[Surgical treatment of renovascular hypertension caused by renal artery stenosis. A retrospective study].
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During a 10 year period 58 patients with renovascular hypertension due to renal artery stenosis were treated surgically. A retrospective analysis of the results was carried out. No perioperative mortalities occurred. Ten percent of the patients developed hypertension again after an average of 27 months. At follow-up (median 65 months), 85% of the patients had normal blood pressure or either no, modest or considerably reduced anti-hypertensive medication. It is concluded that surgical treatment of renovascular hypertension is a safe and effective procedure.Keywords:
Renovascular Hypertension
Renal Artery Obstruction
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RECENT reports have indicated that operative treatment of renovascular hypertension in patients over 50 years of age is not warranted because of high morbidity, high mortality, and poor response.1,2This has not been our experience; of 162 patients with renovascular hypertension who underwent operative treatment, 70 were over 50 years of age and 56 (80%) of these were either cured or improved one year later.3The overall operative mortality was 8.6%, but five of the six operative deaths occurred in patients who were simultaneously undergoing operative treatment for abdominal aortic aneurysm or for occlusive disease. Only one death (1.9%) occurred in a patient in whom operative treatment was limited to the renal arteries. We describe a patient with severe renovascular hypertension and bilateral renal artery stenosis who was treated with bilateral aortorenal bypass grafts and who has had a ten-year serial arteriographic follow-up.
Report of a Case
ARenovascular Hypertension
Renal Artery Obstruction
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We agree with Drs Bush and Kidd thatbilateralrenal artery stenoses are found in approximately 25% of all cases of renovascular hypertension. The largest published series of patients, the Cooperative Study of Renovascular Hypertension, found bilateral renovascular disease in 28% (250 patients) of their patients with renal artery stenosis.1However, many renal artery lesions are functionally insignificant, since unilateral repair often cures or improves hypertension in patients with bilateral stenoses. For example, Schwarten et al2noted that while 14 of their patients had bilateral renal artery stenosis, nine of these patients responded to only unilateral angioplasty. Furthermore, the Cooperative Study of Renovascular Hypertension noted that in patients with bilateral disease who responded to surgery, 83.3% had abnormal rapid-sequence IVPs. Thus, while the sensitivity of the rapid-sequence IVP is lower in detecting bilateral renal artery stenosis, it remains a useful means of uncovering functionally significant renal vascularRenovascular Hypertension
Renal Artery Obstruction
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Renovascular Hypertension
Secondary hypertension
Renal Artery Obstruction
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Renovascular Hypertension
Essential hypertension
Prehypertension
Renal Artery Obstruction
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Atherosclerosis and dysplasia are the most common lesions affecting the renal artery, causing stenosis and renovascular hypertension. Surgical revascularization of the ischemic kidney in properly selected patients has proved to be the treatment of choice. The different pathological characters of dysplastic lesions are examined and compared with the ones of atherosclerotic disease, in surgically treated patients. Correlations between angiographic and histological aspects are also considered. The recognition of these different pathological patterns is important for the selection of the most suitable surgical procedures. The results of a personal technique of arterial reconstruction and angioplasty are reported.
Renovascular Hypertension
Fibromuscular Dysplasia
Renal Artery Obstruction
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Renovascular Hypertension
Secondary hypertension
Renal Artery Obstruction
Essential hypertension
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Abstract Renovascular hypertension is a syndrome which encompasses the physiological response of the kidney to changes in renal blood flow and renal perfusion pressure. Such physiological changes can occur with renal artery occlusion irrespective of the severity of the lesion. We have analyzed hypertensive patients with mild renal artery stenosis and compared them to patients with no stenosis. Renal vein renin sampling from catheterization of the renal vein was performed in all these patients. Patients with mild stenosis had higher renal vein renin ratio (3.01 ± 1.5) than the patients with no stenosis (1.10 ± 0.29; p = 0.002). Patients with mild stenosis were also found to have higher diastolic blood pressure and renal artery resistive indices when compared to patients with no stenosis. We therefore conclude that mild stenosis can precipitate renin‐mediated hypertension in renovascular stenosis and also emphasis that parameters pertinent to renal physiology need to be evaluated before considering treatment options in patients with renal artery stenosis and medical management with RAAS blockade is the preferred modality of therapy for patients with renin‐mediated hypertension.
Renovascular Hypertension
Renal vein
Renal Artery Obstruction
Secondary hypertension
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Renal artery stenosis causes ischemia in the kidney, resulting in renovascular hypertension (RVH) through activation of the renin-angiotensin system (RAS).1 Because RVH is one of the leading causes of curable hypertension, it should not be overlooked. Here, we report a case of RVH attributed to small renal ischemia, in which the causative ischemic lesion was limited enough not to be detected by common screening modalities. A 16-year-old man was referred to our hospital with a 2-month history of hypertension. His blood pressure was 160/100 mm Hg before medication and 140/90 mm Hg after antihypertensive treatment with nifedipine 60 mg and bunazosin 3 mg. The patient showed no abdominal bruit or proteinuria and normal levels of creatinine (0.7 mg/dL) and potassium (3.7 mmol/L). Electrocardiography findings showed high voltage, indicative of left ventricular hypertrophy. Plasma renin activity of 11.7 ng/mL/h and aldosterone level of 187 pg/mL were inappropriately high. Doppler ultrasonography did not show any aortic abnormality or sign of stenosis in each main renal artery. Findings from technetium-99m-diethylenetriaminepentacetic acid renogram showed normal perfusion, function, and drainage from both kidneys. Results from computed tomography (CT) angiographic scan, however, revealed a segmental stenosis in the upper branch of the right renal artery accompanied by a renal artery aneurysm (FigureA). The stenosis caused local hypoperfusion in the limited area <4% of the whole renal parenchyma (FigureA). The angiographic finding was consistent with CT imaging (FigureB), which was suggestive of fibromuscular dysplasia (FMD). Renal venous sampling revealed marked high renin activity in the draining vein of the hypoperfused lesion (92.3 ng/mL/h, 30.8 ng/mL/h, and 18.1 ng/mL/h in draining, right, and left renal vein, respectively). We diagnosed branch-type renovascular hypertension, and performed endovascular angioplasty with 2-mm balloon dilatation (FigureB). Perfusion in the poststenotic lesion was promptly improved after treatment, although the diameter expansion of the treated vessel was only 1 mm (FigureB). One day later, the blood pressure dropped to 120/65 mm Hg without antihypertensive medication (FigureC). One week later, plasma renin activity was reduced to 2.1 ng/mL/h. One month later, renal perfusion in the treated area was maintained (FigureD). Over the following 2 years, he has remained normotensive (110/60 mm Hg). Limited renal ischemia caused by segmental renal artery stenosis. (A) Computed tomography (CT) angiographic scan showing the presence of stenosis and aneurysm in the upper branch of the right renal artery (arrow). The dotted line indicates the limited ischemic area. (B) Pretreatment and post-treatment angiographic images of the right renal artery. Balloon dilatation was performed against the stenotic lesions indicated by arrow heads. (C) Blood pressure before and after the percutaneous transluminal renal angioplasty (PTRA) during hospitalization. (D) CT scan images showing the maintained renal perfusion in the treated area (arrow) 1 month after angioplasty. [Correction added after initial online publication on August 21, 2015: "Doxazosin" was changed to "Bunazosin" in Figure C.] A small area of renal ischemia is sufficient to develop hypertension, because, as in the present case, the resolution of a small ischemia promptly corrected the inappropriate renin secretion and then normalized the blood pressure. Glomerular hypoperfusion following renal ischemia increases renin release from the juxtaglomerular apparatus, causing activation of the RAS and subsequent elevation of systemic blood pressure. Through such mechanisms, even small renal ischemia contributes to various hypertensive conditions. Other renal vascular abnormalities, such as renal arteriovenous fistula and tortuous aberrant renal arteries,2 can also lead to focal renal ischemia and resultant hypertension. Unlike in cases of FMD, angioplasty for atherosclerotic renal artery stenosis is often ineffective,3 because partial ischemia frequently remains in the kidney of that patient through concomitant aortic stiffening and arteriosclerosis in the intrarenal small arteries.4 Furthermore, the present finding speculates that high-renin "essential" hypertension may be partly attributed to small renal ischemia that the clinician does not find. Doppler ultrasonography is a sensitive and noninvasive screening modality for RVH, but remains fairly poor at detecting stenosis of small branch or accessory arteries.1 Although FMD characteristically causes stenosis or aneurysm in the middle to distal portion of the main renal artery, it also occasionally involves the branch renal artery.5 Thus, we cannot exclude FMD-related RVH even if ultrasonography shows no abnormalities, such as in the present case. The present case emphasizes the importance of limited renal ischemia in hypertension development and a pitfall in the diagnosis of RVH. When examining renin-dependent hypertension, we should thoroughly search for renal ischemia. The authors report no specific funding in relation to this research and no conflicts of interest to disclose.
Renovascular Hypertension
Fibromuscular Dysplasia
Right Renal Artery
Renal ischemia
Plasma renin activity
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In an effort to detect renovascular hypertension, clinical characteristics are used to select patients likely to have renal artery stenosis. We prospectively evaluated the ability of commonly used clinical features to predict the presence of renal artery stenosis in 100 hypertensive adults. All subjects had conventional renal arteriography. Renal artery stenosis was diagnosed if there was 50% or more stenosis of a main renal artery. Eighteen of the 100 had renal artery stenosis. The presence of a bruit was strongly associated with renal artery stenosis (P less than .0005). In patients without a bruit, only refractory hypertension was associated with the presence of renal artery stenosis (P = .051). These data suggest that a bruit and refractory hypertension are associated with renal artery stenosis, but that other clinical features investigated may not be and that other means of screening for renovascular disease are needed.
Renovascular Hypertension
Renal Artery Obstruction
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No AccessJournal of UrologyDiseases of Blood Vessels, Hypertension and Renovascular Surgery1 Mar 1984Follow Up Study of 70 Patients With Renal Artery Stenosis Treated by Percutaneous Transluminal Dilatation G.G. Geyskes, C.B.A.J. Puylaert, H.Y. Oei, and E.J. Dorhout Mees G.G. GeyskesG.G. Geyskes More articles by this author , C.B.A.J. PuylaertC.B.A.J. Puylaert More articles by this author , H.Y. OeiH.Y. Oei More articles by this author , and E.J. Dorhout MeesE.J. Dorhout Mees More articles by this author View All Author Informationhttps://doi.org/10.1016/S0022-5347(17)50525-XAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissionsReprints ShareFacebookLinked InTwitterEmail "Follow Up Study of 70 Patients With Renal Artery Stenosis Treated by Percutaneous Transluminal Dilatation." The Journal of Urology, 131(3), pp. 613–614 © 1984 by The American Urological Association Education and Research, Inc.FiguresReferencesRelatedDetails Volume 131Issue 3March 1984Page: 613-614 Advertisement Copyright & Permissions© 1984 by The American Urological Association Education and Research, Inc.MetricsAuthor Information G.G. Geyskes More articles by this author C.B.A.J. Puylaert More articles by this author H.Y. Oei More articles by this author E.J. Dorhout Mees More articles by this author Expand All Advertisement PDF downloadLoading ...
Renovascular Hypertension
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