Vascular anomaly in bilateral ectopic kidney: a case report
© Gokalp et al; licensee BioMed Central Ltd. 2010
Received: 14 October 2009
Accepted: 5 January 2010
Published: 5 January 2010
Ectopic kidney occurs as a result of a halt in migration of kidneys to their normal locations during embryonal period. While kidneys ascend through pelvis, they receive new branches from vessels (iliac and aorta) close to them. When they reach the highest point, they receive new branches from aorta and the former branches degenerate. Renal vessels do not degenerate in the ectopic caudal kidney, more than one accessory and polar arteries may arise. In various studies, a possibility of association between presence of multiple renal arteries and hypertension, has been reported. We aimed to present a case with bilateral ectopic kidney and vascular anomaly associated with hypertension and renal dysfunction.
Ectopic kidney is described as abnormal localization of kidney due to a developmental anomaly and it occurs as a result of a halt in migration of kidneys to their normal locations during embryonal period. More than one anomaly can occur at the same time. While kidneys ascend through pelvis, they receive new branches from vessels (iliac and aorta) close to them. When they reach the highest point, they receive new branches from aorta and the former branches degenerate. If those vessels do not degenerate in the ectopic caudal kidney, more than one accessory and polar arteries may arise [1, 2]. Hypertension is more frequently encountered in cases with more than one renal arteries[3–6]. In the present report, we aimed to present a case with bilateral ectopic kidney and vascular anomaly.
Urinary tract, originating from mesoblast and expanding from cranial to caudal, completes its development after 3 developmental phases: pronephros, mesonephros, and metanephros. The third phase gives rise to the permanent kidneys. Initially, they localize at ventral portion of sacrum and pelvis, close to each other. Along with abdominal and pelvic growth and decrease of body inclination, they follow an ascending route and reach their permanent sites by coming in contact with the adrenal gland at 9th week. First, hila face ventral aspect, however, during ascent, it displays 90 degree medial turn. The hilus of a kidney that attained its final permanent position, faces anterolateral aspect. During ascent, they proceed through a bifurcation formed by umbilical arteries. If one of the kidneys fail to pass this point, it remains within the pelvis next to the common iliac artery. This kidney is called as pelvic or ectopic kidney, and is associated with malrotation [1, 2]. Renal ectopy is a relatively common congenital anomaly and can not be noticed unless it causes any symptomatology. It is most commonly presented with unilateral, pelvic localization along with a minimal left side and male predisposition .
At mesonephros, lateral intersegmental arteries, which are called as urogenital rete arteriosum, provide vascularization. Those arteries build a vascular net that supports adrenal glands, kidneys, and gonads, at both sides of the aorta between 6th cervical and 3th lumbar vertebrae. In other words, kidneys receive branches from blood levels close to them during their ascent. First, renal arteries receive branches from common iliac artery. As the ascent proceeds, kidneys start to receive branches from distal end of the aorta. When they reach the highest level, they receive new branches from aorta, and under normal conditions, the former vessels degenerate and eventually disappear. Permanent renal artery develops from one persistent branch of urogenital rete arteriosum .
The differing origins of renal arteries and commonly encountered variations, are explained by development of mesonephric arteries. Insufficient degeneration of mesonephric arteries, leads to presence of more than one renal artery [1, 5, 6]. Renal artery variations are categorized in 2 groups: "early branching" and "extra renal arteries". While main renal arteries divide into segmental branches at hilus level, a branching occuring more proximal to hilus, is called "early branching". Extra renal arteries are grouped in 2 as follows: hilar (accessory) and polar (aberrant) arteries. While hilar arteries enter kidney through hilus with main renal artery, polar arteries penetrate kidney directly through the capsule from outside of the hilus . In the present case, an accessory artery of the left kidney, originating from starting point of left common iliac artery, and 5 polar (capsular) arteries, were present. The kidney localized at mid level, had a renal artery originating from right common iliac artery, and early branching was present.
Multiple renal veins constitute the most common venous variant and are seen in 15-30% of individuals. Occasionally, single renal vein may divide into branches prior to joining inferior vena cava . In the present case, the kidney localized in the mid level of pelvis had 2 renal veins and the left vein was joining with left renal vein and eventually opening into vena cava inferior.
Renovascular hypertension is defined as a syndrome of arterial hypertension induced by renal perfusion pressure secondary to a vascular lesion . In various studies, a possibility of association between presence of multiple renal arteries and hypertension, has been reported [3, 6]. A study conducted by Glondy B et al. , showed high plasma renin activity in cases with multiple renal arteries, and the authors highlighted that this may lead to a predisposition for hypertension. According to a hypothesis, accesory renal arteries usually have a longer length and a smaller diameter compared to the main artery, and the renal segment supported by this artery display lower blood pressure which cause hypertension by stimulating renin secretion. However, the study performed by Gupta A et al. , showed no association between hypertension risk and accessory renal arteries. In the present case, the association of multiple renal arteries and hypertension/renal failure, is not clear and open to discussion. However, due to presence of studies reflecting an association between presence of multiple renal arteries and hypertension, we believe this possibility should be considered, as well.
CT and MRI are comparable for evaluating renal disease in the majority of patients. MRI angiography was performed in the present case becuse of renal disfunction. There are circumstances in which MRI is, however, the procedure of choice, which includes, patients with allergy to iodine contrast, complicated, particularly calcified, renal cystic lesions and renal masses in which CT images are difficult to interpret. Furthermore, MRI can be used as a problem-solving modality when the CT findings are nondiagnostic. Attempts are being made to use MRI for imaging of renal function, including perfusion, glomerular filtration rate and intrarenal oxygen measurement .
In conclusion, bilateral renal ectopy associated with malrotation is an uncommon anomaly. Due to failure of normal renal ascent and regression, accessory and polar arteries may occur and venous anomalies may accompany. Those arterial anomalies may cause renovascular hypertension and even lead to renal insufficiency. However, further detailed studies are required about this relationship.
Written informed consent was obtained from the parents of the patient for publication of this case report and accompanying images. A copy of the written consent is available for review by the Editor-in-Chief of this journal.
- Sadler TW: Urogenital system. Langman's Medical Embryology. Edited by: Sadler TW. 1990, Baltimore: William and Wilkins, 266-281. 6Google Scholar
- Cocheteux B, Mounier-Vehier C, Gaxotte V, McFadden EP, Francke JP, Beregi JP: Rare variations in renal anatomy and blood supply: CT appearances and embryological background. Eur Radiol. 2001, 11 (5): 779-786. 10.1007/s003300000675.View ArticlePubMedGoogle Scholar
- Bude RO, Forauer AR, Caoili EM, Nghiem HV: Is it necessary to study accessory arteries when screening the renal arteries for renovascular hypertension?. Radiology. 2003, 226 (2): 411-416. 10.1148/radiol.2263011576.View ArticlePubMedGoogle Scholar
- Kem DC, Lyons DF, Wenzl J, Halverstadt D, Yu X: Renin-dependent hypertension caused by nonfocal stenotic aberrant renal arteries: proof of a new syndrome. Hypertension. 2005, 46 (2): 380-385. 10.1161/01.HYP.0000171185.25749.5b.View ArticlePubMedGoogle Scholar
- Glodny B, Cromme S, Reimer P, Lennarz M, Winde G, Vetter H: Hypertension associated with multiple renal arteries may be renin-dependent. J Hypertens. 2000, 18 (10): 1437-1444. 10.1097/00004872-200018100-00011.View ArticlePubMedGoogle Scholar
- Glodny B, Cromme S, Wörtler K, Winde G: A possible explanation for the frequent concomitance of arterial hypertension and multiple renal arteries. Med Hypotheses. 2001, 56 (2): 129-133. 10.1054/mehy.2000.1206.View ArticlePubMedGoogle Scholar
- Cinman NM, Okeke Z, Smith AD: Pelvic kidney: associated diseases and treatment. J Endourol. 2007, 21 (8): 836-842. 10.1089/end.2007.9945.View ArticlePubMedGoogle Scholar
- Satyapal KS, Haffejee AA, Singh B, Ramsaroop L, Robbs JV, Kalideen JM: Additional renal arteries: incidence and morphometry. Surg Radiol Anat. 2001, 23 (1): 33-38. 10.1007/s00276-001-0033-y.View ArticlePubMedGoogle Scholar
- Sampaio FJ, Passos MA: Renal arteries: anatomic study for surgical and radiological practice. Surg Radiol Anat. 1992, 14 (2): 113-117. 10.1007/BF01794885.View ArticlePubMedGoogle Scholar
- Urban BA, Ratner LE, Fishman EK: Three-dimensional Volume-rendered CT Angiography of the Renal Arteries and Veins: Normal Anatomy, Variants, and Clinical Applications. Radiographics. 2001, 21 (2): 373-386.View ArticlePubMedGoogle Scholar
- Tonbul Z, Güney I: Renovasküler hipertansiyon. J Int Med Sci. 2007, 3 (4): 1-10.Google Scholar
- Gupta A, Tello R: Accessory renal arteries are not related to hypertension risk: A review of MR angiography data. AJR. 2004, 182 (6): 1521-1524.View ArticlePubMedGoogle Scholar
- Nikken JJ, Krestin GP: MRI of the kidney-state of the art. Eur Radiol. 2007, 17 (11): 2780-2793. 10.1007/s00330-007-0701-3.PubMed CentralView ArticlePubMedGoogle Scholar
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