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Saudi Journal of Kidney Diseases and Transplantation
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Year : 2003  |  Volume : 14  |  Issue : 4  |  Page : 497-510
Renovascular Hypertension

Nephrology Department, Saudi Hospital at Hajjah, Hudaidah, Yemen

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How to cite this article:
Al-Rohani M. Renovascular Hypertension. Saudi J Kidney Dis Transpl 2003;14:497-510

How to cite this URL:
Al-Rohani M. Renovascular Hypertension. Saudi J Kidney Dis Transpl [serial online] 2003 [cited 2022 Jan 26];14:497-510. Available from: https://www.sjkdt.org/text.asp?2003/14/4/497/32916

   Introduction Top

Renovascular hypertension (RVH) forms approximately 5% of all causes of hyper­tension. This percentage is changing by the increasing number of elderly patients and renal transplants as well as the development of better diagnostic methods. During the last decade, dramatic changes have occurred in the diagnosis and treatment of RVH, which allowed better understanding of RVH and kept it in focus. There is a tendency to avoid invasive diagnostic methods, especially angiography, because of the associated com­plications accompanied by deterioration of renal function. Many methods have been developed in the last decade in order to minimize the side effects and complications of the invasive methods. Nevertheless, angiography still remains the most accurate diagnostic method for RAS.

RVH is a chronically increased blood pressure (BP) because of renal artery stenosis or one of its branches. Inter­national Society of Hypertension (ISH) defined optimal BP as <120/80 mmHg and normal BP as <130/85 mmHg. This is similar to the definition of the Joint National Committee (JNC VI) on Prevention, Detection, Evaluation, and Treatment of High Blood Pressures in U.S. [1] However, the definition of RVH is still not clear. The coexistence of hypertension and renovascular disease (RVD) does not mean that hypertension is due to RVH. Even the demonstration of RAS in hypertensive patient does not necessarily establish the diagnosis of RVH because essential hypertension may accelerate the development of renal artery stenosis, which may occur in the renal arteries as elsewhere. It is necessary to demonstrate that there is also renal ischemia; this is thought to be the stimulus that raises the blood pressure, acting mainly through the renin-angiotensin­aldosterone system (RAAS). [2],[3],[4] Furthermore, the most rigorous definition to be applied to RVH involves the demonstration of a cure or considerable improvement in hypertension after a revascularization procedure in a narrowed renal artery. [5],[6]

   Epidemiology Top

The prevalence of RVH varies according to the population studied and ranges from 1-5% of the hypertensive population. On the other hand, RVH affects 15% - 30% of patients who have clinical criteria suggesting RVD. [7],[8],[9],[10]

The most common causes of RAS are arteriosclerosis (75%) and fibromuscular dysplasia (15%). Other causes are uncommon and form less than 10%, [Table - 1] of the total. The incidence of stenosis increases in patients with coexisting diabetes mellitus.

   Pathophysiology Top

The classic experiments on RVH were published in 1934 by Goldblatt and co-workers, who demonstrated persistent hypertension in dogs by unilateral or bilateral constriction of the renal arteries. [11] Goldblatt postulated that a humoral mechanism could be respon­sible for the hypertension. This was later con­firmed by numerous other workers. RAS leads to hypoperfusion distal to the stenosis causing reduction in preglomerular pressures. Reduced distension and shear stress on the afferent arteriole lead to secretion of renin and proportional production of angiotensin II (Ang II). The reduced pressure in the renal artery attenuates the effect of the endothelial-derived relaxing factor, or nitrous oxide, which opposes the effects of Ang II.

   Renin-Angiotensin-Aldosterone System (RAAS) Top

This system plays an important role in hypertension. This system was intensively studied in animal models and humans. [12] This system has a cascade behavior, which is summarized in [Figure - 1]. [13] It is well esta­blished that Ang II has a major role in hyper­tension. Clarifying this fact helped in the development of the conservative therapy. The activation of RAAS causes vascular vasoconstriction and retention of sodium and water that results in hypertension.

Renin is a key hormone in the generation of the angiotensin. Circulating renin in the plasma is primarily derived from the juxta­glomerular apparatus of the kidney. A group of modified smooth muscle cells in the wall of the terminal portion of the afferent arteriole, known as granular cells, are responsible for the synthesis and secretion of renin within the Juxta glomerular apparatus (JGA). Renin is initially synthesized as an inactive precursor, prorenin, which is trafficked through the Golgi complex and packaged into immature secretory granules or protogranules. During maturation of the granules, the prosequence is cleaved to form active renin, which is then stored in the mature secretory granule. [14] Anderson et al in their examination of immunolabeled, serial cryosections of mice kidney cortex revealed that renin labeling was present only in granular cells of the JGA or the afferent arteriole. [13] Renin-containing granules are somewhat atypical secretory granules, having some features in common with lysosomes; myeloid bodies and vesicular membranes are found as inclusions within the granules, and they contain proteolytic enzymes, including cathepsin B for processing prorenin, cathepsin D, and other acid hydro­lases. [15] One approach to further investigating renin secretion is to compare the sorting and trafficking of renin with that of other proteins trafficked in the same, or in distinct, regulated pathways in granular cells. [13] Active renin is secreted via a stimulus-coupled, regulated secretory pathway in which stored renin is released into the surrounding interstitium from individual granules or by compound exocytosis from multiple granules. In some circumstances, prorenin may also be secreted from immature granules or in smaller vesicles via a constitutive pathway. [16],[17],[18],[19] The produ­ction and effect of renin depends on several inter-related factors,[Table - 2].

Angiotensinogen is a hormone produced by the liver and converted to Ang I by renin, angiotensin I. Thus converting it to Ang II by angiotensin converting enzyme (ACE). Ang II has vasoconstrictive effect on arterioles stimulated aldosterone production and inhibits the renin production [Figure - 1]. The mecha­nisms regulating the intrarenal RAS was studied and showing that the circulating Ang II augments intrarenal Ang II levels. In the glomerulus, Ang II constricts afferent and efferent arterioles but acts more on the efferent arteriole; thereby it can regulate glomerular hemodynamics and filtration. Ang II also induces mesangial cell contraction, leading to alterations in the glomerular ultrafiltration coefficient. [20],[21] In the kidney, Ang II enhances sodium reabsorption directly via activation of the Na/H+ anti-porter in the proximal tubule and indirectly via vaso­constriction of the vasa recta in the loop of Henley. [18] Two types of receptors, AT1 and AT2 receptors, mediate the action of Ang II. While both receptors belong to the seven­transmembrane, G-protein-coupled receptor family, the function and signaling mechanism of these receptor subtypes are quite different. Studying the adult AT2 receptor-null mutant mice, it was found that the AT2 receptor plays a counter-regulatory protective role against the AT1 receptor-mediated antinatruretic and pressor actions of Ang II and that this protective action is mediated by bradykinin and nitric oxide. [22] Brunner et al found that angiotensin blockade markedly decreased blood pressure in the one-clip two-kidney model but had relatively little effect in the one­clip one-kidney model. [23] Actions of Ang II in the kidney have been posited as the major mechanism for maintenance of injurious elevations in glomerular pressure, and redu­ctions in glomerular pressures have been attributed, at least in part, to the removal of the intrarenal effects of Ang II. [24],[25],[26]

Aldosterone is hormone produced by the zona glomerulosa of cortex of the adrenal gland. It causes retention of sodium accom­panied with water leading to hypertension.

The role of Sodium and water in hyper­tension with kidney disease has been studied for a long time. Carlberger and Collste showed that hypertension, is usually sodium­dependent in the bilaterally nephrectomized patient. [27] The relationship between kidney, sodium and hypertension is explained by animal experiments. [28],[29],[30] Dahl et al [30] divided rats into two groups, the salt sensitive rats "S" strain and the salt resistant rats "R" stain. In the "S" rats, hypertension could be exhibited by salt feeding, whereas the "R" rats remained normotensive despite a high salt intake. Furthermore, replacing the kidneys of the "R" rats with kidneys from the "S" rats led to hypertension when these rats were fed a high salt diet. Transplanting kidneys of the "R" into the "S" rats prevented the development of hypertension. [30]

The role of vasoconstrictive substances (endothelin, catecholamines) and the vaso­dilatory substances (prostaglandins, nitric oxide) in relation to RVH is still not clear.

   Pathological Classification of Renal Artery Stenosis Top

Pathological findings of RAS were classified according to the localization and specific character for each type. Harrison and McCormack established a classification system of RAS summarized in [Table - 3].

Arteriosclerosis: is the most common cause of RVH in old persons mostly older than 55 years. It is a progressive disease that may lead to atrophy of the poststenotic kidney and deterioration of renal function. 31 The atheros­clerosis is commonly bilateral and present in two forms, eccentric or concentric lesions located approximately 1 cm from the ostium of the renal artery. [32] Three lesions are distinguished on the basis of the size of the affected vessels; atherosclerosis, which is renal artery atheroma or cholesterol embolism; arte­riosclerosis, which affects medium and small sized arteries, up to the interlobular arteries sized arteries, up to the interlobular arteries and arteriolosclerosis, which involves the afferent and/or efferent glomerular arterioles. [33]

Fibromuscular Dysplasia (FMD): is a common cause of RVH in hypertensive patients mostly younger than 25 years. Small to medium-sized vessels are often affected. Not only renal arteries are affected (60­75%) but also the cervicocranial arteries (25-30%) visceral arteries (9%) and peri­pheral arteries (5%). The etiology of FMD is unknown, but genetic disorder is considered because of high prevalence in certain families of the white population. However hormonal factors are important as well as the effect of some diseases such as pheochromocytoma, neurofibromatosis,  Ehlers-Danlos syndrome More Details type IV, Alport`s syndrome, cystic medial necrosis and coarctation of the aorta. There is evidence that cigarette smoking may be a risk factor. Reported associations include use of ergotamine preparations, methysergide, the rubella syndrome, and hetero-zygous alpha­1-antitrypsin deficiency. [32],[34]

Developmental lesions: most of these stenoses are ostial in their location. They appear to be associated with abnormal intrauterine events that may lead to distortions of all three components of the vessel wall with secondary intimal fibroplasia, fragmentation of the internal elastic lamina, disruptions of the media, and excess accumulations of elastic tissue in the perimedial-subadventitial regions. Renal artery lesions of this type have the external appearance of an hour-glass. They are truly diminutive arteries that are not amenable to balloon angioplasty without risk of rupture. There does not appear to be any sex predi­lection and usually encountered in children at an average age of 10 years. These lesions are associated with neurofibromatosis and often are accompanied by coarctation abdo­minal aorta. Nearly 90% of these patients have multiple renal arteries. This suggests that developmental stenoses evolve during embryonic life as an abnormality of fusion of the two dorsal aortas. [32]


Ischemic renal injury can cause damage to the renal tissue, kidneys structure and function does not return completely normal after management. Fahr was the first who used the term "Nephrosklerose" in 1919. Nephro­sclerosis is marked by lesions that affect the renal vessels, especially the arcuate and inter­lobular arteries. In 80% of patients with arteriosclerosis the kidneys undergo ischemic atrophy in variable degree related to the duration of the disease. Due to ischemia, the glomerular tuft is usually retracted to the hilum and capillary walls are thickened and folded. Hypertrophy of the extracellular matrix is characteristic. The renal tubules become also atrophied and their basement membranes are thickened and may contain eosinophlilic casts. [33]

The role of Ang. II in the development of glomerulosclerosis is not clear. It stimulates the renal mesangial and tubular cells to synthesize the transforming growth factors B (beta) 1 (TGFB1). In the active form, the TGGB1 induces the synthesis of extracellular matrix proteins and prevents their degradation. The effects of Ang. II on the extracellular matrix protein production can be blocked by the AT1 receptor antagoinsts or by neutra­lizing antibodies to TGFB1. [35]

   The Characteristics of Renal Artery Stenosis Top

A- Degree of Stenosis

The exact degree of luminal narrowing representative of significant RAS is not well defined. Hanovici and Zinicda showed that stenosis less than 50% resulted in no pressure gradient pre and post stenosis, and no redu­ction in renal function, whereas a pressure gradient and an absent pyelogram could be shown with a 60% stenosis. [36] Renal arteries were classified according to the degree of stenosis into three categories; mild stenosis (0-59%), severe stenosis (60-99%) and complete occlusion. [37] Furthermore, Lerman et al classified the degree of stenosis to mild (<50%), moderate (50-75%), and severe (76-99%). [38] A functionally significant stenosis was defined as a pressure gradient greater than 15 mm Hg, which is usually associated with RAS greater than 50%. Other studies have used a gradient of 20 mmHg as the cutoff. [6],[39],[40]

B- Location of stenosis

The location of renovascular lesion with regard to aortic lumen is of prognostic imp­ortance. Sos et al [41] classified the lesions according to the distance from the aortic lumen, the stenosis was defined as ostial stenosis located within 5mm from aortic lumen [Figure - 2], nonostial proximal stenosis located within 5-10 mm of the aortic lumen and isolated truncal stenosis located more than 10 mm distally and clearly separated from the aortic lumen. The ostial lesions represent bulky plaques along the aortic wall. They encroach on the origin of the renal artery within 5 mm from the aortic lumen. These represent 11% to 40% of the athero­sclerotic renovascular lesions.

C- Clinical features

The general clinical characteristics of renovascular hypertension are summarized in [Table - 4]. Recurrent pulmonary edema and history of smoking is often present. [42],[43]

   Diagnosis of Renal Artery Stenosis Top

The diagnosis of RVH is complicated because of the absence of a specific clinical picture and the fact that RAS occurs in normo­tensive as well as in patients with essential hypertension. [38],[44] Early diagnosis and treat­ment of patients with RAS can potentially prevent the progressive loss of renal function. We should not only determine the presence of RAS, but also locate it and assess its hemodynamic significance. It is important to have a strategy to screen for the stenosis and to avoid the performance of expensive or invasive imaging studies. At present, color Doppler ultrasound has become the primary screening test. [45] The following is a brief description of commonly used tests in the diagnosis of RAS.

A. Plasma renin activity test (PRA)

This test is a simple screening test for the presence of the stenosis of the renal artery. [11] It is based on the fact that renin level is increased in RAS. PRA can be measured before and after Angiotensin converting enzyme (ACE) inhibition with captopril. This test is consi­dered positive when PRA greater than 12 µg/l/h or 150% of normal. [8],[47] However, its predictive value in the absence of clinical clues of RVH is low. Rarely, PRA can be normal or low in some patients with reno­vascular hypertension. Renin can also be measured by directly sampling the renal veins. A ratio greater than 1.5:1 can be lateralizing and confirms the hemodynamic significance of the stenosis. [47],[48]

B. Color doppler ultrasonography (CDUS)

CDUS has gained popularity as a non­invasive relatively quick and safe procedure. Two types of CDUS have been evaluated: direct assessment of flow velocity in the main renal artery and the waveform mor­phology of the intrarenal artery. [49],[50] CDUS enables detection of hemodynamically insigni­ficant RAS, with 79% sensitivity and 90% negative predictive value. [51] Another study reported detection of more than 60% of RAS with 87% sensitivity and 91% specificity. [52] However, this technique still has limitation in the evaluation of mild stenosis. [53]

C. ACE inhibitor renal scintigraphy (CRS)

This method has 92% sensitivity and 93% specificity. In this test, three isotopes are used; diethylenetriaminepentacetic acid (DTPA) to measure glomerular filtration test (GFR) and Hippuran I 33 of renal blood flow and 99mTc-mercaptoacetyltriglycine (MAG3). The use of 99m Tc-MAG3 is most suitable in patients with renal function impairment. With scintigraphy, we measure the peak activity time that may be delayed in the presence of RAS, and the percentage of the peak activity that remains at 15 and 20 minutes after injection of the isotopes.

D. Conventional renal angiography (CRA)

Conventional renal angiography with contrast media is accepted as the most accurate modality for diagnosis RAS. [54] The use of ionic contrast media was frequently associated with transient renal failure. However, the nonionic contrast media that was developed to decrease this complication had only limited advantage.

E. Intra-arterial digital subtraction angio­graphy (IDSA)

The presence, localization, degree of the stenosis, and hemodynamic significance of RAS can be determined by IDSA. Compared to CRA, the incidence of complications is significantly low, such as exposure to lower concentration of contrast media, avoidance of manipulation of the stenotic lesion with risk of embolization, arterio-venous fistula. [55]

F. Magnetic resonance angiography (MRA)

This method is established as an accurate and safe technique to evaluate the main renal artery and vein with sensitivity and specificity range from 87% to 100%. [55],[56] Using this method allowed to evaluate patients with renal failure, allergy to iodinated contrast material, or difficult arterial access. However, there are a few problems with MR angio­graphy, such as the degradation of image quality in patients with low cardiac output or abdominal aortic aneurysm and difficulty in evaluating the renal artery beyond the most proximal centimeters, decreased ability to differentiate severe stenosis from occlusion, and low ability to locate accessory arteries. MR imaging is contraindicated in the occa­sional patient with metallic implant (pace­maker). Finally, the images may not be clear due to bowel motility and obesity. [52],[53],[57]

G. Three-dimensional gadolinium-enhanced MR angiography

Three-dimensional gadolinium-enhanced MR angiography can be combined with several other sequences to produce a comprehensive approach to renal MR angiography. Gado­linium contrast material can be used safely, even at high doses, in patients with renal failure and older than 55 years. Shortening the imaging times and breath holding for approximately 30 seconds can help to elimi­nate respiratory artifacts. Certain new MR machines now use a test dose-tracking system that will eliminate this pitfall of bolus tracking and circulation time estimation.

However, there are still disadvantages of this technique; first, the resolution is still low to depict segmental stenosis adequately. The second potential problem for some patients is the 25- to 35- second breath hold requirement. Having the patient hyperventilate before the study with nasal oxygen supple­mentation, however, helps the patient hold his or her breath for the study. [5] The renal vein and inferior vena cava can be evaluated by repeating the examination during the venous and equilibrium phases. [56],[58] Patients with severe renal impairment have shown delayed extrarenal elimination routes for Gd DTPA. The elimination half-life has been shown to increase up to 30 hours in patients with severe renal dysfunction. A retrospective study from Mayo clinic examined 151 patients with renal failure (serum creatinine values ranged between 185.6 and 1644.2 µmol/L) showed no evidence of nephrotoxicity. The side effects that were observed in those patients included nausea, vomiting, and headache in1% to 3.6%. [55]

H. Spiral computed tomographic (CT) angiography

This technique has different sensitivities and specificities ranging from 88% to 100% and 77% to 98%, respectively. The introduction of enhanced CT by use of intravenous iodinated contrast material has greatly improved the ability to directly image the proximal renal arteries and vascular lesion. [59] This technique has an advantage over the Gd-enhanced MR angiography, since it is easier to perform by most technicians in routine clinical service. The disadvantages of spiral computed tomo­graphic angiography can be summarized in the use of ionizing radiation and large volume of iodinated contrast material, which is asso­ciated with a higher frequency of anaphylaxis. Moreover, the artifacts from calcification and the limited field of view remain limiting factors of this modality. The image is of limited value in very obese patients or those with low cardiac output. [55]

   Therapy of Renal Artery Stenosis Top

The aim of the treatment is to allow better control of BP, prevent the BP complications, and improve the survival of patient with minimal adverse effects. The choice of treatment depends on many factors such as age of the patient, desired BP control and renal function. The therapeutic methods include drug theray, radiological intervention and surgery. [60] reduction of intake of salt and high cholesterol containing meals, cessation of smoking and avoidance of alcohol can not be overemphasized.

Drug Therapy

Several studies showed high mortality rate in elderly patients treated medically compared to those treated surgically. [61] Even when the blood pressure was adequately controlled pharmacologically, the progression of renal artery disease was not prevented. The five years survival in patients 65 - 74 years of age was 20%, and 9% for patients older than 75 years. [62] The introduction of ACE inhibitors, calcium channel blockers and now Angiotensin II receptor blockers (ARB) helped in better control of BP. We have to remember that the ACE inhibitors, ARB and possibly calcium channel blockers have nephroprotective cardioprotective as well as anti-proteinuric effect. [63],[64] Because the ACE inhibitors can lead to deterioration of renal function in patients with mild to moderate renal failure, the renal function should be monitored for at least 14 days in patients with mild to moderate CRF after starting treatment with ACE inhibitor. This can be repeated for two months, then every two months thereafter. An initial increase in plasma creatinine of 20 - 30 % or less of the initial level is acceptable, but if plasma crea­tinine continues to rise above the critical level, ACE inhibitors should be withdrawn. In patients with bilateral RAS, ACE inhibitors are contraindicated. Furthermore, ACE inhibitors have other side effects such as cough, an~ioedema, hyperkalemia and anemia. [65],[66]

Percutaneous Transluminal Renal Angio­plasty (PTRA)

PTRA is indicated in the treatment of mid and main renal artery. The patients are selected for revascularization if they have recent deterioration in renal function, bilateral renal artery stenosis, stenosis in a single fun­ctioning kidney, flash pulmonary edema, advanced chronic renal failure, reversible azotemia during ACE or ARB therapy, and conditions that cannot be managed medically. [67]

Clinical results of revascularization were evaluated in several studies. It is appropriate to consider the results with atheroma and fibromuscular dysplasia separately. The results for the patients with fibromuscular dysplasia are uniformly good; the rate of success is 90%. [6],[10],[52],[68] Restenosis is uncommon in these patients and the 5-year follow-up angio­grams after angioplasty often show no trace of any stenosis at all. When the stenosis is caused by atheroma, the results of revascu­larization are not satisfactory and associated with high rate of restenosis. Furthermore, in patients with diffuse atheromatous disease, the complication rate is relatively high, and stenting is preferable. However if the PTRA is technically successful in restoring arterial patency, blood pressure and renal functional outcome are broadly similar to those seen after surgical revascularization.

The improvement in hypertension is greater in the fibromuscular than in the atheromatous stenosis. [6],[69] In general, It was fond that BP was normalized in 50% of patients, improved in 42% but was not affected in 8%, whereas in patients with atherosclerosis the respective figures were 19, 51, and 30%. The failure rate of PTRA was 12% more in the atherosclerotic RAS. [69] The complications of angioplasty including deterioration in renal function (5%), hematoma (1.6%) at the puncture site, and azotemia from the dye load, and cholesterol emboli, tend to be more common in the older patients with diffuse atheromatous disease and can affect heart or the central nervous system. Dissection or occlusion (1.6%) of the renal artery may occur, but is rare. [42],[69]

PTRA can be considered as the treatment of choice in patients with fibromuscular stenosis, while it should be restricted in the patients with atheromatous stenosis to those in whom the expected benefits outweigh the risks. In the minority of patients with nonostial renal artery stenoses, PTRA showed 65% 12-month primary patency rates for proximal and 83% for isolated truncal stenoses. [7],[42] The advantages and disadvantage of PTRA in comparison to surgery are summarized in [Table - 5]. [69],[70],[71]

Endovascular Stent Placement

It is important to recognize that the majority of significant renovascular lesions are ostial (11 - 40% of atherosclerotic renovascular lesions). The PTRA often fails to restore arterial patency in ostial stenoses. [51] During the last 10 years, the use of endovascular stent increased in the treatment of RVD. Patient's selection is usually based on the ostial location of stenosis and failure of PTRA. In relation to the GFR changes, only patients with mild renal dysfunction appear to have very good renal functional outcomes. Patients with moderate renal failure (serum creatinine 200 to 350 µmol/L) may stabilize their renal function. However, patients with severe renal failure (s. creatinine > 350 µmol/L) are more likely to progress to ESRF. [6],[7],[42],[72]

There are different types of stents such as the balloon-expandable Palmaz stents, with an unexpanded length of 10, 15, or 20 mm, and the metallic stents for intravascular use. [73],[74] A recent study showed that the stenting is technically superior and clinically comparable to PTRA. [75] Several studies showed that the majority of patients after revascularization had stabilization of renal function, followed by a group of patients who had improvement of or cure of blood pressure and a minority in whom the renal function deteriorated. [58],[76],[77] The restenosis rate at follow up ranges bet­ween 17% and 32%. [57],[77] Stent placement considerably improves patency in ostial stenosis, however, it does not significantly improve primary patency in proximal and isolated truncal renal arterial stenosis in comparison to the PTRA. [78],[79]

Surgical intervention

Leadbetter and Burkland in 1938 were the first to successfully treat renovascular hyper­tension operatively. [80] Since that time, there have been several reviews and reports of surgical revascularization and a variety of techniques have evolved over the past 50 years. It is well established that the surgical revascularization is more suitable for atheros­clerotic RAS compared to PTRA. During the last 30 years, technical changes occurred in the surgical procedures. Autogenous saphenous vein aortorenal bypass was first used by DeWeese at the University of Michigan. This vein bypass proved durable in adults and became the preferred treatment for fibrodysplastic disease. Patch-spatulation of the proximal vein to allow a more perpendi­cular aortic origin of the graft, and distal vein spatulation to provide a more ovoid renal artery anastomoses, has become more common practice. The hypogastric artery is a good alternative for grafting. Synthetic vascular prostheses for renal artery recons­truction are also acceptable. Endarterectomy through an axial aortotomy from the level of the superior mesentric artery to the infrarenal aorta, as well as endarterectomy through the transected infrarenal aorta at the time of concomitant aortic reconstruction, is commonly performed types of renal revas­cularization. These procedures are useful in treating disease affecting multiple renal arteries. In case of bilateral stenoses, an aortic side-to-side or end-to-end anastomosis can be performed.

   Conclusion Top

Renovascular disease is an uncommon disease. Its prevalence is low but it is nece­ssary to be more in focus. Many invasive, less invasive and non-invasive diagnostic screening tests are available. The most of those tests are expensive and it is not cost effective to screen all patients. The differential diagnosis is essential, because there are several therapeutics options. It is necessary to indi­vidualize the treatment of patients with hyper­tension. Long-term outcome with surgical revascularization of renal artery stenosis is good. Long-term outcome of percutaneous renal artery stenting is awaited. The results of PTRA and rate of restenosis are disappointing but it is necessary to have long-term study. With treatment, renal function of most of the treated patients generally improve or at least stabilize and BP can be cured or better controlled.

   References Top

1.Marion Moser, MD, A critique of the world health organization: international society of hypertension guidelines for the management of hypertension, Cardiovascular Reviews and Reports (20) 4: 14, 1999.  Back to cited text no. 1    
2.Jacobson HR. Ischemic renal disease: an overlooked clinical entity? Kidney int 1988; 34:729-43.  Back to cited text no. 2  [PUBMED]  
3.Working Group on Renovascular Hypertension. Detection, evaluation and treatment of renovascular hypertension. Final report. Arch Intern Med 1987;147:820-9.  Back to cited text no. 3    
4.Grim CE, Luft FC, Weinberger MH, Grim CM. Sensitivity and specificity of screening tests for renal vascular hypertension. Ann Intern Med 1979;91:617-22.  Back to cited text no. 4  [PUBMED]  
5.Svetkey LP, Himmelstein SI, Dunnick NR, et al. Prospective analysis of strategies for diagnosing renovascular hypertension. Hypertension 1989;14:247-57.  Back to cited text no. 5  [PUBMED]  
6.Conlon PJ, O'Riordan E, Kalra PA. New insights into the epidemiologic and clinical manifestations of atherosclerotic renovascular disease.Am JKidney Dis 2000;35:573-87.  Back to cited text no. 6    
7.Blum U, Krumme B, Flugel P, et al. Treat­ment of ostial renal-artery stenosis with vascular endoprostheses after unsuccessful balloon angioplasty. N Engl J Med 1997; 336:459-65.  Back to cited text no. 7    
8.Case DB, Laragh JH. Reaetive hyper­reninemia in renovascular hypertension after angiotensin blockag with saralasin or converting enzyme inhibitor. Ann Intern Med 1979;91:153-60.  Back to cited text no. 8  [PUBMED]  
9.Conlon PJ, Athirakul K, Kovalik E, et al. Survival in renal vascular disease. J Am Soc Nephrol 1998;l 9:252-6.  Back to cited text no. 9    
10.Bouyounes BT, Libertino JA. Renovascular hypertension. Curr Opin in Urol 1999;9:111-4.  Back to cited text no. 10    
11.Goldblatt H, Lynch J, Hanzal RF, et al. Studies on experimental hypertension of renal ischemia. J Exp Med 1934;59:347- 79.  Back to cited text no. 11    
12.Egido J. Vasoactive hormones and renal sclerosis, Kidney Int. 1996;49:578-97.  Back to cited text no. 12    
13.Anderson S. Ageing and the renin-angiotensin system. Nephrol Dial Transplant 1997;12: 1093-94.  Back to cited text no. 13  [PUBMED]  [FULLTEXT]
14.Hackenthal, E, Paul M, Ganten D, Taugner R. Morphology, physiology, and molecular biology, of renin secretion. Physiol Rev 1990;70: 1067-116.  Back to cited text no. 14    
15.Taugner R, Whalley A, Angermuller S, Buhrle CP, Hackenthal E. Are the renin­containing granules of juxtaglomerular epithelioid cells modified lysosomes? Cell Tissue Res 1985;239:575-87.  Back to cited text no. 15    
16.Berka JL, Alcorn D, Ryan GB, SkinnerSL. Renin processing studied by immunogold localization of prorenin and renin in granular juxtaglomerular cells in mice treated with enalapril. Cell Tissue Res 1992;268:141-8.  Back to cited text no. 16    
17.Galen FX, Devaux C, Houot AM, et al. Renin biosynthesis by human tumoral juxtaglomerular cells. Evidences for a rennin precursor. J Clin Invest 1983;73: 1144-55.  Back to cited text no. 17    
18.Jurgen Schnermann. The Juxatglomerular apparatus: from anatomical peculiarity to psychological relevance. J Am Soc Nephrol 2003;14:1681-94.  Back to cited text no. 18    
19.Taugner R, Kim SJ, Murakami K, Waldherr R. The fate of prorenin during granulopoiesis in epitheloid cells. Histochemistry 1987;86: 249-53.  Back to cited text no. 19  [PUBMED]  
20.Hall JE. Control of sodium excretion by angiotensin ll: intrarenal mechanisms and blood pressure regulation. Am J Physiol 1986;250:R960-72.  Back to cited text no. 20  [PUBMED]  [FULLTEXT]
21.Edwards RM. Segmental effects of norepinephrine and angiotensin ll on isolated renal microvessels. Am J Physiol 1983;244:F526-34.  Back to cited text no. 21  [PUBMED]  [FULLTEXT]
22.Arima S, Ito S. Angiotensin ll type 2 receptors in the kidney: evidence for endothelial-cell-mediated renal vasodilata­tion; Nephrol Dial Transplant 2000; 15:448-51.  Back to cited text no. 22    
23.Brunner HR, Kirshman JD, Sealey JE, Laragh JH. Hypertension of renal origin: evidence for two different mechanisms. Science 1971;174:1344-6.  Back to cited text no. 23    
24.Anderson S, Rennke HG, Brenner BM. Therapeutic advantage of converting enzyme inhibitors in arresting progressive renal disease associated with systemic hypertension in the rat. J Clin Invest 1986; 77:1993-2000.  Back to cited text no. 24  [PUBMED]  [FULLTEXT]
25.Ibrahim HN, Rosenberg ME, Greene EL, Kren S, Hostetter TH. Aldosterone is a major factor in the progression of renal disease. Kidney Int 1997;52[Suppl 63]: S115-9.  Back to cited text no. 25    
26.Lafayette RA, Mayer G, Park SK, Meyer TW. Angiotensin II receptor blockade limits glomerular injury in rats with reduced renal mass. J Clin Invest 1992;90:766 -71.  Back to cited text no. 26  [PUBMED]  [FULLTEXT]
27.Carlberger G. Collste LG. Hypertension and sodium reten in bilaterally nephrectomised man. Scand J Urol Nephrol 1968;2:151-6.  Back to cited text no. 27    
28.Swales JD Tange JD. The influence of acute sodium depletion on experimental hyper­tension in the rat. J Lab Clin Med 1971;78: 369-79.  Back to cited text no. 28    
29.Dahl LK. Salt and hypertension. Am J Clin Nutr 1972;25:231-44.  Back to cited text no. 29  [PUBMED]  
30.Dahl LK, Heine M. Primary role of renal homografts in setting Chronic Blood Pressure Levels in Rats. Circ Res 1975;36:692-6.  Back to cited text no. 30  [PUBMED]  
31.Schreiber MJ, Pohl MA, Novick AC. The natural history of atherosclerotic and fibrous renal artery disease. Urol Clin North Am 1984;11:383-92.  Back to cited text no. 31  [PUBMED]  
32.Stanley JC. The evolution of surgery for renovascular occlusive disease. Cardiovasc Surg 1994;2:195-202.  Back to cited text no. 32  [PUBMED]  
33.Meyrier A, Simon P, Montseny JJ, et al. Vascular nephropathies and nephrosclerosis: epidemiology and pathophysiology. Adv nephrol - Necker Hosp 1997;26:207-45.  Back to cited text no. 33  [PUBMED]  
34.Begelman S, Olin J. Fibromuscular dysplasia, Curr Opin Rheumatol 2000;12:41-7.  Back to cited text no. 34    
35.Gharavi A, Klotman P. The renin-angio­tensin system as a mediator of renal injury in hypertension. Mt Sinai J. Med 1998; 65:118-24.  Back to cited text no. 35    
36.Hanovici H, Zinicda N. Experimental renal artery stenosis. Diagnostic significance of arterial haemodynamics. J Cardiovasc Surg 1962;3:259-62.  Back to cited text no. 36    
37.Kaplan-Pavlovcill S, Nadja C, Captopril renography and duplex Doppler sonography in the diagnosis of renovascular hypertension. Nephrol Dial Transplant 1998;13:313-7.  Back to cited text no. 37    
38.Lerman LO, Shwartz RS, Grande JP, Romero JC. Noninvasive evaluation of a novel swine model of renal artery stenosis. J Am Soc Nephrol 1999;10:1455-65.  Back to cited text no. 38    
39.Rittgers SE, Norris CS, Barnes RW. Detection of renal artery stenosis: experimental and clinical analysis of velocity waveform. Ultrasound Med Biol 1985;11:523-31.  Back to cited text no. 39  [PUBMED]  
40.Nahman NS Jr, Maniam P, Hernandez RA Jr, et al. Renal artery pressure gradients in patients with angiographic evidence of atherosclerotic renal artery stenosis. Am J Kidney Dis 1994;24:695-99.  Back to cited text no. 40    
41.Sos TA, Pickering TG, Sniderman K, et al. Percutaneous transluminal angioplasty in renovascular hypertension due to atheroma or fibromuscular dysplasia. N Engl J Med 1983;309:274-9.  Back to cited text no. 41  [PUBMED]  
42.Baumgartner I, Von Aesch K, Do DD, Triller J, Birrer M, Mahler F. Stent placement in ostial and nonostial atherosclerotic renal arterial stenoses: a prospective follow-up study. Radiology 2000;216:498-505.  Back to cited text no. 42  [PUBMED]  [FULLTEXT]
43.Sos TA, Trost DW. Renal vascular disease as cause of hypertension, Curr opin Nephrol hypertens 1995; 4:76-81.  Back to cited text no. 43    
44.Holley KE, Hunt JC. Renal artery stenosis: a clinical-pathologic study in normotensive and hypertensive patients. Am J Med 1964; 37:14-22.  Back to cited text no. 44    
45.Lencioni R, Pinto S Napoli V, Bartolozzi C. Noninvasive assessment of renal artery stenosis: current imaging protocols and future directions in ultrasonography. J Comput Assist Tomogr 1999;23:S95-100 (suppl.1).  Back to cited text no. 45    
46.Locatelli F, Marcelli D, Conte F, et al. Cardiovascular disease in chronic renal failure: the challenge continues. Nephrol Dial Transplant 2000;15:69-80.  Back to cited text no. 46    
47.Muller FB, Sealey JE, Case DB, et al. The captopril test for identifying renovascular disease in hypertensive patients. Am J Med 1986;80:633-44.  Back to cited text no. 47  [PUBMED]  [FULLTEXT]
48.Schohn DC, Jahn HA, Schmitt RL. Predictability of standardized captopril-test in hypertension in end-stage renal failure. Kidney Int 1988;34(Suppl 25):145-8.  Back to cited text no. 48    
49.Soulez G, Oliva VL, Turpin S, et al. Imaging of renovascular hypertension: respective values of renal scintigraphy, renal doppler US, and MR angiography. Radiographics. 2000;20:1355-68.  Back to cited text no. 49    
50.Metcalfe W, Reid AW, Geddes CC. Prevalence of angiographic atherosclerotic renal artery disease and its relationship to the anatomical extent of peripheral vascular atherosclerosis. Nephrol Dial Transplant 1999;14:105-108.  Back to cited text no. 50  [PUBMED]  [FULLTEXT]
51.Miralles M, Covas MI, Martinez Miralles E, Cairols M, Cotillas J, Santiso MA. Captopril test and renal duplex scanning for the primary screening of renovascular disease, Am J Hypertens 1997;10:1290-6.  Back to cited text no. 51    
52.De Cobelli F, Venturini M, Vanzulli A et al. Renal arterial stenosis: prospective comparison of color doppler US and Breath-hold, three­dimensional, dynamic, gadolinium-enhanced MR angiography. Radiology. 2000;214:373-80.  Back to cited text no. 52    
53.Kent KC, Edelman RR, Kim D, Steinman TI, Porter DH, Skillman JJ. Magnetic resonance imaging: a reliable test for the evaluation of proximal atherosclerosic renal arterial stenosis. J Vas Surg 1999; 13:311- 28.  Back to cited text no. 53    
54.Hillman BJ. Imaging advances in the diagnosis of renovascular hypertension. Am J Roentgenol 1989;153:5-14.  Back to cited text no. 54    
55.Ghantous et al Evaluating Patients with Renal Failure for Renal Artery Stenosis with Gadolinium-Enhanced Magnetic Resonance Angiography. AJKD vol.32 No 1 (Jan) 1999; 36 -42.  Back to cited text no. 55    
56.Bakker J, Beek FJ, Beutler JJ, et al. Renal artery stenosis and accessory renal arteries: Accuracy of detection and visualization with gadolinium-enhanced breath-hold MR angiography. Radiology 1998;207:497-504.  Back to cited text no. 56  [PUBMED]  
57.Rees CR, Niblett R, Snead D: United State multicenter study of Palmaz - Schatz stents in the renal arteries. CIIRSE Annual Meeting and interventional Radiological Society of Europe. Crete, June 1994.  Back to cited text no. 57    
58.Qian Dong, Schoenbergso, Carlos RC, et al. Diagnosis of renal vascular disease with MR angiography. Radiographics 1999;19: 1535-54.  Back to cited text no. 58    
59.Sarkar SD,Siegel DN. Invited commentary. Radiographics 2000;20:1368-72.  Back to cited text no. 59    
60.Hunt JC, Sheps SG, Harrisson EG Jr, Strong CG, Bernatz PE. Renal and renovascular hypertension. A reasoned approach to diagnosis and management. Arch Intern Med 1974;133:988-99.  Back to cited text no. 60    
61.Schwenger V, Zeier M, Ritz E. Antihyper­tensive therapy in renal patients - benefits and difficulties. Nephron 1999; 83:202-13.  Back to cited text no. 61  [PUBMED]  [FULLTEXT]
62.Hirshberg B, Sasson T, Grinblat I, Shustin L, Rubinger D. Prolonged renal dysfunction secondary to renal artery stenosis in the elderly - it is never too late. Nephrol Dial Transplant 1998;13: 982-84.  Back to cited text no. 62  [PUBMED]  [FULLTEXT]
63.Michel JB, Dussaule JC, Choudat L, et al. Effects of antihypertensive treatment in one-clip, two kidney hypertension in rats. Kidney int 1986;29:1011-20.  Back to cited text no. 63  [PUBMED]  
64.Mervaala E, Dehmel B, Gross V et al. Angiotensin-converting enzyme inhibation and AT1 receptor blockade modify the pressure-natriuresis relationship by additive mechanisms in rats with human renin and angiotensinogen genes. J Am Soc Nephrol 1999;10:1669-80.  Back to cited text no. 64    
65.Kuroda S, Nishida N, Uzu T, et al. Prevalence of renal artery stenosis in autopsy patients with stroke. Stroke 2000; 31:61-5.  Back to cited text no. 65  [PUBMED]  [FULLTEXT]
66.Jensen G, Zachrisson BF, Delin K, Volkmann R, Aurell M. Treatment of renovascular hypertension: one year results of renal angioplasty. Kidney Int 1995;48: 1936-45.  Back to cited text no. 66  [PUBMED]  
67.Leertouwer TC, Gussenhoven EJ, Bosch JL, et al. Stent placement for renal arterial stenosis: where do we stand? A meta anlysis. Radiology 2000;216:78-85.  Back to cited text no. 67    
68.Schwarten DE, Yune HY, Klatte EC, Grim CE, Weinberger MH. Clinical experience with percutaneous transluminal angioplasty (PTA) of stenotic renal arteries. Radiology 1980;135:601-4.  Back to cited text no. 68  [PUBMED]  
69.Morganti A. Renal angioplasty: better for treating hypertension or for rescuing renal function? J hypertens 1999;17:1659-65.  Back to cited text no. 69  [PUBMED]  [FULLTEXT]
70.Weinberger MH, Yum MN, Grim CE, Luft FC, Klatte EC, Donahue JP. Percutaneous transluminal angioplasty for renal artery stenosis in a solitary functioning kidney. Ann Intern Med 1979;91:684-8.  Back to cited text no. 70    
71.Kaplan NM. Clinical hypertension Baltimore, Md: Williams & Wilkins, 1990; 303-324.  Back to cited text no. 71    
72.Textore SC, Wilcox CS. Renal artery stenosis: a common, treatable cause of renal failure? Annu Rev Med 2001;52:421-42.  Back to cited text no. 72    
73.Dotter CT. Transluminally-placed coilspring endarterial tube grafts. Long-term patency in canine popliteal artery. Invest Radiol 1969: 4(5):329-32.  Back to cited text no. 73    
74.Palmaz JC, Sibbitt RR, Reuter SR, Tio FO, Rice WJ. Expandable intraluminal graft: a preliminary study. Work in progress. Radiology 1985;156 (1):73-7.  Back to cited text no. 74    
75.Watson PS, Hadjipetrou P, Cox SV, Piemonte TC, Eisenhauer AC. Effect of renal artery stenting on renal function and size in patients with atherosclerotic renovascular disease. Circulation 2000; 102:1671-7.  Back to cited text no. 75  [PUBMED]  [FULLTEXT]
76.Rousseau H, Joffre F. Stents in renal arteries: long term follow up with Wallstent. Abstract presented at IV course on vascular and interventional radiology 1994, Las Palmas Canary Islands Spain.  Back to cited text no. 76    
77.Baumgartner I, Von Aesch K, Do DD, et al. Stent placement in ostial and nonostial atherosclerotic renal arterial stenosis: a prospective follow-up study. Radiology 2000;216:498-505.  Back to cited text no. 77  [PUBMED]  [FULLTEXT]
78.Alcazar JM, Rodicio JL. Ischemic nephro­pathy: clinical characteristics and treatment. Am J Kidney Dis 2000;36:885-93.  Back to cited text no. 78    
79.Neymark E, LaBerge JM, Hirose R, et al. Arteriographic detection of renovascular disease in potential renal donors: incidence and effect on donor surgery. Radiology 2000;214:755-60.  Back to cited text no. 79  [PUBMED]  [FULLTEXT]
80.Leadbetter WF, Burkland GE. Hyper­tension in unilateral renal disease. J. Urology 1938; 39: 611-26.  Back to cited text no. 80    

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