(Radiographics. 2000;20:1355-1368.)
© RSNA, 2000
Imaging of Renovascular Hypertension: Respective Values of Renal Scintigraphy, Renal Doppler US, and MR Angiography1
Gilles Soulez, MD ,
Vincent L. Oliva, MD ,
Sophie Turpin, MD ,
Raymond Lambert, MD ,
Viviane Nicolet, MD and
Eric Therasse, MD
1 From the Department of Radiology, Notre-Dame Hospital, Centre Hospitalier de l'Université de Montréal, 1560 rue Sherbrooke East, Montreal, Quebec, Canada H2L 4M1 (G.S., V.L.O., V.N.); and the Departments of Nuclear Medicine (S.T., R.L.) and Radiology (E.T.), Hotel-Dieu Hospital, Centre Hospitalier de l'Université de Montréal. Presented as a scientific exhibit at the 1998 RSNA scientific assembly. Received May 6, 1999; revision requested June 29; final revision received September 8; accepted September 9. Address correspondence to G.S. (e-mail: gsoulez@netcom.ca).
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Abstract
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Renovascular hypertension affects 15%–30% of patients who have clinical criteria suggestive of renovascular disease. Noninvasive screening is crucial for patient selection prior to conventional angiography and renal revascularization. Renal scintigraphy has been reported to be sensitive for detection of renovascular hypertension, but some of its limitations (eg, in the setting of bilateral renal artery stenosis and renal failure) should be considered. Doppler ultrasonography (US) allows direct evaluation of the renal arteries as well as transrenal Doppler waveform analysis, but it remains operator dependent. Gadolinium-enhanced magnetic resonance (MR) angiography is becoming an excellent alternative to conventional angiography. The main limiting factors of this technique are inadequate visualization of segmental and accessory renal arteries as well as a tendency toward overestimation of stenoses. Given the high cost and low availability of MR angiography, scintigraphy and Doppler US should be considered the primary studies in screening for renovascular hypertension. MR angiography could be reserved for patients with inconclusive scintigraphic and Doppler US results, patients with high clinical suspicion of renovascular hypertension, and patients with a contraindication to conventional angiography.
Index Terms: Angiotensin-converting enzyme (ACE), 81.1217 • Hypertension, renovascular, 89.72 • Kidney, radionuclide studies, 81.1217 • Radionuclide imaging, comparative studies, 81.12174 • Renal arteries, MR, 961.12942 • Renal arteries, stenosis or obstruction, 961.72 • Renal arteries, US, 961.12984
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LEARNING OBJECTIVES FOR TEST 4
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After reading this article and taking the test, the reader will be able to:
- List the spectrum of clinical and radiologic findings in patients with RVH.
- Describe the technical aspects of the different imaging studies used in investigation of RVH.
- Discuss the roles and limitations of the different imaging studies used in diagnosis of RVH.
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Introduction
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The term renovascular hypertension (RVH) pertains to the causal relationship between a renal artery stenosis (RAS) and its clinical consequences, namely, hypertension or renal failure. Among the population of hypertensive patients, approximately 1%–5% have true RVH (1). However, among patients with a significant RAS, only two-thirds show improvement of hypertension after revascularization and 27%–80% show improvement or stabilization of renal function. When left untreated, atheromatous RAS tends to worsen, leading to renal artery thrombosis (2). In addition, medical treatment of RVH has been proved to be less effective than percutaneous or surgical revascularization (3–5). Therefore, patients suspected of having RVH should undergo adequate screening.
RVH can be suspected by using several clinical criteria (Table 1), in the presence of which the prevalence of RVH is 20%–30% (6). In this selected population, the investigation should be extended to noninvasive studies that will allow detection of RAS. ACE inhibitor scintigraphy, Doppler ultrasonography (US), and magnetic resonance (MR) angiography of the renal arteries can be used in combination to achieve adequate screening of patients prior to conventional angiography or revascularization. This article describes the roles of these three modalities in diagnosis of RVH and presents an algorithm for their use.
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Causes of RAS
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Although a variety of pathologic lesions may cause RVH, the most common is stenosis of the renal artery caused by atherosclerosis or, less commonly, fibromuscular dysplasia. The main features of these two entities are summarized in Table 2. In general, atheromatous lesions involve the proximal renal artery, whereas fibromuscular dysplasia involves the distal main renal artery and segmental renal arteries. Consequently, diagnostic tests that demonstrate only the proximal renal arteries, such as MR angiography or Doppler US limited to the main renal arteries, can be of less value in patients with suspected fibromuscular dysplasia.
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ACE Inhibitor Scintigraphy
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It has been demonstrated that a kidney with RVH may exhibit impaired function during ACE inhibition. This phenomenon is observed mainly in patients with bilateral RAS or with arterial
stenosis in a solitary kidney; it is believed to be caused by disruption of the autoregulation system of the glomerular filtration rate (GFR), which becomes dependent on angiotensin II under conditions of low perfusion. Although a decline in the GFR can be induced by ACE inhibition in the affected kidney of patients with unilateral RAS, the contralateral kidney preserves the overall renal function.
In patients with unilateral RAS, a unilateral change in renal function induced by ACE inhibition can be revealed with scintigraphy (7,8). In these patients, ACE inhibitor scintigraphy induces significant changes in the time-activity curves of the affected kidney in comparison with baseline scintigraphy. Such changes are not observed in patients with nonsignificant RAS or normal renal arteries. ACE inhibitor scintigraphy is performed 1 hour after an oral dose of 25 mg of captopril or 15 minutes after an intravenous dose of 0.04 mg/kg of enalapril maleate. ACE inhibitor therapy should be stopped 2–5 days prior to the study according to the half-life (9), and adequate hydration must be ensured. Blood pressure should be monitored during the test. Baseline and ACE inhibitor scintigraphy are performed after intravenous injection of technetium-99m mercaptoacetyltriglycine (MAG3), iodine-131 orthoiodohippurate (OIH), or Tc-99m diethylenetriaminepentaacetic acid (DTPA). Sequential images and scintigraphic curves are obtained for 30 minutes after injection of the radiopharmaceutical. Time-activity curves are generated from the renal cortex and pelvis. Renal uptake is measured at 1–2-minute intervals after injection.
Tc-99m MAG3 and I-131 OIH are excreted by means of tubular secretion, and Tc-99m DTPA is excreted by means of glomerular filtration. In patients with RAS, ACE inhibitors induce renal retention of the radiopharmaceutical due to decreased urinary output secondary to reduced GFR. Scintigraphic abnormalities provoked by ACE inhibitors can be reversed with balloon dilation (Fig 1).
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Figure 1a. Renovascular disease in a 60-year-old patient. (a) Baseline scintigram (posterior view) obtained with Tc-99m MAG3 shows mild and nonspecific abnormalities, with decreased amplitude and delayed peaking of the left renal curve (arrowhead) relative to the right renal curve (solid arrow). The time reference (open arrow) is 30 minutes. (b) Scintigram (posterior view) obtained after administration of captopril shows diminished uptake in the left kidney, with an abnormal curve (solid arrow) suggesting left-sided renovascular disease. The time reference (open arrow) is 30 minutes. (c) Aortogram shows a severe stenosis of the left renal artery. (d) Angiogram obtained after angioplasty and stent placement shows wide patency of the left renal artery. (e) Scintigraphic curves (top left, left renal collecting system; top right, left renal cortex; bottom left, right renal collecting system; bottom right, right renal cortex) obtained after correction of RAS show normalization of the captopril scintigraphic curve for the left kidney (top curves). The curves were obtained over 30 minutes. CA = cortical peak activity (between 1 and 3 minutes), CBF = curve with background correction, CR = cortical residual activity (between 20 and 23 minutes).
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Figure 1b. Renovascular disease in a 60-year-old patient. (a) Baseline scintigram (posterior view) obtained with Tc-99m MAG3 shows mild and nonspecific abnormalities, with decreased amplitude and delayed peaking of the left renal curve (arrowhead) relative to the right renal curve (solid arrow). The time reference (open arrow) is 30 minutes. (b) Scintigram (posterior view) obtained after administration of captopril shows diminished uptake in the left kidney, with an abnormal curve (solid arrow) suggesting left-sided renovascular disease. The time reference (open arrow) is 30 minutes. (c) Aortogram shows a severe stenosis of the left renal artery. (d) Angiogram obtained after angioplasty and stent placement shows wide patency of the left renal artery. (e) Scintigraphic curves (top left, left renal collecting system; top right, left renal cortex; bottom left, right renal collecting system; bottom right, right renal cortex) obtained after correction of RAS show normalization of the captopril scintigraphic curve for the left kidney (top curves). The curves were obtained over 30 minutes. CA = cortical peak activity (between 1 and 3 minutes), CBF = curve with background correction, CR = cortical residual activity (between 20 and 23 minutes).
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Figure 1c. Renovascular disease in a 60-year-old patient. (a) Baseline scintigram (posterior view) obtained with Tc-99m MAG3 shows mild and nonspecific abnormalities, with decreased amplitude and delayed peaking of the left renal curve (arrowhead) relative to the right renal curve (solid arrow). The time reference (open arrow) is 30 minutes. (b) Scintigram (posterior view) obtained after administration of captopril shows diminished uptake in the left kidney, with an abnormal curve (solid arrow) suggesting left-sided renovascular disease. The time reference (open arrow) is 30 minutes. (c) Aortogram shows a severe stenosis of the left renal artery. (d) Angiogram obtained after angioplasty and stent placement shows wide patency of the left renal artery. (e) Scintigraphic curves (top left, left renal collecting system; top right, left renal cortex; bottom left, right renal collecting system; bottom right, right renal cortex) obtained after correction of RAS show normalization of the captopril scintigraphic curve for the left kidney (top curves). The curves were obtained over 30 minutes. CA = cortical peak activity (between 1 and 3 minutes), CBF = curve with background correction, CR = cortical residual activity (between 20 and 23 minutes).
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Figure 1d. Renovascular disease in a 60-year-old patient. (a) Baseline scintigram (posterior view) obtained with Tc-99m MAG3 shows mild and nonspecific abnormalities, with decreased amplitude and delayed peaking of the left renal curve (arrowhead) relative to the right renal curve (solid arrow). The time reference (open arrow) is 30 minutes. (b) Scintigram (posterior view) obtained after administration of captopril shows diminished uptake in the left kidney, with an abnormal curve (solid arrow) suggesting left-sided renovascular disease. The time reference (open arrow) is 30 minutes. (c) Aortogram shows a severe stenosis of the left renal artery. (d) Angiogram obtained after angioplasty and stent placement shows wide patency of the left renal artery. (e) Scintigraphic curves (top left, left renal collecting system; top right, left renal cortex; bottom left, right renal collecting system; bottom right, right renal cortex) obtained after correction of RAS show normalization of the captopril scintigraphic curve for the left kidney (top curves). The curves were obtained over 30 minutes. CA = cortical peak activity (between 1 and 3 minutes), CBF = curve with background correction, CR = cortical residual activity (between 20 and 23 minutes).
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Figure 1e. Renovascular disease in a 60-year-old patient. (a) Baseline scintigram (posterior view) obtained with Tc-99m MAG3 shows mild and nonspecific abnormalities, with decreased amplitude and delayed peaking of the left renal curve (arrowhead) relative to the right renal curve (solid arrow). The time reference (open arrow) is 30 minutes. (b) Scintigram (posterior view) obtained after administration of captopril shows diminished uptake in the left kidney, with an abnormal curve (solid arrow) suggesting left-sided renovascular disease. The time reference (open arrow) is 30 minutes. (c) Aortogram shows a severe stenosis of the left renal artery. (d) Angiogram obtained after angioplasty and stent placement shows wide patency of the left renal artery. (e) Scintigraphic curves (top left, left renal collecting system; top right, left renal cortex; bottom left, right renal collecting system; bottom right, right renal cortex) obtained after correction of RAS show normalization of the captopril scintigraphic curve for the left kidney (top curves). The curves were obtained over 30 minutes. CA = cortical peak activity (between 1 and 3 minutes), CBF = curve with background correction, CR = cortical residual activity (between 20 and 23 minutes).
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In selected high-risk populations, ACE inhibitor scintigraphy can be very accurate. Its sensitivity for detection of RAS 70% or greater in diameter varies between 51% and 96% (mean, 82%) (10). Its positive predictive value for detection of RAS associated with clinical improvement in hypertension after revascularization varies between 51% and 100% (mean, 85%). However, ACE inhibitor scintigraphy is much less sensitive and specific in unselected patients. Bilateral RAS, impaired renal function, urinary obstruction, and chronic intake of ACE inhibitors are other factors that lower the sensitivity of ACE inhibitor scintigraphy (Fig 2). The latter factor is the reason for withholding ACE inhibitors for 2–5 days (depending on the half-life) before the study. When performed under the right conditions, ACE inhibitor scintigraphy is a useful tool. Moreover, careful analysis of the scintigram may allow detection of stenotic accessory arteries (Fig 3).
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Figure 2a. Indeterminate scintigraphic results in a 70-year-old patient with renal insufficiency. Baseline (a) and captopril (b) Tc-99m DTPA scintigrams (sequential images obtained at 2-minute intervals from top left to bottom right) show poor demonstration of both kidneys. No conclusion could be drawn about the possibility of renovascular disease.
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Figure 2b. Indeterminate scintigraphic results in a 70-year-old patient with renal insufficiency. Baseline (a) and captopril (b) Tc-99m DTPA scintigrams (sequential images obtained at 2-minute intervals from top left to bottom right) show poor demonstration of both kidneys. No conclusion could be drawn about the possibility of renovascular disease.
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Figure 3a. Stenotic accessory artery in a 55-year-old patient with hypertension. (a) Baseline Tc-99m DTPA scintigrams (sequential posterior views obtained at 2-minute intervals from top left to bottom right) show slight retention of the radiopharmaceutical in the left renal pelvis. (b) Captopril scintigrams show markedly decreased uptake in the upper half of the right kidney, a finding consistent with renovascular disease of a polar artery.
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Figure 3b. Stenotic accessory artery in a 55-year-old patient with hypertension. (a) Baseline Tc-99m DTPA scintigrams (sequential posterior views obtained at 2-minute intervals from top left to bottom right) show slight retention of the radiopharmaceutical in the left renal pelvis. (b) Captopril scintigrams show markedly decreased uptake in the upper half of the right kidney, a finding consistent with renovascular disease of a polar artery.
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ACE inhibitor scintigrams should be interpreted as consistent with a low, intermediate, or high probability of renovascular disease. The most specific diagnostic criterion for RVH at
scintigraphy is an ACE inhibitor–induced change on the scintigram. The general interpretive criteria are as follows (9):
1. A normal ACE inhibitor scintigram indicates a low probability (<10%) of RVH.
2. A small, poorly functioning kidney (<30% uptake with a time to maximum activity [Tmax] 
2 minutes) that shows no change on the ACE inhibitor scintigram and bilateral symmetric abnormalities such as cortical retention of tubular agents indicate an intermediate probability of RVH.
3. Criteria associated with a high probability of RVH include worsening of the scintigraphic curve, reduction in the relative uptake, prolongation of the renal and parenchymal transit time, increase in the 20-minute/peak uptake ratio, and prolongation of Tmax.
Specific interpretive criteria for Tc-99m MAG3 and I-131 OIH scintigrams are as follows (9): Unilateral parenchymal retention after ACE inhibition is the most important criterion for Tc-99m MAG3 and I-131 OIH scintigraphy and represents a high probability (>90%) of RVH. Parenchymal retention can be demonstrated as a change in the 20-minute/peak uptake ratio of 0.15 or greater, a significantly prolonged transit time, or a change in the scintigraphic grade (Fig 4). Parenchymal retention can also be demonstrated as a delay in excretion of the tracer into the renal pelvis of greater than 2 minutes after administration of ACE inhibitors or an increase in the Tmax of at least 2 minutes or 40%. A greater than 10% change in the relative uptake of Tc-99m MAG3 or I-131 OIH after ACE inhibition is uncommon but represents a high probability of RVH.
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Figure 4. Patterns of scintigraphic curves. 0 = normal, 1 = minor abnormalities but with Tmax greater than 5 minutes and (for Tc-99m MAG3 and I-131 OIH scintigrams) 20-minute/peak uptake ratio greater than 0.3, 2 = marked delayed excretion rate with preserved washout phase, 3 = delayed excretion rate without washout phase (accumulation curve), 4 = renal failure pattern with measurable kidney uptake, 5 = renal failure pattern without measurable kidney uptake (blood background-type curve).
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Doppler US
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Doppler US has the advantages of being noninvasive and inexpensive. However, considerable controversy exists with regard to the role of Doppler US in screening for RAS. Two approaches are used to detect RAS with Doppler US: direct visualization of the renal arteries and analysis of intrarenal Doppler waveforms.
Direct Visualization of the Renal Arteries
The first approach involves direct scanning of the main renal arteries with color or power Doppler US followed by analysis of renal artery velocity with spectral Doppler US (Fig 5). An anterior or anterolateral approach usually allows exploration of both renal arteries with an adequate angle of insonation. A coronal approach can be used when bowel gas is present. Owing to various factors such as gas interposition or the anatomy of the left renal artery, a complete examination of both renal arteries can be achieved in only 50%–90% of cases (11–13). Signal enhancement can be achieved by administering contrast agents that facilitate visualization of the renal arteries (Fig 6). However, the clinical impact of US contrast agents remains to be determined (14), and the potential of contrast agents to increase the maximum Doppler shift remains controversial (15).
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Figure 5a. Severe stenosis in a patient with a solitary left kidney who experienced recurring hypertension and renal failure 3 months after stent placement in the left renal artery. (a) Doppler spectrum from the proximal left renal artery shows flow acceleration of close to 300 cm/sec inside the stent. (b) Intrarenal Doppler spectrum shows a waveform with a pulsus tardus configuration, which indicates severe hemodynamic repercussions. (c) Arteriogram shows severe stenosis inside the stent (arrow). Thrombosis of the infrarenal aorta is also noted.
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Figure 5b. Severe stenosis in a patient with a solitary left kidney who experienced recurring hypertension and renal failure 3 months after stent placement in the left renal artery. (a) Doppler spectrum from the proximal left renal artery shows flow acceleration of close to 300 cm/sec inside the stent. (b) Intrarenal Doppler spectrum shows a waveform with a pulsus tardus configuration, which indicates severe hemodynamic repercussions. (c) Arteriogram shows severe stenosis inside the stent (arrow). Thrombosis of the infrarenal aorta is also noted.
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Figure 5c. Severe stenosis in a patient with a solitary left kidney who experienced recurring hypertension and renal failure 3 months after stent placement in the left renal artery. (a) Doppler spectrum from the proximal left renal artery shows flow acceleration of close to 300 cm/sec inside the stent. (b) Intrarenal Doppler spectrum shows a waveform with a pulsus tardus configuration, which indicates severe hemodynamic repercussions. (c) Arteriogram shows severe stenosis inside the stent (arrow). Thrombosis of the infrarenal aorta is also noted.
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Figure 6a. Signal enhancement with a contrast agent. (a) Gray-scale US scan of the abdominal aorta obtained with a right coronal approach shows the left renal artery (arrows). However, results of duplex US were nondiagnostic. (b) Color Doppler US scan obtained after injection of a contrast agent shows strong signal inside the aorta and left renal artery (arrow). The enhanced signal allowed evaluation of the left renal artery with pulsed Doppler US. (Courtesy of Michel Lafortune, MD, Hôpital Saint-Luc, Centre Hospitalier de l'Université de Montréal, Quebec, Canada.)
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Figure 6b. Signal enhancement with a contrast agent. (a) Gray-scale US scan of the abdominal aorta obtained with a right coronal approach shows the left renal artery (arrows). However, results of duplex US were nondiagnostic. (b) Color Doppler US scan obtained after injection of a contrast agent shows strong signal inside the aorta and left renal artery (arrow). The enhanced signal allowed evaluation of the left renal artery with pulsed Doppler US. (Courtesy of Michel Lafortune, MD, Hôpital Saint-Luc, Centre Hospitalier de l'Université de Montréal, Quebec, Canada.)
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Four criteria are used to diagnose significant proximal stenosis or occlusion of a renal artery: (a) An increase in peak systolic velocity in the renal artery (in the literature, the threshold for significant RAS is 100–200 cm/sec); (b) a renal-to-aortic ratio of peak systolic velocity greater than 3.5; (c) turbulent flow in the poststenotic area; and (d) visualization of the renal artery without detectable Doppler signal, a finding that indicates occlusion.
Accessory renal arteries and bowel gas interposition are the main limiting factors in direct scanning of the renal arteries. Therefore, recent studies have demonstrated mixed results, with sensitivities of 0%–93% for detection of RAS (11–13,16).
Analysis of Intra-renal Doppler Waveforms
The segmental renal arteries are evaluated by means of a translumbar approach. Therefore, technical failure occurs in only 0%–2% of kidneys studied. The different segments of the kidneys
must be scanned systematically to detect a stenosis of a segmental or accessory renal artery (Fig 7). A dampened appearance (pulsus tardus) of an intrarenal Doppler waveform indicates stenosis (Fig 5) (16,17). The presence of an early systolic peak can be interpreted as a sign of normality; however, the absence of an early systolic peak does not necessarily indicate stenosis (18,19). Detection of significant RAS can be based on a pattern recognition approach (Fig 8).
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Figure 7a. Stenosis of an accessory renal artery in a patient with recent acceleration of hypertension. (a) Doppler spectrum from the left kidney shows a waveform with a pulsus tardus configuration, which is consistent with severe RAS. (b) Doppler spectrum from the upper right kidney shows a normal waveform. (c) Doppler spectrum from the lower pole of the right kidney shows a waveform with a delayed systolic upstroke (arrow), which suggests stenosis of an accessory or branch renal artery. (d) Abdominal aortogram shows severe stenosis of the left renal artery (arrow). The origins of the right main and accessory renal arteries are not adequately visualized. (e) Selective arteriogram of the main right renal artery shows no stenosis. (f) Arteriogram of an accessory artery to the right lower pole shows ostial stenosis.
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Figure 7b. Stenosis of an accessory renal artery in a patient with recent acceleration of hypertension. (a) Doppler spectrum from the left kidney shows a waveform with a pulsus tardus configuration, which is consistent with severe RAS. (b) Doppler spectrum from the upper right kidney shows a normal waveform. (c) Doppler spectrum from the lower pole of the right kidney shows a waveform with a delayed systolic upstroke (arrow), which suggests stenosis of an accessory or branch renal artery. (d) Abdominal aortogram shows severe stenosis of the left renal artery (arrow). The origins of the right main and accessory renal arteries are not adequately visualized. (e) Selective arteriogram of the main right renal artery shows no stenosis. (f) Arteriogram of an accessory artery to the right lower pole shows ostial stenosis.
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Figure 7c. Stenosis of an accessory renal artery in a patient with recent acceleration of hypertension. (a) Doppler spectrum from the left kidney shows a waveform with a pulsus tardus configuration, which is consistent with severe RAS. (b) Doppler spectrum from the upper right kidney shows a normal waveform. (c) Doppler spectrum from the lower pole of the right kidney shows a waveform with a delayed systolic upstroke (arrow), which suggests stenosis of an accessory or branch renal artery. (d) Abdominal aortogram shows severe stenosis of the left renal artery (arrow). The origins of the right main and accessory renal arteries are not adequately visualized. (e) Selective arteriogram of the main right renal artery shows no stenosis. (f) Arteriogram of an accessory artery to the right lower pole shows ostial stenosis.
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Figure 7d. Stenosis of an accessory renal artery in a patient with recent acceleration of hypertension. (a) Doppler spectrum from the left kidney shows a waveform with a pulsus tardus configuration, which is consistent with severe RAS. (b) Doppler spectrum from the upper right kidney shows a normal waveform. (c) Doppler spectrum from the lower pole of the right kidney shows a waveform with a delayed systolic upstroke (arrow), which suggests stenosis of an accessory or branch renal artery. (d) Abdominal aortogram shows severe stenosis of the left renal artery (arrow). The origins of the right main and accessory renal arteries are not adequately visualized. (e) Selective arteriogram of the main right renal artery shows no stenosis. (f) Arteriogram of an accessory artery to the right lower pole shows ostial stenosis.
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Figure 7e. Stenosis of an accessory renal artery in a patient with recent acceleration of hypertension. (a) Doppler spectrum from the left kidney shows a waveform with a pulsus tardus configuration, which is consistent with severe RAS. (b) Doppler spectrum from the upper right kidney shows a normal waveform. (c) Doppler spectrum from the lower pole of the right kidney shows a waveform with a delayed systolic upstroke (arrow), which suggests stenosis of an accessory or branch renal artery. (d) Abdominal aortogram shows severe stenosis of the left renal artery (arrow). The origins of the right main and accessory renal arteries are not adequately visualized. (e) Selective arteriogram of the main right renal artery shows no stenosis. (f) Arteriogram of an accessory artery to the right lower pole shows ostial stenosis.
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Figure 7f. Stenosis of an accessory renal artery in a patient with recent acceleration of hypertension. (a) Doppler spectrum from the left kidney shows a waveform with a pulsus tardus configuration, which is consistent with severe RAS. (b) Doppler spectrum from the upper right kidney shows a normal waveform. (c) Doppler spectrum from the lower pole of the right kidney shows a waveform with a delayed systolic upstroke (arrow), which suggests stenosis of an accessory or branch renal artery. (d) Abdominal aortogram shows severe stenosis of the left renal artery (arrow). The origins of the right main and accessory renal arteries are not adequately visualized. (e) Selective arteriogram of the main right renal artery shows no stenosis. (f) Arteriogram of an accessory artery to the right lower pole shows ostial stenosis.
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Figure 8. Doppler waveform patterns. Types A and B represent normal Doppler spectra. In type A, a peak is present at the end of the early rise. In type B, no peak is present but the rise remains straight. Note that waveform VI is considered normal despite the high compliance peak; this particular type is most commonly seen in young patients. Type C represents abnormal spectra with varying degrees of a slowed early rise.
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Several quantitative criteria have been proposed for detection of significant RAS: (a) acceleration of less than 370–470 cm/sec, (b) time of acceleration greater than 0.05–0.08 seconds, and (c) change in resistive index of greater than 5% between the right and left kidneys. The early systolic acceleration seems to be the best predictor of RAS (19,20). This quantity should be measured along the initial portion of the systolic rise and should not include the late compliance peak (Fig 9).
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Figure 9. Normal Doppler waveform with straight early upstroke and high compliance peak. One should measure acceleration along the initial portion of the upstroke (dotted line), avoiding the compliance peak.
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When combined morphologic and quantitative criteria are used, the sensitivity for detection of RAS 70% or greater in diameter is 72%–92%. Administration of captopril can improve detection of RAS (Fig 10), especially for RAS 50% or greater in diameter (20).
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Figure 10a. Renovascular disease in a patient with severe hypertension. (a) Intrarenal Doppler spectrum from the left kidney shows a waveform with a straight systolic upstroke (arrows). (b) Intrarenal Doppler spectrum obtained after oral administration of 25 mg of captopril shows a waveform with a frankly abnormal systolic upstroke and a slowed early rise. (c) Arteriogram shows stenosis of the left renal artery.
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Figure 10b. Renovascular disease in a patient with severe hypertension. (a) Intrarenal Doppler spectrum from the left kidney shows a waveform with a straight systolic upstroke (arrows). (b) Intrarenal Doppler spectrum obtained after oral administration of 25 mg of captopril shows a waveform with a frankly abnormal systolic upstroke and a slowed early rise. (c) Arteriogram shows stenosis of the left renal artery.
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Figure 10c. Renovascular disease in a patient with severe hypertension. (a) Intrarenal Doppler spectrum from the left kidney shows a waveform with a straight systolic upstroke (arrows). (b) Intrarenal Doppler spectrum obtained after oral administration of 25 mg of captopril shows a waveform with a frankly abnormal systolic upstroke and a slowed early rise. (c) Arteriogram shows stenosis of the left renal artery.
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Few data are available concerning the value of Doppler US in prediction of clinical success after correction of RAS. A positive predictive value of 85% (comparable with that of ACE inhibitor scintigraphy) has been reported for cure of or improvement in hypertension after percutaneous transluminal angioplasty (21). In our recent experience (22), Doppler US had a positive predictive value of 67% for cure of or improvement in hypertension (66% for scintigraphy) and 95% for improvement in or stabilization of renal failure (79% for scintigraphy) after correction of RAS.
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MR Angiography
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Gadolinium-enhanced MR angiography is now available on high-field-strength imaging systems with high performance gradients, which are capable of performing breath-hold three-dimensional spoiled gradient-echo imaging with short repetition times and echo times. The angiographic contrast is the result of the T1-shortening effect of the intravenously administered paramagnetic contrast agent. Blood is rendered bright, whereas stationary tissues remain dark. Subtraction of nonenhanced images removes all background signals and improves the vessel-to-background signal. Usually, a double dose of gadolinium contrast material (0.2 mmol/kg) is injected at a rate of 1.5–2 mL/sec.
Timing the contrast material injection to the start of image acquisition is crucial to obtain adequate arterial signal and avoid venous or soft-tissue enhancement. At many institutions, a bolus timing acquisition is performed with a small injection of 1–2 mL of gadolinium contrast material before the three-dimensional MR angiography sequence to measure the time between the peripheral injection and peak enhancement (Tpeak) (23). The time delay from the beginning of the injection to the start of acquisition can then be calculated as follows: Tdelay = Tpeak + Tinjection/2 - Tacquisition/2. Alternatively, the acquisition can be started 1–2 seconds before the time of peak enhancement.
In addition, bolus tracking methods have recently become available on certain units, allowing automatic triggering of the acquisition with the arrival of the bolus. Current bolus tracking techniques include line scanning methods, such as Smart Prep (GE Medical Systems, Milwaukee, Wis) or MR fluoroscopy. To maximize the timing with the bolus and the breath hold, new k-space readout algorithms are being implemented in which the center of k space is read out first, allowing contrast-related information to be acquired during the beginning of the breath hold, when there is maximum gadolinium enhancement. The periphery of k space is interpreted last, near the end of the breath hold.
Maximum-intensity projection images are created to provide an angiographic image (Fig 11). On maximum-intensity projection images, areas of lower signal intensity within the blood vessels may be lost. Therefore, interpretation of the source images is important to correlate stenotic lesions, small vessels, kidney size, and cortical thickness (Fig 12). Multiplanar projection images are helpful for analyzing the renal artery ostia. They can also be used in cases of superimposition of the left renal vein (Fig 13).
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Figure 11a. Renovascular disease in a patient with hypertension and two right renal arteries. (a) Coronal maximum-intensity projection image from MR angiography shows an eccentric atheromatous lesion of the abdominal aorta adjacent to the upper right renal artery (black arrow); however, this lesion does not cause stenosis. The lower right renal artery has a proximal stenosis (arrowhead). A stenosis of the left renal artery is also demonstrated (white arrow). (b) Conventional aortogram shows the findings seen on the MR angiogram (a) with good correlation.
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Figure 11b. Renovascular disease in a patient with hypertension and two right renal arteries. (a) Coronal maximum-intensity projection image from MR angiography shows an eccentric atheromatous lesion of the abdominal aorta adjacent to the upper right renal artery (black arrow); however, this lesion does not cause stenosis. The lower right renal artery has a proximal stenosis (arrowhead). A stenosis of the left renal artery is also demonstrated (white arrow). (b) Conventional aortogram shows the findings seen on the MR angiogram (a) with good correlation.
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Figure 12a. Severe bilateral RAS in a patient with renal insufficiency and an aortobifemoral bypass. (a) Coronal maximum-intensity projection image from MR angiography shows severe bilateral renal stenoses (arrows), which appear as short occlusions. (b) Coronal source MR image shows left renal atrophy, suggesting that the left-sided stenosis is more severe. A large renal cyst is also seen. (c, d) Selective arteriograms show a 70% stenosis of the right renal artery (c) and a 90% stenosis of the left renal artery (d).
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Figure 12b. Severe bilateral RAS in a patient with renal insufficiency and an aortobifemoral bypass. (a) Coronal maximum-intensity projection image from MR angiography shows severe bilateral renal stenoses (arrows), which appear as short occlusions. (b) Coronal source MR image shows left renal atrophy, suggesting that the left-sided stenosis is more severe. A large renal cyst is also seen. (c, d) Selective arteriograms show a 70% stenosis of the right renal artery (c) and a 90% stenosis of the left renal artery (d).
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Figure 12c. Severe bilateral RAS in a patient with renal insufficiency and an aortobifemoral bypass. (a) Coronal maximum-intensity projection image from MR angiography shows severe bilateral renal stenoses (arrows), which appear as short occlusions. (b) Coronal source MR image shows left renal atrophy, suggesting that the left-sided stenosis is more severe. A large renal cyst is also seen. (c, d) Selective arteriograms show a 70% stenosis of the right renal artery (c) and a 90% stenosis of the left renal artery (d).
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Figure 12d. Severe bilateral RAS in a patient with renal insufficiency and an aortobifemoral bypass. (a) Coronal maximum-intensity projection image from MR angiography shows severe bilateral renal stenoses (arrows), which appear as short occlusions. (b) Coronal source MR image shows left renal atrophy, suggesting that the left-sided stenosis is more severe. A large renal cyst is also seen. (c, d) Selective arteriograms show a 70% stenosis of the right renal artery (c) and a 90% stenosis of the left renal artery (d).
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Figure 13a. Superimposition of the left renal vein in a patient with hypertension. (a) Coronal MR angiogram does not show the left renal artery clearly due to superimposition of the left renal vein. (b) Axial multiplanar reconstruction image shows both the artery and the vein clearly.
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Figure 13b. Superimposition of the left renal vein in a patient with hypertension. (a) Coronal MR angiogram does not show the left renal artery clearly due to superimposition of the left renal vein. (b) Axial multiplanar reconstruction image shows both the artery and the vein clearly.
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Most series have shown excellent correlation between conventional angiography and MR angiography (sensitivity >95% and specificity >90%) for detection of RAS 50% or greater in diameter (24). Relative to conventional angiography, there is a tendency with MR angiography to overestimate moderate stenosis (Fig 14). In addition, detection of accessory arteries is sometimes problematic (Figs 14, 15).
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Figure 14a. Overestimation of stenosis in a patient with hypertension. (a) Coronal MR angiogram shows severe stenosis of the left main renal artery. No accessory artery is seen. (b) Conventional aortogram shows the stenosis of the left main renal artery, which was slightly overestimated on the MR angiogram (a). In addition, a small accessory artery is demonstrated at the upper pole of the kidney (arrowhead).
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Figure 14b. Overestimation of stenosis in a patient with hypertension. (a) Coronal MR angiogram shows severe stenosis of the left main renal artery. No accessory artery is seen. (b) Conventional aortogram shows the stenosis of the left main renal artery, which was slightly overestimated on the MR angiogram (a). In addition, a small accessory artery is demonstrated at the upper pole of the kidney (arrowhead).
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Figure 15a. Accessory artery in a 35-year-old patient with severe hypertension. (a) Coronal MR angiogram shows irregularities of the distal third of both main renal arteries, an appearance suggestive of fibromuscular dysplasia. (b) Conventional aortogram shows fibromuscular dysplasia involving both renal arteries. A possible accessory artery is seen on the right side (arrow). (c, d) Selective arteriograms of the right (c) and left (d) main renal arteries show mild fibromuscular dysplasia. Note the small parenchymal defect at the upper pole of the right kidney from the accessory artery.
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Figure 15b. Accessory artery in a 35-year-old patient with severe hypertension. (a) Coronal MR angiogram shows irregularities of the distal third of both main renal arteries, an appearance suggestive of fibromuscular dysplasia. (b) Conventional aortogram shows fibromuscular dysplasia involving both renal arteries. A possible accessory artery is seen on the right side (arrow). (c, d) Selective arteriograms of the right (c) and left (d) main renal arteries show mild fibromuscular dysplasia. Note the small parenchymal defect at the upper pole of the right kidney from the accessory artery.
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Figure 15c. Accessory artery in a 35-year-old patient with severe hypertension. (a) Coronal MR angiogram shows irregularities of the distal third of both main renal arteries, an appearance suggestive of fibromuscular dysplasia. (b) Conventional aortogram shows fibromuscular dysplasia involving both renal arteries. A possible accessory artery is seen on the right side (arrow). (c, d) Selective arteriograms of the right (c) and left (d) main renal arteries show mild fibromuscular dysplasia. Note the small parenchymal defect at the upper pole of the right kidney from the accessory artery.
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Figure 15d. Accessory artery in a 35-year-old patient with severe hypertension. (a) Coronal MR angiogram shows irregularities of the distal third of both main renal arteries, an appearance suggestive of fibromuscular dysplasia. (b) Conventional aortogram shows fibromuscular dysplasia involving both renal arteries. A possible accessory artery is seen on the right side (arrow). (c, d) Selective arteriograms of the right (c) and left (d) main renal arteries show mild fibromuscular dysplasia. Note the small parenchymal defect at the upper pole of the right kidney from the accessory artery.
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The main limitations of MR angiography are (a) evaluation of branch vessels, (b) the presence of a metallic stent, (c) detection of accessory arteries, and (d) evaluation of small renal arteries. Even though evaluation of renal artery branches is not always easy with MR angiography, detection of fibromuscular dysplasia involving the main renal artery is sometimes possible (Fig 15).
Functional information can be added by measuring renal flow with cine phase-contrast imaging (25). Diffusion and perfusion imaging can also be used to measure renal ischemia, but these techniques are under investigation. To our knowledge, there are no data on the value of functional MR imaging in predicting the response to renal revascularization.
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Conclusions
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The main challenge is not to detect all cases of RAS 50% or greater in diameter but to identify stenoses that will benefit from revascularization. Another major issue is avoidance of unnecessary diagnostic angiography, especially in patients with renal failure.
From this perspective, screening should begin with a functional investigation such as Doppler US or scintigraphy. In a center with good expertise with Doppler US, the cost-effectiveness of this technique is probably superior to that of scintigraphy. MR angiography, with its higher cost and lesser availability, should be reserved for patients with indeterminate functional imaging results, patients with normal functional imaging results but high clinical suspicion of RVH, and patients with abnormal functional imaging results who have a contraindication to conventional angiography, such as renal failure or a history of allergy to iodinated contrast material (Fig 16).
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Footnotes
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See the commentary by Sarkar and Siegel.
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Abstract
LEARNING OBJECTIVES FOR TEST...
