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Genitourinary Imaging |
1 From the Department of Radiology-MRI, New York University, 530 First Ave, HCC Basement, New York, NY 10016. From the 1999 RSNA scientific assembly. Received December 14, 2000; revision requested February 4, 2001; revision received February 21; accepted March 19. Supported in part by a 1998 RSNA Research and Education Fund Seed Grant, National Institutes of Health grant K23-DK02814, and a Society of Computed Body Tomography/Magnetic Resonance Lauterbur Award. Address correspondence to V.S.L. (e-mail: lee@mri.med.nyu.edu).
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ABSTRACT |
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 TOP ABSTRACT INTRODUCTIONMATERIALS AND METHODS RESULTS DISCUSSIONREFERENCES |
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MATERIALS AND METHODS: Thirty-two patients underwent MR renography (turbo fast low-angle shot sequence: repetition time, 5 msec; echo time, 2.3 msec; flip angle, 15°; one coronal image acquired every 2 seconds for 4 minutes) following intravenous injection of 2 mL of gadopentetate dimeglumine, which was repeated following intravenous injection of an ACE inhibitor. Contrast material–enhanced MR angiography was also performed. On the basis of renographic findings, renal cortex and renal medulla enhancement curves and normalized enhancement ratios were analyzed.
RESULTS: The cortex and medulla showed an early transient period of enhancement within 20 seconds (vascular phase). During 1–2 minutes, a second, gradual increase in medullary enhancement, reflecting transit of filtered contrast material, was observed that was significantly greater in patients with a serum creatinine level less than 2 mg/dL (177 µmol/L) than in those with a level of 2 mg/dL or greater (P < .01). After injection of the ACE inhibitor, patients with elevated creatinine levels showed low renal medullary enhancement regardless of the presence of renal artery stenosis (RAS). However, in patients with creatinine less than 2 mg/dL, medullary enhancement ratios after injection of the ACE inhibitor were consistently lower in patients with RAS of 50% or greater than in those without stenosis (P = .02 to .08).
CONCLUSION: Low-dose MR renography can be performed in the clinical setting before and after injection of an ACE inhibitor, and its potential use for evaluating decreased renal function as a consequence of RAS is promising.
Index terms: Kidney, function, 81.12143, 81.12144 • Magnetic resonance (MR), vascular studies, 961.12942, 961.12943 • Renal arteries, stenosis or obstruction, 961.72
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INTRODUCTION |
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TOPABSTRACTINTRODUCTIONMATERIALS AND METHODS RESULTS DISCUSSIONREFERENCES |
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Magnetic resonance (MR) imaging has the potential to provide a comprehensive anatomic and physiologic evaluation of disease in patients suspected of having RVD. Numerous studies have established the accuracy of gadolinium-enhanced MR angiography in the identification of RAS when compared with conventional angiography (6–8, for example). Moreover, the contrast agents typically used in MR imaging, such as gadopentetate dimeglumine, have useful physiologic properties for the evaluation of renal function. As with its scintigraphic counterpart, technetium 99m diethylenetriaminepentaacetic acid (DTPA), gadopentetate dimeglumine (Magnevist; Berlex Laboratories, Wayne, NJ) is freely filtered at the glomerulus without tubular secretion or reabsorption. Thus, its clearance can be used to estimate creatinine clearance and glomerular filtration rate (9–12). Furthermore, the high T1 relaxivity of the agent allows direct visualization of tracer quantities of gadopentetate dimeglumine with T1-weighted MR imaging, an approach referred to as MR renography.
Several groups of authors have established the feasibility of MR renography, although typical doses of gadolinium-based contrast material ranged from 0.05–0.20 mmol per kilogram of body weight (10,13–22). These relatively high doses of contrast material can cause signal loss due to T2* effects, which leads to ambiguities in the relationship between contrast material concentration and signal intensity. Also, repeated administration of these doses, such as after injection of an angiotensin converting enzyme (ACE) inhibitor, can compromise the performance of contrast material–enhanced MR angiography in the same setting, thereby limiting clinical applicability for the diagnosis of RVD.
Our group has observed that doses of contrast material of 1–2 mL (approximately 0.005–0.010 mmol/kg) result in distinct renal cortical and medullary enhancement. Among the advantages of lower doses are the potential for contrast quantification and the option for repeated studies without affecting the performance of contrast-enhanced MR angiography in the same examination. The purpose of our investigation was to develop and test low-dose MR renography performed both without and with an ACE inhibitor and conducted in conjunction with gadolinium-enhanced MR angiography for the diagnosis of RVD.
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MATERIALS AND METHODS |
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TOPABSTRACTINTRODUCTIONMATERIALS AND METHODS RESULTS DISCUSSIONREFERENCES |
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The following diagnostic criteria were considered to indicate an increased risk of RVD: hypertension refractory to medication (n = 22, 69%); onset at less than 20 years of age or after age 50 years (n = 14, 44%); peripheral, coronary, or carotid atherosclerotic disease (n = 15, 47%); sudden onset or worsening of hypertension (n = 13, 41%); abdominal or flank bruit (n = 2, 6%); and hypertensive retinopathy (n = 3, 9%) (23). The majority (n = 20, 63%) of patients met more than one diagnostic criterion. For 14 (44%) patients, an ACE inhibitor was part of the routine medicine regimen at the time of examination, and it was not discontinued for this study because of the reluctance of the referring physicians. This subset of patients underwent the same MR imaging protocol, including imaging before and after injection of an intravenous dose of ACE inhibitor, as the remaining 18 patients. The mean serum creatinine level was 1.9 mg/dL ± 1.2 (168 µmol/L ± 106). Twenty (63%) patients had serum creatinine levels less than 2 mg/dL (177 µmol/L) (mean, 1.1 mg/dL ± 0.3) (97 µmol/L ± 27), while for the remainder, the mean creatinine level was 3.0 mg/dL ± 1.1 (265 µmol/L ± 97).
The rationale for use of an ACE inhibitor was based on established experience with nuclear scintigraphic studies (23). In patients with RAS and reduced renal perfusion, decreases in perfusion pressure detected by the juxtaglomerular apparatus lead to activation of the renin-angiotensin axis. One product of this activation, angiotensin II, causes systemic vasoconstriction, systemic blood pressure elevation, and constriction of the efferent arteriole of the glomerulus, thereby resulting in normal or near-normal filtration pressure and glomerular filtration rate. As a consequence, patients with compensated RAS may not manifest decreased perfusion or filtration on scintigraphic renal studies. ACE inhibitors block the conversion of angiotensin I to angiotensin II, thereby reversing the efferent arteriolar constriction and, thus, can cause a decrease in glomerular filtration rate. With the disease unmasked, the abnormal physiology caused by RAS can be diagnosed more accurately at scintigraphy. We hypothesize that the same would be true for MR renography.
MR Imaging Protocol
To minimize the risk of hypotension after injection of ACE inhibitor, all patients were instructed to drink 2 cups of water just before the study. A 22-gauge intravenous catheter was placed in an antecubital vein and attached to a power injector (Spectris; Medrad, Pittsburgh, Pa). During the entire examination, an MR-compatible blood pressure monitor (Multigas 9500; MR Equipment, Bay Shore, NY) was used to record blood pressure and pulse at baseline and following ACE inhibitor injection. The cuff was placed on the upper part of the arm contralateral to the intravenous catheter.
All patients underwent imaging at 1.5 T (Vision; Siemens Medical Systems, Erlangen, Germany [25 mT/m maximum gradient strength and 600-µsec rise time]) with use of a torso phased-array coil. The patient’s arms were propped up at the sides by using small cushions to minimize potential wraparound artifacts during coronal imaging.
After routine transverse breath-hold T1-weighted gradient-echo imaging (repetition time msec/echo time msec of 160–180/4.1, 90° flip angle) through the kidneys and adrenal glands, a three-dimensional spoiled gradient-echo (3.8/1.3, 25° flip angle) image set was first acquired without contrast material to serve as a mask for subtraction from contrast-enhanced MR angiographic images. Subsequently, MR renographic images were obtained both before and 10–15 minutes after a slow intravenous injection of the ACE inhibitor (enalaprilat, Vasotec; Merck, West Point, Pa) at a dose of 0.04 mg/kg (up to a maximum of 2.5 mg, injected during 3–4 minutes). Blood pressure and pulse rates were recorded before injection and at 5–10-minute intervals thereafter for at least 40 minutes or until blood pressure returned to within 10% of baseline. Patients were questioned repeatedly for symptoms during the course of the examination. Contrast-enhanced MR angiography was then performed following the two MR renographic acquisitions. For the entire MR study, patients received a total of 25 mL of gadopentetate dimeglumine, for a mean dose of 0.16 mmol/kg.
MR Renography
The MR renographic protocol consisted of alternating transverse and coronal acquisitions with a magnetization-prepared spoiled gradient-echo sequence (turbo fast low-angle shot, with 5.0/2.3/300 [inversion time msec], flip angle of 15°, section thickness of 8 mm, field of view of 350–450 mm, 256 x 128 matrix, and rectangular field of view optimized to each patient’s body habitus). Images were acquired one per second for 4 minutes following injection of 2 mL (mean dose, 0.013 mmol/kg) of gadopentetate dimeglumine and a 20-mL saline flush. By alternating the plane of acquisition, transverse and coronal images were obtained every 2 seconds. Breath holding was intermittently performed to minimize motion effects. Patients were instructed to hold their breath in expiration for as long as possible in the first 30 seconds of the 4-minute acquisition. This was followed by a 20-second free breathing interval. Then a 10-second breath hold and 50-second free breathing period were serially repeated for the remainder of the acquisition.
MR Angiography
MR angiographic acquisitions were performed in the oblique-coronal plane with use of an interpolated three-dimensional spoiled gradient-echo sequence (3.8/1.3, flip angle of 25°, field of view of 350–400 mm, 256 x 160 matrix, and rectangular field of view depending on body habitus). Slab thickness ranged from 70 to 120 mm; 1.0–2.5-mm section thickness was achieved in the section-select direction by using sinc interpolation or zero filling (uninterpolated section thickness, 2–5 mm). Image acquisition times were all shorter than 25 seconds, and patients were instructed to hold their breath at end expiration for better reproducibility. A nonenhanced image was acquired first to serve as a mask for subtraction. Subsequently, patient circulation time (mean, 21 seconds ± 5) was determined on the basis of the time to peak aortic enhancement on the transverse MR renographic images and was used to time the arterial phase angiographic acquisition to ensure maximal arterial enhancement (24). For MR angiography, all patients received an intravenous injection of 21 mL of gadopentetate dimeglumine (mean dose, 0.14 mmol/kg ± 0.03) at a rate of 2 mL/sec, with use of the power injector, followed by a 20-mL saline flush.
Image Analysis
MR renography.—MR renographic images were analyzed by research assistants under the supervision of one radiologist (V.S.L.). On all coronal images, regions of interest were placed over renal cortex and medulla, while on transverse images, regions of interest were placed over the aorta. Anatomic regions of the kidney were defined on the MR renographic image with greatest corticomedullary differentiation, typically 2–6 seconds after peak enhancement of the abdominal aorta. Mean signal intensity for each region was computed for all coronal renographic images. In 90% of cases, signal intensities from more than 40 pixels (range, 40–100 pixels) were averaged for each compartment. In six atrophic kidneys, smaller regions of interest had to be used. Regions of interest were manually adjusted on renographic images to compensate for respiratory-induced renal motion, particularly on images from the latter portion of the first 30-second breath hold.
To correct for possible variation in MR signal intensity in patients due to variable receiver gain and coil positioning, aorta, renal cortex, and renal medulla enhancement values (SIi) were standardized relative to baseline values (SI0), prior to contrast material administration according to the calculation (SIi - SI0)/SI0 and plotted against time. These relative signal intensity values were used for all analyses.
Cortical and medullary enhancement curves exhibited an initial peak within 30 seconds of contrast material arrival in the aorta (termed the vascular peak), which marked the arrival of contrast material in the arterioles and capillaries of each compartment. For all kidneys, we measured the relative signal intensity values at 1, 2, 3, and 4 minutes following injection. To adjust for differences in the amount and rate of contrast material delivered to the kidney, either because of slight differences in volumes of contrast material delivered or because of differences in individual cardiac output, we normalized all relative signal intensity measurements to the area under the cortical vascular peak, Ap, which was measured from the onset of enhancement for 30 seconds. On the basis of indicator-dilution theory, Ap can be considered a parameter that reflects renal blood flow and the quantity of contrast material administered (25). Cortical and medullary enhancement ratios at 1, 2, 3, and 4 minutes following initiation of contrast material administration were therefore defined as the relative signal intensities at each of those times divided by Ap.
MR angiography.—MR angiographic images were viewed at the satellite workstation (Siemens Medical Systems) with use of standard multiplanar and maximum intensity projection reconstruction images. The highest degree of stenosis for each renal artery was classified as a diameter reduction of 50% or greater or less than 50% on the basis of the source images from contrast-enhanced MR angiography with use of multiplanar reformatting. The images were evaluated prospectively by an MR radiologist blinded to MR renographic results.
Conventional Angiography and Clinical Follow-up
After MR imaging, eight (25%) patients with RAS at MR angiography were referred for digital subtraction angiography within 3 months. All studies were performed with a femoral artery approach with a 5-F pigtail catheter. Selective injections of diseased renal arteries were also performed. The angiographic studies were interpreted by a staff radiologist, who was unaware of the results of the MR angiographic and MR renographic studies. Conventional angiographic reports were used to classify stenoses as resulting in diameter reduction of 50% or greater or less than 50%.
One year after the study, clinic chart review and patient interviews were conducted by research assistants under the supervision of one investigator (V.S.L.) to evaluate the patients’ subsequent clinical course.
Statistical Analysis
Because the assumption of independence between kidneys could not be made, analyses were performed with the patient as the unit, by using averaged (left and right) measures of both kidneys for each patient. A one-tailed Student t test was performed to compare renographic parameters for patients with or without RAS and according to whether the serum creatinine level was less than 2 mg/dL or was 2 mg/dL or greater. The use of a one-tailed t test was based on the expectation from scintigraphic renography literature that renal enhancement would be lower in patients with elevated creatinine or RAS. A one-tailed Student t test was also used to compare ACE inhibitor–enhanced MR renographic measures between patients with and those without arterial stenosis, with the expectation that medullary enhancement ratios would be lower in patients with RAS.
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RESULTS |
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TOPABSTRACTINTRODUCTIONMATERIALS AND METHODS RESULTS DISCUSSIONREFERENCES |
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MR Angiography
MR angiography was successfully performed in all 32 patients. Overall, 20 (31%) of 64 main renal arteries demonstrated 50% or greater stenosis at MR angiography, which corresponded to 13 (41%) of 32 patients. Thus, 19 of 32 patients had no substantial RAS. Bilateral RAS was found in seven (22%) of the 32 patients. In four (13%) patients, single accessory renal arteries, none of which had significant stenosis, were identified at MR angiography.
MR Renography: Association with Renal Function
We observed distinct patterns of cortical and medullary enhancement in the kidneys in patients with normal serum creatinine levels (Fig 1, n = 20). In all 40 kidneys of patients with serum creatinine levels less than 2 mg/dL, both the cortex and medulla demonstrated an early transient period of enhancement within the first 20 seconds after contrast medium injection (Fig 2). Presumably, this corresponded to the first pass of contrast material through the blood vessels; therefore, we referred to it as the vascular phase. After a small decrease in medullary enhancement, a gradual second increase in enhancement was seen during 1–2 minutes. Cortical enhancement decreased and then plateaued during 2–4 minutes.
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.01).
ACE Inhibitor–enhanced MR Renography: Association with RAS
To evaluate enhancement parameters for baseline and ACE inhibitor–enhanced MR renography, enhancement ratios (relative signal intensities normalized to the area under the cortical vascular peak, Ap) were compared. For the 15 patients with serum creatinine levels less than 2 mg/dL and without RAS, 1–4-minute cortical and medullary enhancement ratios were not significantly different at baseline and after injection of an ACE inhibitor.
When we compared medullary enhancement ratios at 1, 2, 3, and 4 minutes for patients with RAS (bilateral stenosis 
50%, n = 7) versus those without RAS (n = 19), we found no significant difference in measurements performed without an ACE inhibitor (P = .13 to .42). After injection of the ACE inhibitor, medullary enhancement ratios were slightly lower for patients with RAS than for those without RAS (P = .1 to .2, Table).
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In four of the six patients who underwent interventional therapy, baseline serum creatinine levels were 2 mg/dL or greater. Although serum creatinine levels were stable following therapy in all four patients, all continued to experience hypertension, with systolic blood pressure greater than 160 mm Hg or diastolic blood pressure greater than 90 mm Hg at 1-year follow-up. Each of the two patients with normal baseline serum creatinine levels (1.1 mg/dL [97 µmol/L] and 1.5 mg/dL [133 µmol/L]) underwent successful unilateral angioplasty or stent placement with resulting decreases in blood pressure.
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DISCUSSION |
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TOPABSTRACTINTRODUCTIONMATERIALS AND METHODS RESULTS DISCUSSIONREFERENCES |
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Our observations that patients with impaired renal function have markedly less medullary enhancement from 1 to 4 minutes following contrast material injection are consistent with this interpretation of the medullary enhancement pattern. Diminished glomerular filtration should result in reduced amounts of filtered contrast material and, consequently, delayed and diminished medullary enhancement. These results are also in agreement with scintigraphic findings in patients with diminished renal function where radionuclide activity of the kidneys during 1–3 minutes after injection is measurably lower (27). Our results are consistent with those in a study (15) of 11 pediatric patients (mean age, 12 years), in which the delay in corticomedullary junction time, which reflects delayed and diminished medullary enhancement, correlated well (r = -0.63) with 24-hour creatinine clearance values. Our preliminary results support the continued investigation of MR renography as a tool for quantifying individual renal function with the further potential application of measuring intrarenal regional function.
The low-dose gadolinium-enhanced MR renographic method we developed has the advantage of allowing repeated measures in conjunction with contrast-enhanced MR angiography. With this feature, we were able to test the feasibility of MR renography performed before and after injection of the ACE inhibitor with the expectation that, as in captopril 99mTc DTPA renography, the use of an ACE inhibitor might improve the detection of abnormal renal physiology caused by RAS. In our series of 32 patients, all tolerated the standard intravenous dose of the ACE inhibitor. Although four (13%) patients experienced blood pressure declines of greater than 20% of baseline, none became symptomatic, and all blood pressures recovered with an intravenous bolus injection of 250 mL of normal saline. Our preliminary results support the feasibility and safety of administering an ACE inhibitor during MR evaluation, provided blood pressure is carefully monitored.
To our knowledge, three groups of authors tested the use of an ACE inhibitor to improve the detection of RAS with use of MR renography, two in animal models (19,21) and one in a study of 15 human patients with hypertension (16). Findings in these studies showed that the delay in medullary enhancement observed in the presence of RAS was, in some cases, greater following injection of an ACE inhibitor. Grenier et al (16) also observed one case of a segmental perfusion abnormality (limited to the upper two-thirds of the kidney) that corresponded to an interlobular artery stenosis at conventional angiography. They concluded that regional abnormalities that were not discernable at scintigraphy could be detected with MR renography. In the same study, the authors reported good correlation between MR renography with 0.1 mmol/kg of gadolinium-based contrast material and 99mTc mercaptoacetyltriglycine, or MAG3, renography.
In our study, medullary enhancement ratios were not significantly different between patients with RAS and those without when renography was performed without an ACE inhibitor. With an ACE inhibitor, however, medullary enhancement ratios in those with normal serum creatinine levels were consistently lower among those with RAS than in those without RAS, which suggests a pattern of physiology similar to that observed with captopril renography.
There are several limitations in our study. First, a large subset of patients (14 of 32) continued to receive chronic ACE inhibitor therapy that was not discontinued for this examination. The sensitivity of captopril renography for the detection of RAS was shown to be diminished from 98% (39 of 40) in patients not taking ACE inhibitors to 75% (12 of 16) in patients taking them (28). Second, we relied on the relatively insensitive serum creatinine level as a measure of renal function. Further validation studies are needed with use of more accurate measures of renal function, such as creatinine clearance or 99mTc DTPA clearance. Third, we relied on MR angiography for the diagnosis of significant RAS. Although the accuracy of MR angiography for the diagnosis of RAS is high when compared with that with conventional angiography (6–8), evidence of response to revascularization therapy is needed for the true diagnosis of renovascular disease. Finally, our MR renographic approach may be limited in its ability to augment the diagnosis of RVD in patients with renal insufficiency. In this subpopulation, we observed diminished medullary enhancement regardless of the presence or absence of RAS so that changes in medullary enhancement following injection of the ACE inhibitor were not detectable. It is possible that none of these patients had truly physiologically significant RAS. Nevertheless, a similar limitation was observed for radioisotope renography (29). Further modifications or refinements in the MR renographic method may be needed for the diagnosis of RVD in patients with renal insufficiency, possibly including the use of larger doses of contrast material (30) or longer acquisition times, perhaps as long as 20–30 minutes, as in captopril scintigraphy.
Our technique relied on alternating transverse and coronal two-dimensional acquisitions through the abdomen, the transverse section for aortic enhancement measurements and the coronal section for renography. With technical advances in MR hardware and software, fast three-dimensional renographic acquisitions may become possible that will enable more comprehensive imaging, including the aorta and total renal parenchyma, as well as evaluation of the renal collecting system and ureter (31).
Our initial experience shows that low-dose MR renography can be performed feasibly in the clinical setting both before and after injection of an ACE inhibitor and in conjunction with gadolinium-enhanced MR angiography and that its potential use for evaluating decreased renal function as a consequence of RAS is promising. In particular, MR renography could play a role as an adjunct to MR angiography in the evaluation of disease in patients with mild-to-moderate RAS to predict better who will benefit from revascularization. However, evaluation of tests to diagnose RVD is difficult because, although correlation with angiography is usually used as the reference standard, true confirmation of the diagnosis of RVD requires demonstration of a physiologic response following revascularization. Larger long-term investigations are clearly warranted.
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FOOTNOTES |
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Author contributions: Guarantor of integrity of entire study, V.S.L.; study concepts, V.S.L.; study design, V.S.L., N.M.R., G.A.K., H.R., G.J.; literature research, V.S.L., N.M.R.; clinical studies, V.S.L., N.M.R., G.A.K.; experimental studies, G.J., H.R.; data acquisition, V.S.L., N.M.R., G.A.K.; data analysis/interpretation, V.S.L., H.R., G.J.; statistical analysis, V.S.L., H.R.; manuscript preparation, definition of intellectual content, editing, revision/review, and final version approval, all authors.
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REFERENCES |
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TOPABSTRACTINTRODUCTIONMATERIALS AND METHODS RESULTS DISCUSSIONREFERENCES |
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