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1 Both authors: Department of Radiology, Boston University Medical Center, 88 E Newton St., Boston, MA 02118.
Received July 30, 2003;
accepted after revision November 18, 2003.
Address correspondence to A. Gupta
(avgupta{at}bmc.org).
Abstract
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MATERIALS AND METHODS. From 1996 to 2002, 185 hypertensive patients underwent MR angiography of the renal arteries at our institution for assessment of renal artery stenosis. MR angiograms were obtained using a 1.5-T magnet, IV gadolinium, and 3D gradient-echo sequences. Interpretations of the MR angiograms were retrospectively reviewed.
RESULTS. Of 185 hypertensive patients, 45 (24%) showed accessory
renal arteries. Of these 45 patients, nine (20%) showed renal artery stenosis
and 36 (80%) showed no significant stenosis. Of the 140 patients with a single
renal artery, 42 (30%) showed renal artery stenosis and 98 (70%) showed no
stenosis. The odds ratio of renal artery stenosis in the accessory renal
artery group versus the single renal artery group was 0.58 (95% confidence
interval, 0.26–1.3%), which is not statistically significant at a power
of 0.85 (
2 = 1.705; p = 1.0).
CONCLUSION. We found no statistically significant difference in the prevalence of renal artery stenosis between patients with accessory renal arteries and those without accessory renal arteries. Assuming that the presence of two separate causes of hypertension in the same patient would be unlikely, this finding implies that accessory renal arteries are a vascular anomaly and not a direct cause of hypertension. The findings are potentially relevant in refuting the theory of accessory renal arteries as an anatomically treatable cause of hypertension.
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Although several possible etiologies for high blood pressure have been described, 90–95% of cases of hypertension have no definable cause and are termed "essential hypertension" and treated medically [1]. Renal artery stenosis, usually due to atherosclerosis, has been established as a vascular cause of hypertension because of the activation of the renin-angiotensin system [1, 2]. In low-pressure states, such as hypovolemia or hypotension, perfusion to the kidneys is decreased. In response, renin secretion increases in an attempt to raise systemic blood pressure to normal levels. This protective mechanism maintains blood pressure in the normal range, but it also may contribute to hypertension in patients with stenotic renal arteries. In patients with renal artery stenosis, the kidney receives relatively less blood flow from the narrowed renal artery, leading to renin hypersecretion and an abnormally elevated blood pressure via activation of the renin-angiotensin system. The identification of renal artery stenosis has been helpful in defining treatments aimed at correcting the stenosis, such as angioplasty and stenting of narrowed arteries. These treatments have, for the most part, been successful in reducing hypertension attributable to renal artery stenosis [1].
A second hypothesis regarding renovascular hypertension has been raised: Accessory renal arteries, which are seen in 25–50% of normal subjects (based on autopsy data), may lead to hypertension via activation of the renin-angiotensin system [2–7]. Accessory renal arteries are aberrant arterial branches originating directly from the aorta, usually serving a small portion of the kidney [3–5]. During embryogenesis, the kidneys ascend from their original sacral location to their final location in the upper retroperitoneum. As the kidneys ascend during the sixth through ninth weeks of gestation, they maintain their arterial supply by becoming progressively revascularized by a series of arterial sprouts from the aorta. These transient aortic branches regress in a sequential fashion, and each kidney is finally left with a single main renal artery when ascent has been completed. Failure of one of the transient arteries to regress may result in an accessory renal artery [3].
Accessory renal arteries tend to be longer and narrower than the main renal arteries, resulting in lower perfusion pressure and higher resistance across the artery. Indeed, the anecdotally reported observations that portions of the kidney served by accessory renal arteries tend to exhibit delayed parenchymal enhancement on angiographic studies have appeared in the literature. These reports have led to the suggestion that the relative lack of perfusion in the renal parenchyma served by the slower flow and lower pressure of accessory renal arteries results in increased renin secretion and subsequent development of hypertension [4].
MR angiography has become a proven imaging technique for detecting renal artery stenosis and accessory renal arteries [2, 8–12] (Figs. 1 and 2). The goal of our investigation was to determine the relation, if any, between the presence of accessory renal arteries and hypertension risk, using MR angiography. Although anecdotal evidence and small studies describing a link between these two factors are abundant, a single-site cohort or cross-sectional study to address this question has, to our knowledge, been lacking. With this article, we sought to present the data from our patient population on this supposed link. To the best of our knowledge, no prior studies examining the relationship between hypertension and accessory renal arteries have been performed using MR angiography.
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Clarification of any relationship between accessory renal arteries and hypertension risk is important before considering aggressive therapies. Embolization of accessory renal arteries has been suggested as a treatment for renovascular hypertension attributable to duplicate arteries [5]. In fact, partial nephrectomy has been performed in the pediatric population for hypertension due to segmental intrarenal stenosis [13].
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Criteria for inclusion in our study were a history of hypertension, with blood pressure exceeding 160/90 mm Hg confirmed through chart review. Normotensive patients and those referred for workup for a renal mass or pretransplantation assessment were excluded.
MR Angiography
MR angiography was performed on a 1.5-T system (Gyroscan, Philips Medical
Systems) using a quadrature body coil for signal transmission and reception.
Sequences used included axial T2-weighted turbo spin-echo (TR range/TE range,
2,000–4,000/80–100; turbo factor, 2–16; slice thickness,
5–8 mm with a gap of 1 mm, field of view, 340–540 mm; number of
excitations, 2–4); axial T1-weighted spinecho
(200–400/10–30; slice thickness, 5 mm with a gap of 1 mm; field of
view, 340–450 mm; number of excitations, 2; with respiratory and flow
compensation); and gradient-echo time-of-flight (TR/TE, 25/6.9; flip angle,
40°; number of excitations, 2) performed without cardiac gating
In addition, dynamic gadopentetate dimeglumine–enhanced (Magnevist,
Berlex) MR angiography was performed using a 3D gradient-recalled echo
sequence (10/3; flip angle, 40°; number of excitations, 1; slice
thickness, 2 mm with a 1-mm overlap) acquired during breath-holding in the
coronal plane centered over the renal artery origins with a 3D fast spoiled
gradient-echo sequence (TR/TEmin, 10/3; flip angle, 40°; number
of excitations, 1) acquired during the bolus administration of 0.1 mmol/kg of
body weight of gadopentetate dimeglumine (
20 mL) followed by a 50-mL
normal saline flush. The total 70 mL of fluid was administered over 60 sec by
hand with scanning initiated at the beginning of bolus administration.
Acquisition time was 23–32 sec. No saturation pulses were applied.
Maximum-intensity-projection images were generated in the coronal plane every
15°.
Images were interpreted by an attending radiologist trained in body MRI and a radiology resident or fellow. Clinical histories, such as the presence of hypertension, were available to the radiologists at the time of image interpretation. Criteria for defining significant renal artery stenosis included a narrowing of 50% or greater. Accessory renal arteries were defined as arteries arising directly from the aorta and terminating in a portion of the kidney.
Statistical Analysis
We plotted the number of patients with and without renal artery stenosis
against the presence or absence of accessory renal arteries on a 2 x 2
contingency table. The odds ratio between the incidence of accessory renal
arteries and renal artery stenosis was calculated with a power of 0.85.
Chi-square analysis and Fisher's exact test were performed to evaluate any
correlation between the incidence of accessory renal arteries and renal artery
stenosis.
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2 = 1.705;
p = 1.0).
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Of the 45 patients with accessory renal arteries, one patient (2.2%) showed stenosis of the accessory artery without stenosis of either main renal artery. No patients had coexisting stenosis of an accessory artery and either main renal artery.
Additionally, we found that among 51 patients with renal artery stenosis,
nine (17.6%) had accessory renal arteries and 42 (82.4%) had a single renal
artery (Table 2). Among the 134
patients without renal artery stenosis, 36 (26.9%) had accessory renal
arteries and 98 (73.1%) had a single renal artery. The odds ratio of accessory
renal arteries in the renal artery stenosis group versus accessory renal
arteries in the group without renal artery stenosis was 0.58 (95% CI,
0.26–1.3; 2 = 1.705, p = 1.0), which is not
statistically significant at a power of 0.85.
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The incidence of accessory renal artery stenosis in the absence of main renal artery stenosis has recently been described as 1.5% in a population of 68 patients in a study using catheter angiography [15]. In our study we found that of 45 patients with accessory renal arteries, a similar proportion, 2.2%, had accessory renal artery stenosis in the absence of main renal artery stenosis; no patients in our study population had coexistent stenosis of both the accessory and the main renal arteries.
Angiographic dilatation or occlusion of accessory renal arteries has been suggested as a method of relieving hypertension attributed to duplicate renal arteries [5]. Recently, partial nephrectomy has been proposed as a treatment for patients with segmental or regional intrarenal stenosis, and performance of partial nephrectomies in the hypertensive pediatric population has been reported [13]. Our data suggest that such aggressive therapy may be unwarranted.
We recognize several limitations of our study. First, we limited our study population to hypertensive patients only, which may have introduced a selection bias that might have adversely affected outcomes. Additionally, ours was a retrospective analysis in which the referring history of hypertension was known at the time of examination, which may also have introduced bias. Finally, our sample size was limited to a power of 0.85.
We have concluded that accessory renal arteries are not related to hypertension risk. Our study represented a diverse cross section of the hypertensive patient population. To our knowledge, no prior studies examining the relationship between hypertension risk and accessory renal arteries using MR angiography have been performed. We believe that this study can be important as a guide in the selection of therapy for renovascular hypertension and as a warning against aggressive antihypertensive treatment aimed at correcting accessory renal arteries.
Acknowledgments
We thank Janet Greene of the Department of Radiology at Boston University
Medical Center for the tabulation of MRI reports and patient demographic
information.
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