis and Treatment

2011; Elsevier BV; Volume: 86; Issue: 7 Linguagem: Inglês

10.4065/mcp.2011.0181

1942-5546

David Lao, Punit S. Parasher, Kerry C. Cho, Yerem Yeghiazarians,

Vascular anomalies and interventions

Renal artery stenosis (RAS) is characterized by a heterogeneous group of pathophysiologic entities, of which fibromuscular dysplasia and atherosclerotic RAS (ARAS) are the most common. Whether and which patients should undergo revascularization for ARAS is controversial. The general consensus is that all patients with ARAS should receive intensive medical treatment. The latest randomized clinical trials have increased confusion regarding recommendations for revascularization for ARAS. Although revascularization is not indicated in all patients with ARAS, experts agree that it should be considered in some patients, especially those with unstable angina, unexplained pulmonary edema, and hemodynamically significant ARAS with either worsening renal function or with difficult to control hypertension. A search of the literature was performed using PubMed and entering the search terms renal artery stenosis, atherosclerotic renal artery stenosis, and renal artery stenosis AND hypertension to retrieve the most recent publications on diagnosis and treatment of ARAS. In this review, we analyze the pathways related to hypertension in ARAS, the optimal invasive and noninvasive modalities for evaluating the renal arteries, and the available therapies for ARAS and assess future tools and algorithms that may prove useful in evaluating patients for renal revascularization therapy. Renal artery stenosis (RAS) is characterized by a heterogeneous group of pathophysiologic entities, of which fibromuscular dysplasia and atherosclerotic RAS (ARAS) are the most common. Whether and which patients should undergo revascularization for ARAS is controversial. The general consensus is that all patients with ARAS should receive intensive medical treatment. The latest randomized clinical trials have increased confusion regarding recommendations for revascularization for ARAS. Although revascularization is not indicated in all patients with ARAS, experts agree that it should be considered in some patients, especially those with unstable angina, unexplained pulmonary edema, and hemodynamically significant ARAS with either worsening renal function or with difficult to control hypertension. A search of the literature was performed using PubMed and entering the search terms renal artery stenosis, atherosclerotic renal artery stenosis, and renal artery stenosis AND hypertension to retrieve the most recent publications on diagnosis and treatment of ARAS. In this review, we analyze the pathways related to hypertension in ARAS, the optimal invasive and noninvasive modalities for evaluating the renal arteries, and the available therapies for ARAS and assess future tools and algorithms that may prove useful in evaluating patients for renal revascularization therapy. Renal artery stenosis (RAS), narrowing of the renal arteries, is caused by a heterogeneous group of conditions, including atherosclerosis, fibromuscular dysplasia (FMD), vasculitis, neurofibromatosis, congenital bands, and extrinsic compression, and radiation.1Dubel GJ Murphy TP The role of percutaneous revascularization for renal artery stenosis.Vasc Med. 2008; 13: 141-156Crossref PubMed Scopus (37) Google Scholar Atherosclerosis accounts for approximately 90% of the lesions that obstruct blood flow to the renal arteries. Atherosclerotic renal artery stenosis (ARAS) typically involves the ostium and/or proximal one-third of the renal artery and often the adjacent aorta.2Kaatee R Beek FJ Verschuyl EJ et al.Atherosclerotic renal artery stenosis: ostial or truncal?.Radiology. 1996; 199: 637-640PubMed Google Scholar However, segmental and diffuse intrarenal atherosclerosis may also be observed, especially in advanced cases.3Safian RD Textor SC Renal-artery stenosis.N Engl J Med. 2001; 344: 431-442Crossref PubMed Scopus (900) Google Scholar We reviewed the literature using PubMed to search for relevant recent publications with the terms renal artery stenosis, atherosclerotic renal artery stenosis, and renal artery stenosis AND hypertension. This review highlights salient points of the pathophysiology, diagnosis, and treatment of ARAS. The prevalence of ARAS increases with advancing age and with the presence of traditional cardiovascular risk factors. Among patients with hypertension, ARAS is observed in only 1% to 6%,4Simon N Franklin SS Bleifer KH Maxwell MH Clinical characteristics of renovascular hypertension.JAMA. 1972; 220: 1209-1218Crossref PubMed Scopus (267) Google Scholar, 5Ram CV Renovascular hypertension.Curr Opin Nephrol Hypertens. 1997; 6: 575-579Crossref PubMed Scopus (33) Google Scholar, 6Vokonas PS Kannel WB Cupples LA Epidemiology and risk of hypertension in the elderly: the Framingham Study.J Hypertens Suppl. 1988; 6: S3-S9PubMed Google Scholar whereas the incidence of ARAS is more than 30% in patients undergoing cardiac catheterization7Harding MB Smith LR Himmelstein SI et al.Renal artery stenosis: prevalence and associated risk factors in patients undergoing routine cardiac catheterization.J Am Soc Nephrol. 1992; 2: 1608-1616PubMed Google Scholar, 8Buller CE Nogareda JG Ramanathan K et al.The profile of cardiac patients with renal artery stenosis.J Am Coll Cardiol. 2004; 43: 1606-1613Abstract Full Text Full Text PDF PubMed Scopus (133) Google Scholar and more than 50% in elderly patients with known atherosclerotic disease.9Miralles M Corominas A Cotillas J Castro F Clara A Vidal-Barraquer F Screening for carotid and renal artery stenoses in patients with aortoiliac disease.Ann Vasc Surg. 1998; 12: 17-22Abstract Full Text PDF PubMed Scopus (51) Google Scholar, 10Swartbol P Parsson H Thorvinger B Norgren L To what extent does peripheral vascular disease and hypertension predict renal artery stenosis?.Int Angiol. 1994; 13: 109-114PubMed Google Scholar In a study of 170 patients with ARAS who were followed up with serial duplex scans, the cumulative incidence of disease progression was 51% 5 years after diagnosis.11Caps MT Perissinotto C Zierler RE et al.Prospective study of atherosclerotic disease progression in the renal artery.Circulation. 1998; 98: 2866-2872Crossref PubMed Scopus (359) Google Scholar In a pooled review of 5 trials using serial arteriography, 49% of all renal arteries examined demonstrated progression of stenosis during follow-up ranging from 6 to 180 months.12Greco BA Breyer JA The natural history of renal artery stenosis: who should be evaluated for suspected ischemic nephropathy?.Semin Nephrol. 1996; 16: 2-11PubMed Google Scholar Atherosclerotic renal artery stenosis results in a progressive loss of renal mass and function over time. In a subgroup of patients with renovascular hypertension and 60% obstruction, renal atrophy occurred in 21%.13Dean RH Kieffer RW Smith BM et al.Renovascular hypertension: anatomic and renal function changes during drug therapy.Arch Surg. 1981; 116: 1408-1415Crossref PubMed Scopus (280) Google Scholar, 14Tollefson DF Ernst CB Natural history of atherosclerotic renal artery stenosis associated with aortic disease.J Vasc Surg. 1991; 14: 327-331Abstract Full Text Full Text PDF PubMed Scopus (260) Google Scholar Historical data suggest that up to 27% of patients with ARAS will develop chronic renal failure within 6 years.15Wollenweber J Sheps SG Davis GD Clinical course of atherosclerotic renovascular disease.Am J Cardiol. 1968; 21: 60-71Abstract Full Text PDF PubMed Scopus (245) Google Scholar A prospective angiographic study revealed that ARAS was the cause of end-stage renal disease in 14% of patients in whom dialysis was newly initiated7Harding MB Smith LR Himmelstein SI et al.Renal artery stenosis: prevalence and associated risk factors in patients undergoing routine cardiac catheterization.J Am Soc Nephrol. 1992; 2: 1608-1616PubMed Google Scholar; thus, early detection and appropriate treatment of ARAS could have important economic consequences. The presence of ARAS is known to predict adverse coronary events. In the Cardiovascular Health Study, patients diagnosed as having ARAS had a higher incidence of hospitalization for angina, myocardial infarction, and coronary revascularization.16Edwards MS Craven TE Burke GL Dean RH Hansen KJ Renovascular disease and the risk of adverse coronary events in the elderly: a prospective, population-based study.Arch Intern Med. 2005; 165: 207-213Crossref PubMed Scopus (128) Google Scholar In a cohort of patients with ARAS detected at the time of coronary angiography, the 4-year survival rate was 65% for those with vs 86% for those without ARAS.17Conlon PJ Athirakul K Kovalik E et al.Survival in renal vascular disease.J Am Soc Nephrol. 1998; 9: 252-256PubMed Google Scholar The pathophysiology of hypertension in patients with RAS due to FMD was well-described in the seminal work on animal models of hypertension by Goldblatt18Goldblatt H Experimental hypertension induced by renal ischemia: Harvey Lecture, May 19, 1938.Bull N Y Acad Med. 1938; 14 (Accessed May 3, 2011.): 523-553http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1911248/pdf/bullnyacadmed00606-0004.pdfPubMed Google Scholar in the 1930s. This model describes renin-dependent hypertension in patients with FMD, but it does not adequately describe the etiology of hypertension in patients with ARAS, in whom the mechanisms of hypertension are more complex. Article Highlights •Renal artery stenosis (RAS) is caused by a heterogeneous group of conditions that lead to narrowing of the renal arteries; ARAS produces 90% of the lesions that obstruct blood flow•The mechanism of hypertension and cardiac morbidity in patients with ARAS is complex and often is not strictly renin-dependent; the interplay between the direct vasculotoxic effects of renin, the proinflammatory and neurohormonal effects of circulating angiotensin II, and the endocrinologic effects of aldosterone leads to an increase in total blood volume•Ultrasonography is widely accepted as the first-line diagnostic imaging test because of its availability and cost•Invasive renal angiography can be useful in evaluating ARAS and can be used in combination with adjunctive invasive tools, such as fractional flow reserve to measure translesional pressure gradients•All patients with ARAS require intensive antihypertensive agents and lipid-lowering agents; they should stop smoking, and antiplatelet therapy should be considered•Renal revascularization therapy is controversial; the only class I indication for renal revascularization under current guidelines is for hemodynamically significant ARAS in the setting of recurrent, unexplained congestive heart failure or sudden, unexplained pulmonary edema•Patients should undergo an evaluation of renal ischemia and of baseline renal function before undergoing renal revascularization therapy Article Highlights •Renal artery stenosis (RAS) is caused by a heterogeneous group of conditions that lead to narrowing of the renal arteries; ARAS produces 90% of the lesions that obstruct blood flow•The mechanism of hypertension and cardiac morbidity in patients with ARAS is complex and often is not strictly renin-dependent; the interplay between the direct vasculotoxic effects of renin, the proinflammatory and neurohormonal effects of circulating angiotensin II, and the endocrinologic effects of aldosterone leads to an increase in total blood volume•Ultrasonography is widely accepted as the first-line diagnostic imaging test because of its availability and cost•Invasive renal angiography can be useful in evaluating ARAS and can be used in combination with adjunctive invasive tools, such as fractional flow reserve to measure translesional pressure gradients•All patients with ARAS require intensive antihypertensive agents and lipid-lowering agents; they should stop smoking, and antiplatelet therapy should be considered•Renal revascularization therapy is controversial; the only class I indication for renal revascularization under current guidelines is for hemodynamically significant ARAS in the setting of recurrent, unexplained congestive heart failure or sudden, unexplained pulmonary edema•Patients should undergo an evaluation of renal ischemia and of baseline renal function before undergoing renal revascularization therapy Well-established animal studies have clearly shown that decreased renal artery perfusion leads to a cascade of events, starting with the production of renin.1Dubel GJ Murphy TP The role of percutaneous revascularization for renal artery stenosis.Vasc Med. 2008; 13: 141-156Crossref PubMed Scopus (37) Google Scholar, 19Gomez RA Sequeira Lopez ML Who and where is the renal baroreceptor? The connexin hypothesis.Kidney Int. 2009; 75: 460-462Crossref PubMed Scopus (19) Google Scholar, 20Skinner SL McCubbin JW Page IH Control of renin secretion.Circ Res. 1964; 15: 64-76Crossref PubMed Scopus (108) Google Scholar Renin promotes conversion of angiotensinogen to angiotensin I, which is converted to angiotensin II by angiotensin I converting enzyme, which also inactivates kinins that promote hypotension.21Erdos EG Angiotensin I converting enzyme.Circ Res. 1975; 36: 247-255Crossref PubMed Scopus (372) Google Scholar The largest store of angiotensin I converting enzyme is found in the pulmonary vasculature, where it plays an important role in the regulation of systemic blood pressure.22Aiken JW Vane JR Renin–angiotensin system: inhibition of converting enzyme in isolated tissues.Nature. 1970; 228: 30-34Crossref PubMed Scopus (90) Google Scholar In addition to causing hypertension by being directly vasoconstrictive, angiotensin II promotes hypertension by increasing total blood volume through its effect on aldosterone and by potentiating the vasoconstrictor response to circulating norepinephrine.23Reid IA Interactions between ANG II, sympathetic nervous system, and baroreceptor reflexes in regulation of blood pressure.Am J Physiol. 1992; 262: E763-E778PubMed Google Scholar Goldblatt's work has been expounded on to suggest 3 phases of renovascular hypertension as demonstrated in animal models. In stage I (acute occlusion) and stage II (occlusion for days/weeks), the blood pressure and plasma renin/angiotensin II levels are elevated, and elimination of the obstruction leads to normalization of both blood pressure and plasma renin/angiotensin II levels. In stage III, the occlusion is prolonged for months, plasma renin/angiotensin levels are no longer elevated, and elimination of the obstruction does not lead to normalization of blood pressure.24Glorioso N Laragh JH Rappelli A Renovascular Hypertension: Pathophysiology, Diagnosis, and Treatment. Raven Press Books, Ltd, New York, NY1987Google Scholar Although these stages were described in animal models, stage III may reflect hypertension seen in patients with ARAS who do not appear to have strict renin-dependence. Patients with ARAS and low renin/angiotensin II levels may have improvement in hypertension after renal revascularization, but the results are unreliable. In summary, activation of the sympathetic and central nervous systems, increasing total blood volume via aldosterone, and the direct pressor effects of angiotensin II in the setting of ARAS are thought to contribute to hypertension.25Johansson M Elam M Rundqvist B et al.Increased sympathetic nerve activity in renovascular hypertension.Circulation. 1999; 99: 2537-2542Crossref PubMed Scopus (165) Google Scholar, 26Mathias CJ Kooner JS Peart S Neurogenic components of hypertension in human renal artery stenosis.Clin Exp Hypertens A. 1987; 9: 293-306Crossref PubMed Scopus (21) Google Scholar Several studies have suggested that ARAS results in cardiac morbidity that is disproportionate to the degree of hypertension.15Wollenweber J Sheps SG Davis GD Clinical course of atherosclerotic renovascular disease.Am J Cardiol. 1968; 21: 60-71Abstract Full Text PDF PubMed Scopus (245) Google Scholar, 27Conlon PJ Little MA Pieper K Mark DB Severity of renal vascular disease predicts mortality in patients undergoing coronary angiography.Kidney Int. 2001; 60: 1490-1497Crossref PubMed Scopus (288) Google Scholar, 28Isles C Main J O'Connell J et al.Survival associated with renovascular disease in Glasgow and Newcastle: a collaborative study.Scott Med J. 1990; 35: 70-73PubMed Google Scholar Multiple pathways account for this because angiotensin II has been associated with a range of proinflammatory and toxic cardiovascular effects, including myocardial fibrosis,29Vasan RS Evans JC Benjamin EJ et al.Relations of serum aldosterone to cardiac structure: gender-related differences in the Framingham Heart Study.Hypertension. 2004; 43: 957-962Crossref PubMed Scopus (116) Google Scholar arterial medial hypertrophy, smooth muscle cell proliferation, endothelial cell dysfunction, and plaque rupture.30Meyrier A Vascular mechanisms of renal fibrosis: vasculonephropathies and arterial hypertension [article in French].Bull Acad Natl Med. 1999; 183: 33-45PubMed Google Scholar, 31Nakashima H Suzuki H Ohtsu H et al.Angiotensin II regulates vascular and endothelial dysfunction: recent topics of angiotensin II type-1 receptor signaling in the vasculature.Curr Vasc Pharmacol. 2006; 4: 67-78Crossref PubMed Scopus (117) Google Scholar Renin has also been associated with vasculotoxic and nephrotoxic effects.32Volpe M Camargo MJ Mueller FB et al.Relation of plasma renin to end organ damage and to protection of K+ feeding in strokeprone hypertensive rats.Hypertension. 1990; 15: 318-326Crossref PubMed Scopus (128) Google Scholar Oxidative stress has been implicated in the ischemic and hypertensive parenchymal renal injury related to ARAS.33Lerman LO Nath KA Rodriguez-Porcel M et al.Increased oxidative stress in experimental renovascular hypertension.Hypertension. 2001; 37: 541-546Crossref PubMed Google Scholar, 34Parildar M Parildar Z Oran I Kabaroglu C Memis A Bayindir O Nitric oxide and oxidative stress in atherosclerotic renovascular hypertension: effect of endovascular treatment.J Vasc Interv Radiol. 2003; 14: 887-892Abstract Full Text Full Text PDF PubMed Scopus (17) Google Scholar Clinical clues to the presence of ARAS are listed in Table 1.35Hirsch AT Haskal ZJ Hertzer NR et al.ACC/AHA 2005 guidelines for the management of patients with peripheral arterial disease (lower extremity, renal, mesenteric, and abdominal aortic): executive summary a collaborative report from the American Association for Vascular Surgery/Society for Vascular Surgery, Society for Cardiovascular Angiography and Interventions, Society for Vascular Medicine and Biology, Society of Interventional Radiology, and the ACC/AHA Task Force on Practice Guidelines (Writing Committee to Develop Guidelines for the Management of Patients With Peripheral Arterial Disease).J Am Coll Cardiol. 2006; 47: 1239-1312Abstract Full Text Full Text PDF PubMed Scopus (1070) Google Scholar On the basis of the American Heart Association (AHA) guidelines, screening and revascularization should be considered in patients who present in the setting of the clinical scenarios outlined in Table 2.35Hirsch AT Haskal ZJ Hertzer NR et al.ACC/AHA 2005 guidelines for the management of patients with peripheral arterial disease (lower extremity, renal, mesenteric, and abdominal aortic): executive summary a collaborative report from the American Association for Vascular Surgery/Society for Vascular Surgery, Society for Cardiovascular Angiography and Interventions, Society for Vascular Medicine and Biology, Society of Interventional Radiology, and the ACC/AHA Task Force on Practice Guidelines (Writing Committee to Develop Guidelines for the Management of Patients With Peripheral Arterial Disease).J Am Coll Cardiol. 2006; 47: 1239-1312Abstract Full Text Full Text PDF PubMed Scopus (1070) Google Scholar, 36Rundback JH Sacks D Kent KC AHA Councils on Cardiovascular Radiology, High Blood Pressure Research, Kidney in Cardiovascular Disease, Cardio-Thoracic and Vascular Surgery Clinical Cardiology Society of Interventional Radiology FDA Device Forum Committee American Heart Association et al.Guidelines for the reporting of renal artery revascularization in clinical trials.Circulation. 2002; 106: 1572-1585Crossref PubMed Scopus (226) Google Scholar The Joint National Committee stated that more extensive testing in patients with identifiable causes of ARAS is typically not necessary unless blood pressure control is not achieved while the patient is receiving maximal antihypertensive therapy.37Chobanian AV Bakris GL Black HR et al.Seventh report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure.Hypertension. 2003; 42: 1206-1252Crossref PubMed Scopus (10557) Google ScholarTABLE 1Clinical Clues to the Diagnosis of Atherosclerotic Renal Artery StenosisFrom J Am Coll Cardiol,35Hirsch AT Haskal ZJ Hertzer NR et al.ACC/AHA 2005 guidelines for the management of patients with peripheral arterial disease (lower extremity, renal, mesenteric, and abdominal aortic): executive summary a collaborative report from the American Association for Vascular Surgery/Society for Vascular Surgery, Society for Cardiovascular Angiography and Interventions, Society for Vascular Medicine and Biology, Society of Interventional Radiology, and the ACC/AHA Task Force on Practice Guidelines (Writing Committee to Develop Guidelines for the Management of Patients With Peripheral Arterial Disease).J Am Coll Cardiol. 2006; 47: 1239-1312Abstract Full Text Full Text PDF PubMed Scopus (1070) Google Scholar with permission of the American Heart Association. 1.Onset of hypertension before age 30 y or severe hypertension after age 55 y (class I, level of evidence [LOE] B)2.Accelerated, resistant, or malignant hypertension (class I, LOE C)3.Development of new azotemia or worsening renal function after administration of an angiotensin-converting enzyme inhibitor or angiotensin receptor blocker (class I, LOE B)4.Unexplained atrophie kidney or size discrepancy >1.5 cm between kidneys (class I, LOE B)5.Sudden, unexplained pulmonary edema (class I, LOE B)6.Unexplained renal dysfunction, including patients starting renal replacement treatment (class II, LOE B)7.Multivessel coronary artery disease or peripheral arterial disease (class IIb, LOE B)8.Unexplained congestive heart failure or refractory angina (class IIb. LOE C) Open table in a new tab TABLE 2American Heart Association Recommendations for Revascularization of Atherosclerotic Renal Artery Stenosis (ARAS)Adapted from J Am Coll Cardiol?35Hirsch AT Haskal ZJ Hertzer NR et al.ACC/AHA 2005 guidelines for the management of patients with peripheral arterial disease (lower extremity, renal, mesenteric, and abdominal aortic): executive summary a collaborative report from the American Association for Vascular Surgery/Society for Vascular Surgery, Society for Cardiovascular Angiography and Interventions, Society for Vascular Medicine and Biology, Society of Interventional Radiology, and the ACC/AHA Task Force on Practice Guidelines (Writing Committee to Develop Guidelines for the Management of Patients With Peripheral Arterial Disease).J Am Coll Cardiol. 2006; 47: 1239-1312Abstract Full Text Full Text PDF PubMed Scopus (1070) Google Scholar Asymptomatic stenosis Percutaneous revascularization can be considered for treatment of an asymptomatic bilateral or solitary viable kidney with hemodynamically significant ARAS (class IIb, level of evidence [LOE] C)Usefulness of percutaneous revascularization of asymptomatic unilateral hemodynamically significant ARAS in a viable kidney is not well established and is currently clinically unproved (class IIb, LOE C)Hypertension Percutaneous revascularization is reasonable for patients with hemodynamically significant ARAS and accelerated hypertension, resistant hypertension, malignant hypertension, hypertension with unexplained unilateral small kidney, and hypertension with intolerance to drug treatment (class IIa, LOE B)Preservation of renal function Percutaneous revascularization is reasonable for patients with ARAS and progressive chronic kidney disease with bilateral ARAS or ARAS of a solitary functioning kidney (class IIa, LOE B)Percutaneous revascularization can be considered for patients with ARAS and chronic renal insufficiency with unilateral ARAS (class IIb, LOE C)Effect of ARAS on congestive heart failure and unstable angina Percutaneous revascularization is indicated for patients with hemodynamically significant ARAS and recurrent, unexplained congestive heart failure or sudden, unexplained pulmonary edema (class I, LOE B)Percutaneous revascularization is reasonable for patients with hemodynamically significant ARAS and unstable angina (class IIa, LOE B) Open table in a new tab Magnetic resonance angiography (MRA), helical computed tomographic angiography (CTA), Doppler ultrasonography, renal scintigraphy (ie, captopril scan), invasive angiography, peripheral renin levels, and renal vein renin sampling have all been used as screening tests to detect ARAS. Renal vein renin sampling, peripheral renin levels, and renal scintigraphy are not generally recommended for ARAS screening because of their low sensitivity and low specifity.38Napoli V Pinto S Bargellini I et al.Duplex ultrasonographic study of the renal arteries before and after renal artery stenting.Eur Radiol. 2002; 12: 796-803Crossref PubMed Scopus (36) Google Scholar, 39Radermacher J Chavan A Bleck J et al.Use of Doppler ultrasonography to predict the outcome of therapy for renal-artery stenosis.N Engl J Med. 2001; 344: 410-417Crossref PubMed Scopus (669) Google Scholar, 40Grenier N Trillaud H Combe C et al.Diagnosis of renovascular hypertension: feasibility of captopril-sensitized dynamic MR imaging and comparison with captopril scintigraphy.AJR Am J Roentgenol. 1996; 166: 835-843Crossref PubMed Scopus (71) Google Scholar For an imaging study to be considered optimal, the following 4 objectives must be met: (1) ARAS must be detected and characterized on the basis of anatomic and hemodynamic severity; (2) anatomic consequences of ARAS on the artery itself and on the kidney must be assessed (eg, severe ARAS can result in poststenotic dilatation of the artery, which can be detected by CTA and MRA, and also in shrinkage of the renal parenchyma, with the kidney being 90 cm/s) and low RRI (<75-80) indicate no microvascular disease or increased resistance.39Radermacher J Chavan A Bleck J et al.Use of Doppler ultrasonography to predict the outcome of therapy for renal-artery stenosis.N Engl J Med. 2001; 344: 410-417Crossref PubMed Scopus (669) Google Scholar, 44Mukherjee D Bhatt DL Robbins M et al.Renal artery end diastolic velocity and renal artery resistance index as predictors of outcome after renal stenting.Am J Cardiol. 2001; 88: 1064-1066Abstract Full Text Full Text PDF PubMed Scopus (22) Google Scholar Spectral broadening and increased velocity on ultrasonography are markers of hemodynamically significant stenoses. For example, a renoaortic velocity ratio (defined as the renal artery peak systolic velocity/aortic peak systolic velocity) greater than 3.5 has been correlated to 60% stenosis,45Olin JW Piedmonte MR Young JR DeAnna S Grubb M Childs MB The utility of duplex ultrasound scanning of the renal arteries for diagnosing significant renal artery stenosis.Ann Intern Med. 1995; 122: 833-838Crossref PubMed Scopus (367) Google Scholar whereas a renal artery peak systolic velocity greater than 150 cm/s correlates to 50% stenosis, and a velocity greater than 180 cm/s correlates to 60% stenosis.45Olin JW Piedmonte MR Young JR DeAnna S Grubb M Childs MB The utility of duplex ultrasound scanning of the renal arteries for diagnosing significant renal artery stenosis.Ann Intern Med. 1995; 122: 833-838Crossref PubMed Scopus (367) Google Scholar, 46Kohler TR Zierler RE Martin RL et al.Noninvasive diagnosis of renal artery stenosis by ultrasonic duplex scanning.J Vasc Surg. 1986; 4: 450-456PubMed Scopus (216) Google Scholar, 47Taylor DC Kettler MD Moneta GL et al.Duplex ultrasound scanning in the diagnosis of renal artery stenosis: a prospective evaluation.J Vasc Surg. 1988; 7: