AUTHOR AND EDITOR INFORMATION

Section 1 of 12  

• Authors and Editors
• Introduction
• Differentials
• Radiograph
• CT SCAN
• MRI
• Ultrasound
• Nuclear Medicine
• Angiography
• Intervention
• Multimedia
• References

INTRODUCTION

Section 2 of 12  

• Authors and Editors
• Introduction
• Differentials
• Radiograph
• CT SCAN
• MRI
• Ultrasound
• Nuclear Medicine
• Angiography
• Intervention
• Multimedia
• References

Background

Renovascular hypertension (RVHT) denotes nonessential hypertension  in which a causal relationship exists between anatomically evident arterial occlusive disease and elevated blood pressure. RVHT is the clinical consequence of renin-angiotensin-aldosterone activation as a result of renal ischemia. Renal artery stenosis (RAS) is a major cause of RVHT and accounts for 1-10% of the 50 million cases of hypertension in the United States.

Apart from the casual relationship of occlusive renal artery disease and hypertension, RAS is also being increasingly recognized as an important cause of chronic renal failure. In older patients, atherosclerosis is the most common cause of RAS. RAS due to atherosclerosis is generally a progressive disease with increasing luminal narrowing, which may eventually compromise renal blood flow and renal function and structure.

Arterial dysplasias (AD) are uncommon angiopathy associated with heterogeneous histologic changes that may affect the carotid circulation and the visceral and peripheral arteries. Medial fibroplasia (MFP), as a cause of RAS usually affects young to middle-aged adults, mostly women, but it can also affect children. It is an important cause of RVHT in children. The average age range of patients with MFP is 30-40 years. The youngest patient with MFP of the renal artery was reportedly 6 months old.

Ultimately, MFP results in arterial stenosis, which causes organ ischemia or infarction. The clinical manifestations reflect the arteries involved which most commonly manifests as hypertension due to RAS or as strokes due to carotid artery disease. MFP is one of the most important mimics of vasculitis.

Although MFP is a pathologic diagnosis, characteristic change is seen at vascular imaging. The most common finding is the string-of-beads appearance caused by areas of relative stenoses or webs alternating with small fusiform or saccular aneurysms of the artery. Approximately 10-30% of patients with RAS have MFP.

Diagnostic imaging plays an essential role in the diagnosis and treatment of RVHT. With an aging population and a possible increase in the prevalence of RAS and ischemic nephropathy, radiologists will play an increasing role both in the diagnosis and treatment of RVHT.

Pathophysiology

Development of RVHT

RVHT is the clinical consequence of renin-angiotensin-aldosterone activation. Since Goldblatt's work in 1934, RVHT has become increasingly recognized as a cause of clinically difficult-to-control hypertension and chronic renal insufficiency. Goldblatt demonstrated that occlusion of the renal artery causes ischemia, which then causes an elevation of blood pressure by triggering the release of renin. Increased renin levels help in the conversion of angiotensin I to angiotensin II, causing severe vasoconstriction, aldosterone release. The ultimate cascade of events depends on the presence of a functioning contralateral kidney.

The development of RVHT involves the activation of both limbs of the renin-angiotensin-aldosterone system and depends on the presence or absence of a contralateral kidney. Unilateral renal ischemia initiates an increased secretion of renin, which accelerates the conversion of angiotensin I to angiotensin II and which enhances the adrenal release of aldosterone. Aldosterone-mediated sodium and water retention is efficiently handled by the noncompromised kidney, precluding the volume from contributing to the angiotensin II–mediated hypertension.

Atherosclerotic disease is usually diffuse and may involve both kidneys, leaving a solitary ischemic kidney that has little reserve capacity for sodium and water excretion; hence, volume plays an additive role in the hypertension. An ischemic solitary kidney is unable to perform the pressure diuresis required to handle the aldosterone-induced sodium and water retention. Thus, the resultant volume load further contributes to the hypertension and also suppresses the production of renin by the stenotic kidney.

Angiotensin II causes vasoconstriction of both afferent and efferent arterioles, with a preferential affect on the efferent side. Under physiologic conditions, efferent tone is essential to the maintenance of intraglomerular pressure. Angiotensin blockade increases efferent renal arterial blood flow, resulting in an increased intraglomerular pressure and optimized glomerular filtration rate (GFR).

In a kidney rendered ischemic by RAS with a reduced afferent blood flow, the intraglomerular pressure and glomerular filtration are maintained by angiotensin II–mediated efferent vasoconstriction. Removal of the efferent vasoconstriction effect by using angiotensin blockade in the ischemic kidney may reduce the GFR. Angiotensin blockade can be achieved by the use of angiotensin-converting enzyme (ACE) inhibitors.

The use of ACE inhibitors causes a deterioration of renal function in some patients with renovascular disease; this effect is particularly pronounced in patients with in bilateral RAS. Because angiotensin predominantly affects the efferent renal arteriole, the decrease in renal blood flow caused by afferent vasoconstriction is less than the decrease in the GFR caused by efferent vasoconstriction. The net result is a decrease in the filtration fraction. By blockading angiotensin, ACE inhibitors eliminate efferent vasoconstriction and cause a decrease in the intraglomerular pressure and the GFR.

Normally, the perfusion of the kidney is increased by as much as 5 times, as compared with that of other organs, because it drives glomerular capillary filtration. Both glomerular capillary hydrostatic pressure and renal blood flow are essential components of the GFR.

In patients with RAS, chronic ischemia produces adaptive changes in the kidney that are more pronounced in the tubular tissue. These changes include tubular cell atrophy, atrophy of the glomerular tuft, patchy inflammation and fibrosis of tubular cells, tubular sclerosis, thickening and duplication of the Bowman capsule, and intrarenal arterial medial thickening. In RAS, the GFR is dependent on angiotensin II and other modulators that maintain the balance between the afferent and efferent arteries. However, when perfusion pressure decreases below 70-85 mm Hg, maintaining an adequate GFR may no longer be possible. Significant functional impairment of autoregulation, leading to a decrease in the GFR, is not likely to be observed until arterial luminal narrowing exceeds 50%.

In adults, renovascular disease tends to appear at different times, and it affects the sexes differently. Atherosclerotic disease affects mainly the proximal third of the main renal artery, and it is most common among older men. Fibromuscular dysplasia (FMD) involves the distal two thirds and branches of the renal arteries, and it is most common among younger women.

Other conditions that may be associated with RVHT include cholesterol embolic disease, acute arterial thrombosis or embolism, aortic dissection, neurofibromatosis, renal arterial trauma, arterial aneurysm, arteriovenous malformation of the renal artery, and polyarteritis nodosa and other vasculitides.

Evolution of RVHT

The evolution of RVHT has been described as having 3 stages.

In the first stage, the immediate elevation of blood pressure is a direct result of increased levels of renin. Over days to weeks, the blood pressure remains elevated, but the course and presence of elevated renin levels depends on the presence and function of the contralateral kidney. The mechanism by which hypertension is produced in patients with renovascular disease thus changes over time and varies with the sodium balance. With a normally functioning contralateral kidney, volume expansion is avoided, and renin levels remain high. The 2 kidneys function out of synch: The ischemic stenotic kidney produces excessive renin and retains sodium, whereas the comparatively normal kidney continues to excrete sodium and water to maintain normal volume levels. The end result is systemic hypertension that is renin and angiotensin mediated.

In the second phase, in the setting of an ischemic solitary kidney, sodium and water retention, together with the vasopressor effects of angiotensin II, act to maintain renal perfusion pressure. The stimulus to produce renin is impaired, and renin levels thus decrease. In these circumstances, angiotensin II no longer drives the hypertensive state, but the high blood pressure instead results from volume expansion. Thus, perfusion pressure tends to be maintained at the expense of systemic hypertension and volume retention.

Renal perfusion may return to normal if blood flow is normalized during the first 2 phases, and the blood pressure soon returns to a normal level.

In the third phase, hypertension persists, even after patency of the renal artery is restored. Once phase 3 is reached, restoration of renal blood flow may not normalize the blood pressure, presumably because of secondary irreversible vascular or renal parenchymal disease.

Atherosclerosis

How the initial arterial epithelial injury occurs in patients with atherosclerosis is not clear. Nevertheless, lipid abnormalities, hypertension, cigarette smoking, diabetes mellitus, viral infection, immune injury, and increased homocysteine levels have all been implicated in contributing to the endothelial injury. At the site of the endothelial atheromatous lesion, permeability to plasma macromolecules (eg, low-density lipoproteins) is increased, with a subsequent increased turnover of endothelial cells, smooth muscle cells, and intimal macrophages. When atherogenic lipoproteins exceed a certain critical mass, the mechanical forces may enhance lipoprotein infiltration in these regions, leading to early atheromatous lesions.

Atherosclerotic RAS may progress in as many as one third of patients, and ongoing ischemic renal parenchymal damage is of concern. Furthermore, despite adequate blood pressure control, this condition is associated with reduced renal perfusion pressures, and renal function may deteriorate.

Studies about the natural history of atheromatous RAS obtained by means of sequential abdominal aortography or duplex sonography in patients with documented and medially treated RAS have shown that progressive arterial obstruction occurs in 42-53% of patients within the first 2 years of follow-up. In patients with a high-degree RAS, the rate of progression to complete renal artery occlusion in these studies is 9-16%. In a study of 85 patients at the Cleveland Clinic who were followed up for 3-172 months, mild-to-moderate stenosis remained unchanged upon follow-up, but 39% of patients, lesions >75% progressed to total occlusion (Schreiber, 1984).

Aterial dysplasia

Leadbetter and Burkland first reported AD of a renal artery in 1938 when they removed an ectopic kidney in a 5-year old boy that presented with sustained hypertension. FMD may involve any layer of a visceral artery, and it may be classified as intimal, medial, or adventitial. The medial variety can be subdivided into several more categories.

In 1967, McCormack et al classified AD on the basis of the primary site of involvement of arterial wall, as determined histologically. Their classification of fibrosing lesions of renal arteries included the categories of intimal fibroplasia, medial fibrosis with microaneurysms, subadventitial fibroplasia and fibromuscular hyperplasia. They first coined the term chain of beads to describe radiographic changes in MFP of the renal artery. The term has subsequently been modified to string of beads. MFP is the most common variety of AD and represents 85% of the cases. The string-of-beads sign is classically seen in MFP.

A similar radiographic appearance can be caused by subadventitial fibroplasia, but in this variant, the size of the aneurysms does not exceed the diameter of the renal artery. MFP may appear as a single stenosis of a visceral artery, but it is more often seen as multiple stenoses with intervening outpouchings forming a chain. Radiographically, this is depicted as a string-of-beads sign.

Histologically, MFP can be subdivided into 2 types: a peripheral form and a diffuse form. The peripheral form generally affects the outer media, replacing the smooth muscle with fibrous-appearing tissue. The diffuse form affects the media more extensively, with replacement of the media with fibrous tissue interspaced by medial thinning. The media can be completely absent in some areas, giving rise to aneurysmal dilatation. Although FMD was initially described in the renal arteries, many other visceral arteries are now known to be involved, and multiple visceral artery aneurysms have been reported.

Although the pathogenesis is not completely understood, humoral, mechanical, and genetic factors may play a role, as may mural ischemia. Hormonal factors have been implicated because MFP and subadventitial fibroplasias are found predominantly in women. The common association with ptotic kidneys has supported the mechanical theory in which stretching of the renal artery may be responsible for the development of FMD.

Ischemia due to inadequate nutrition of the renal artery by the vasa vasora has also been implicated. A deficiency of alpha-1-antitrypsin has also been implicated in the development of various disorders affecting medium-sized arteries, including those affected by intracranial aneurysms, cervicocephalic arterial dissections, and FMD. Some have suggested that a heterozygous alpha-1-antitrypsin deficiency may be a genetic risk factor for FMD.

The natural history of MFP is relatively benign with progression occurring in only a minority of patients. Anatomic progression of MFP in the renal artery has been reported 12-66% in patients with main renal artery disease. However, renal function deterioration, as assessed by measuring the serum creatinine level or a reduction in renal size, seldom occurs despite progression of RAS as demonstrated angiographically.

Complete obstruction of renal artery leading to total renal infarction has been reported. Studying potential artery donors with angiographic evidence of AD, Goncharenko et al found that 26% developed hypertension, as compared with 6% of age-sex matched control subjects. Medical treatment of MFP associated hypertension poses the risk of a further reduction of renal blood flow, which may result in ischemic atrophy or even total infarction of the involved kidney. Isolated renal artery dissection is a rare condition that has also been reported in association with MFP.

Hepatic and superior mesenteric involvement in FMD occurs less frequently, and sporadic cases of severe intestinal ischemia and hepatic artery aneurysm rupture have been reported. FMD is a rare cause of abdominal aortic aneurysm. The consequences of RAS are hypertension, which may be particularly difficult to control or which may require the use of multiple antihypertensive agents (with increased adverse effects), and a progressive loss of renal function is possible. In addition, the discovery of atherosclerotic renal vascular disease frequently occurs in the setting of generalized vascular disease (eg, cerebral, cardiac, peripheral disease), with the consequences associated with disease in those vascular beds.

Neurofibromatosis

Neurofibromatosis is a rare cause of RAS and usually secondary to a direct effect of fibrous proliferation of the intima or media. Less commonly, neurofibromatous tissue may affect the adventitia, producing periarterial fibrosis indistinguishable from other causes of RAS. These lesions are usually at the origin of the artery, and they may be bilateral.

Congenital stenosis

Congenital stenosis (coarctation of renal artery) is extremely rare and assumed congenital because of its discovery in early life. This type of stenosis is generally confined to the main renal artery, and it may be associated with aortic coarctation. Some cases may eventually involve changes related to arteritis, FMD, or neurofibromatosis.

Transplant RAS

Transplant RAS is seen in about 10% of patients after renal transplantation, and it is the most important cause of treatable hypertension. In renal transplantation patients, RAS may occur as a complication of surgery, as transplant rejection, or as intrinsic vascular disease; this RAS usually occurs in the first year after surgery and rarely after the third year. The presentation is usually with hypertension and, occasionally, an elevated serum creatinine level.

The extent to which the RAS stenosis contributes to the hypertension is difficult to determine because rejection is frequent cause of vascular disease, and systemic hypertension often accompanies rejection. Of the 20% of patients with normal blood pressure and renal failure, 50% become hypertensive after renal transplantation. With this complex background and the ever-present complication of graft rejection and acute tubular necrosis, one may loose sight of RAS as a treatable cause of hypertension.

Frequency

United States

RVHT is the most common type of secondary hypertension, accounting for less than 1% of cases in unselected populations and as many as 30% of cases in selected populations. Studies suggest that ischemic nephropathy may be responsible for 5-22% of advanced renal disease in all patients older than 50 years. FMD accounts for approximately 25% of all cases of RVHT, and it is a common cause of hypertension in children. RVHT occurs in approximately 6 of 100,000 people.

International

The international prevalence of RVHT is not known, but no data suggest that the incidence differ from that in the United States.

Mortality/Morbidity

• In patients with hypertension, atherosclerotic renal artery disease is a strong predictor of increased mortality relative to the general population. In the setting of renal dysfunction, RVHT is associated with the greatest mortality rate.
• Major complications of RVHT include end-organ damage due to chronically uncontrolled hypertension and progressive renal insufficiency, which is an important sequel of chronic renal ischemia. (See also Pathophysiology).
• The prognosis of patients with RVHT is difficult to ascertain because it varies with the degree of RAS, the response of the patient to antihypertensive therapy, and the effectiveness of revascularization procedures.

Race

RVHT is less common in African Americans than in persons of other races.

• In 2 studies of patients with severe hypertension, the incidence was 27-45% in white Americans compared with 8-19% in African Americans.
• RVHT occurs more often in white men and in blacks of both sexes.

Sex

• All types of AD, except intimal fibroplasia, more commonly affect women than men. For intimal fibroplasias, the male-female distribution is equal. For FMD, the male-to-female ratio is 1:3-5.
• RVHT is most common in younger women and older men. In younger women, RVHT most commonly develops as a result of FMD affecting the distal two thirds of the renal arteries and their branches. In older men, RVHT most often develops as a result of atherosclerotic disease that affects the proximal third of the main renal artery.
• Although the incidence of atherosclerotic RVHT is independent of sex, Crowley et al showed that female sex is an independent predictor of renovascular disease progression. Other such predictors are older age, elevated serum creatinine level, coronary artery disease, peripheral vascular disease, hypertension, and cerebrovascular disease.

Age

The age of onset depends on the cause of the damage to the renal blood vessels. The average age range is 30-40 years. RVHT tends to occur in patients younger than 30 years or older than 50 years. The youngest patient with FMD of the renal artery was reportedly 6 months old.

• RVHT often occurs in men older than 45 years with atherosclerosis and in women younger than 45 years with AD.
• Around 10% of children with AD also have RVHT. FMD generally affects young-to-middle-aged adults, mostly women; however, it can affect children as well. FMD is an important cause of RVHT in children.
• In 1964, Holley et al reported data from 295 consecutive autopsies. The mean age at death was 61 years. The prevalence of RAS was 27% among 256 patients identified as having history of hypertension, whereas 56% had significant stenosis (>50% luminal narrowing). Among normotensive patients, 17% had severe RAS (>80% luminal narrowing). Among those older than 70 years, 62% had severe RAS. Another similar autopsy study showed that 5% of patients older than 64 years had severe stenosis; this rate increased to 18% in patients aged 65-74 years and to 42% for patients older than 75 years.

Anatomy

Although classified as dorsal branches, the renal arteries usually arise as lateral aortic branches slightly below the disk between L1 and L2. Rarely, the renal arteries may arise below the inferior aspect of D12 or below the lower border of L2.

The position of the kidney is variable, and although most renal arteries arise between L1 and L2, the length of the renal arteries and the angle between the aorta and the renal arteries varies. The lower the kidneys are, the longer and more acutely angulated are the renal arteries.

The right renal artery may originate slightly anterior to the coronal plane. Supplemental renal arteries may be problematic for the angiographer because they may be difficult to find and the catheter tip may obstruct the orifice. Their origin of renal arteries may again be variable, and these arteries may arise from D11 down to the iliac vessels. Furthermore, supplemental branches may arise from visceral arteries.

Cadaveric studies have shown that single renal arteries are bilaterally present in 72% of cases. The kidney may be divided into dorsal and ventral segments, and the arteries to these segments may be identified on angiograms. The intrarenal branches of renal arteries taper uniformly. The intralobar branches repeatedly branch to give rise to arcuate arteries. The interlobular arteries arise from the arcuate arteries, where they extend into the renal cortex in a parallel fashion.

AD may affect the main renal arteries and the intralobar arteries. With severe RAS, extensive collateral circulation develops via the capsular, peripelvic, and periureteric systems. These collaterals involve the capsular, lumbar, internal iliac, lower intercostal, and gonadal arteries. The collateral channels are coiled, tortuous, and enormously lengthened in comparison to normal arteries.

Clinical Details

Clinical criteria for the presence of RVHT include the following:

• Difficult-to-control hypertension despite adequate medical treatment
• Hypertension with renal failure or progressive renal insufficiency
• Accelerated or malignant hypertension
• Severe hypertension (diastolic blood pressure >120 mm Hg) or resistant hypertension
• Hypertension with an asymmetric kidney
• Paradoxical worsening of hypertension with diuretic therapy
• Hypertension refractory to standard therapy
• Onset of hypertension occurring in patients younger than 30 years or older than 50 years
• Abrupt onset of hypertension
• Symptoms of atherosclerotic disease elsewhere
• Negative family history of hypertension
• Cigarette smoking or use of other tobacco products
• Renal failure with ACE inhibition
• Recurrent pulmonary edema (flash edema)
• Advanced funduscopic changes
• Clear abdominal bruit (This is heard in 46% of patients with RVHT. Bruit is also heard in 9% of patients with essential hypertension; however, innocent bruits are common in younger individuals.)
• Systolic-diastolic bruits (In combination with hypertension, these are suggestive of RVHT.)

Risk factors associated with the development of atherosclerotic RAS include the following:

• Carotid artery disease
• Coronary artery disease
• Diabetes mellitus
• Hypertension (high blood pressure)
• Obesity 
• Older age
• Peripheral vascular disease (vascular disease in the extremities, eg, the legs)
• Smoking 
• Familial history of AD RAS (often present)

Preferred Examination

The preferred imaging method in a patient with suspected of RAS is controversial. Accurate identification of patients with correctable RVHT can be difficult with use of standard noninvasive techniques, such as sonography, because they provide only indirect evidence of the presence of RAS. On the contrary, invasive techniques, which are much more accurate, some have the potential of nephrotoxicity. If so, invasive methods can cause deterioration of renal function and procedure-related complications at the site of arterial puncture or catheter-induced embolism.

Gilfeather et al evaluated conventional angiography versus gadolinium-enhanced magnetic resonance angiography (MRA) in 54 patients and 107 kidneys. The study showed that, in 70 kidneys (65%), the average degree of stenosis reported by readers assessing both modalities differed by 10% or less.

In 22 cases (21%), MRA caused overestimation of the stenosis by more than 10% relative to the results of conventional angiography. In 15 cases (14%), MRA caused underestimation of the stenosis by more than 10%. MRA produces excellent contrast-enhanced angiograms without the risk of iodinated compounds and radiation exposure. MRA provides accurate information about the number of renal arteries, the size of the kidneys, and the presence of anatomic variants. The obvious advantages of conventional angiography are its usefulness in determining the clinical importance of suspicious lesions and the ability to concurrently perform endovascular intervention.

Hypertensive urography is of historical interest and no longer used as a screening technique for RAS. CO₂ angiography is also obsolete with MRA and gadolinium imaging. CT angiography (CTA) with maximum intensity projection (MIP) and the quantitative measurement of stenosis is an accurate noninvasive technique in the diagnosis of visceral artery stenosis; this is fast becoming the diagnostic tool of choice with angiography reserved in cases in which vascular intervention is planned.

Doppler sonography can be used to measure the velocity of blood flow. It is a noninvasive technique, and it has high sensitivity in expert hands. Color flow Doppler may demonstrate disorganized flow patterns and high velocity flow stream associated with hemodynamically significant stenosis. Radionuclide renography technetium-mercaptoacetyltriglycine (MAG3)-captopril has a high sensitivity and specificity, and it adds a physiologic element to the diagnosis of RAS.

Limitations of Techniques

The acceptance of radionuclide renography as a primary screening tool for RAS has been hindered by the lack of standardized protocols.

Doppler ultrasonography is operator dependent, time consuming, and cumbersome. Doppler sonography examination is affected by anatomic, technical, patient-related, or pathologic factors.

CTA or MRA may cause the clinician to overlook mild cases of FMD that are detectable with digital subtraction angiography (DSA). Most of the false-negative and false-positive findings of RAS arise from accessory renal arteries. MRI is expensive, and its availability is limited.

Measurements of the size of RAS on angiograms (an important clinical consideration) are imprecise, and do not permit assessment of the cross-sectional area or, more importantly, the flow through the stenotic segment. The various histologic types of FMD are difficult to distinguish on angiograms; this limitation has important clinical bearing from a prognostic point of view.

All techniques do not relate to the predictive value of the cure aspect in reestablishing renal perfusion.

DIFFERENTIALS

Section 3 of 12  

• Authors and Editors
• Introduction
• Differentials
• Radiograph
• CT SCAN
• MRI
• Ultrasound
• Nuclear Medicine
• Angiography
• Intervention
• Multimedia
• References

Other Problems to be Considered

Systemic necrotizing vasculitis
Binswanger disease
Grange syndrome
Acute renal failure
Albuminuria
Atherosclerosis
Renal failure
Chronic glomerulonephritis
Essential and other causes of hypertension
Malignant hypertension
Nephropathy
Atherogenesis

Standing waves in the renal arteries appear as multiple serrated indentations, symmetrically distributed at evenly spaced intervals. These waves are of no pathologic significance and may represent arterial spasm. They may also affect intrarenal branches.

A fibrous musculotendinous band may cause extrinsic compression of the renal artery.

Atheroma, FMD, thrombus, embolus, or arteritis may cause branch RAS.

Klippel-Trenaunay syndrome is a congenital angiodysplasia consisting of a triad of angiomas, osteohypertrophy and venous varicosities. Visceral involvement is not uncommon and may cause life-threatening complications.

RADIOGRAPH

Section 4 of 12  

• Authors and Editors
• Introduction
• Differentials
• Radiograph
• CT SCAN
• MRI
• Ultrasound
• Nuclear Medicine
• Angiography
• Intervention
• Multimedia
• References

Findings

For the detection of RAS, hypertensive urography for RAS, is obsolete.

Degree of Confidence

Hypertensive urography is of historical interest only. It is no longer used as a screening technique for RAS because of its inconsistent results. The urogram may be normal in the presence of established RAS.

CT SCAN

Section 5 of 12  

• Authors and Editors
• Introduction
• Differentials
• Radiograph
• CT SCAN
• MRI
• Ultrasound
• Nuclear Medicine
• Angiography
• Intervention
• Multimedia
• References

Findings

CTA with MIP and quantitative measurement of stenosis is an accurate noninvasive technique in the diagnosis of RAS. The advent of spiral and multisection CT scanning has made CTA feasible. Continuous scanning through an area of interest during a single breath hold provides sufficient data to reconstruct 3-dimensional (3D) images.

Many scanning protocols are available. The general consensus is that both a timed bolus and rapid injection rate improves image quality. No positive oral contrast material should be used because it results in severe degradation of the image quality. Immediately before the procedure, the patient ingests water, and glucagon is then given intravenously to diminish bowel movement and maximize bowel distension. The 3 most common techniques used for 3D reconstruction are MIP, shaded-surface display (SSD), and volume rendering. MIP is often the single most useful technique for 3D reconstructions.

Accessory renal arteries are reliably identified by means of CTA. In either the mainstem artery or its intrarenal branches, RAS is detected with a high degree of accuracy.

Degree of Confidence

The sensitivity and specificity of the spiral CT in detecting RAS are approximately 98% and 94%, respectively. In patients with a plasma creatinine concentration higher than 1.7 mg/dL, the accuracy is lower (93% sensitivity, 81% specificity), possibly because of reduced renal blood flow. Because most of the false-negative and false-positive findings arise from accessory renal arteries, the accuracy in detecting RAS of the main renal artery may be as good as that of angiography.

False Positives/Negatives

In their recent paper, Andreoni et al raised concerns that CTA or MRA may cause clinicians to overlook mild cases of DSA-detectable AD. Most of the false-negative and false-positive findings of RAS are related to accessory renal arteries.

MRI

Section 6 of 12  

• Authors and Editors
• Introduction
• Differentials
• Radiograph
• CT SCAN
• MRI
• Ultrasound
• Nuclear Medicine
• Angiography
• Intervention
• Multimedia
• References

Findings

MRA is fast becoming a clinical standard for the safe and noninvasive detection of RAS, aneurysms, and occlusions. A comprehensive examination includes both 3D dynamic gadolinium-enhanced and 3D phase-contrast MRA techniques, which allow an evaluation of the renal arteries and other visceral arteries. The 3D phase-contrast technique is flow based and subject to dephasing in the presence of significant arterial stenosis. The 3D gadolinium-enhanced MRA method produces excellent contrast angiograms without the risk of iodinated compounds or radiation exposure.

MRA provides accurate information about the number of renal arteries, the size of the kidneys, and the presence of anatomic variants.

Gadolinium-based contrast agents (gadopentetate dimeglumine [Magnevist], gadobenate dimeglumine [MultiHance], gadodiamide [Omniscan], gadoversetamide [OptiMARK], gadoteridol [ProHance]) have recently been linked to the development of nephrogenic systemic fibrosis (NSF) or nephrogenic fibrosing dermopathy (NFD). For more information, see the eMedicine topic Nephrogenic Fibrosing Dermopathy. The disease has occurred in patients with moderate to end-stage renal disease after being given a gadolinium-based contrast agent to enhance MRI or MRA scans.

As of late December 2006, the FDA had received reports of 90 such cases. Worldwide, over 200 cases have been reported, according to the FDA. NSF/NFD is a debilitating and sometimes fatal disease. Characteristics include red or dark patches on the skin; burning, itching, swelling, hardening, and tightening of the skin; yellow spots on the whites of the eyes; joint stiffness with trouble moving or straightening the arms, hands, legs, or feet; pain deep in the hip bones or ribs; and muscle weakness. For more information, see the FDA Public Health Advisory or Medscape.

Degree of Confidence

Gadolinium-enhanced MRA has been proven to have a high sensitivity for detecting stenosis in the main and accessory renal arteries. At present, MRA provides anatomic information regarding a vascular stenosis but little information is provided about the functional significance of a stenosis. Recent reports indicate that 3D MRA with gadolinium-based contrast agents (which have a low potential for nephrotoxicity) has a sensitivity of 96-100% and a specificity of 71-96% for the detection of a main RAS of greater than 50%.

When combined with cardiac synchronization, 3D MRA can sharply delineate the entire length of the major renal arteries. However, MRA remains suboptimal for the detection of hemodynamically significant lesions of distal, intrarenal, and accessory renal arteries, which may cause physiologically significant RAS.

Limitations of MRA include its costs and lack of availability. Contraindications to MRA include claustrophobia and metallic implants, such as a pacemaker or surgical clip.

False Positives/Negatives

In their recent paper, Andreoni et al raised concerns that CTA or MRA may cause clinicians to overlook mild cases of DSA-detectable AD. Although false-negative studies in RAS are rare, a tendency to overestimate stenoses occurs, and this overestimation may lead to a false-positive diagnosis. To some extent, this tendency to overestimate stenoses can be compensated for by performing phase-contrast MRA, a type of MRA based on accumulated phase differences.

ULTRASOUND

Section 7 of 12  

• Authors and Editors
• Introduction
• Differentials
• Radiograph
• CT SCAN
• MRI
• Ultrasound
• Nuclear Medicine
• Angiography
• Intervention
• Multimedia
• References

Findings

The diagnosis of RAS is based on systolic and diastolic velocity changes throughout the length of the renal artery. Renal artery flow patterns can be classified into 4 categories: (1) normal, (2) diameter-reducing stenosis less than 60%, (3) diameter-reducing stenosis more than 60%, or (4) renal artery occlusion.

The peak systolic velocity in normal renal arteries averages 120 cm/s ±12, with an average peak systolic aortic velocity of 60 m/s ±15. Both velocities decrease with age.

The kidneys offer a low-resistance vascular bed; thus the Doppler spectral waveform from the normal kidney is that of a constant forward diastolic flow. In renal parenchymal disease there is increased vascular resistance, which in turn causes a decrease in the diastolic flow component and an increase in the pulsatility of the Doppler spectral waveform. Parenchymal diastolic flow velocities less than 20% of the peak systolic velocities are consistent with renal parenchymal disease.

In RAS, the peak systolic velocity increases by more than 150 cm/s for angles less than 60° or 180 cm/s for angles greater than 70°. Poststenotic spectral broadening may be present with or without flow reversal. Flow may be absent during diastole in a stenosis of more than 50%. A ratio of the peak systolic renal artery velocity to the aortic peak systolic velocity of 3.5 or more is said to be predictive of a stenosis of more than 60%.

Certain indirect Doppler sonographic signs have been described for RAS. One such sign is the presence of tardus-pavus pulse-demonstrated by a gradual slope of Doppler waveform during systole (pulse time increase of greater than 0.07-0.12 s) and attenuated Doppler waveform amplitude (peak systolic velocity less than 20-30 cm/s). The acceleration index is determined by dividing the slope of the systolic upstroke (in kilohertz per second) by the carrier Doppler frequency, and an acceleration time is the time interval between the onset of systole and the initial peak. The acceleration index in RAS is greater than 3 m/s². The resistive index in RAS is usually less than 0.56. The early systolic peak may be absent in RAS.

Color flow Doppler imaging may demonstrate disorganized flow patterns and a high velocity flow stream associated with hemodynamically significant stenosis. A false-negative diagnosis may occur with accessory renal artery, whereas a false-positive diagnosis may be made with coarctation of aorta.

RAS in a transplanted kidney is seen in about 10% of patients after renal transplantation, raising the questions of whether RAS it is the cause of post-transplant hypertension. The site of stenosis is not at anastomotic site in most patients; this suggests the possibility of focal rejection (with edema/fibrosis) as the cause of the hypertension. Duplex and color Doppler sonography has greatly impacted the diagnosis of RAS. The most reliable Doppler criteria for stenosis are a high velocity jet and distal turbulence.

Degree of Confidence

Doppler sonography has several limitations in the diagnosis of RAS. These include patient-related factors, anatomic factors, technical factors, and pathologic factors.

Patient factors include bowel gas, obesity, respiratory renal movements, and poor patient compliance. Anatomic factors include multiple renal arteries (16-28%), variation of renal veins (used as imaging landmarks), horseshoe kidneys, and crossed ectopia.

Technical factors include false-positive examinations due to suboptimal angles, variation in operator experience, incomplete examination (because complete renal evaluation is cumbersome), the need to visualize the entire length of artery, transmitted cardiac and/or aortic pulsation (which may obscure renal waveforms), and different emphasis on variable parameters. Pathologic factors include false tracings (which may be recorded from large collateral vessels and a reconstituted main renal artery) and variable causes of RAS that affects different sites (eg, atheroma, fibromuscular hyperplasia, vasculitis, arteriovenous fistula, retroperitoneal fibrosis, neurofibromatosis).

False Positives/Negatives

A false-negative diagnosis may occur with accessory renal artery, whereas a false-positive diagnosis may be made with coarctation of the aorta.

NUCLEAR MEDICINE

Section 8 of 12  

• Authors and Editors
• Introduction
• Differentials
• Radiograph
• CT SCAN
• MRI
• Ultrasound
• Nuclear Medicine
• Angiography
• Intervention
• Multimedia
• References

Findings

Standard renography with iodine-131–labeled ortho-iodohippurate (OIH) is of historical interest and no longer performed in the investigation of RAS.

The effect of the ACE inhibitor captopril on RAS was first described by Majd et al in 1983. They observed virtually no radionuclide uptake on diethylene triamine pentaacetic acid (DTPA) images in a patient with hypertension receiving captopril therapy. A repeat DTPA renogram performed in the same patient after cessation of captopril therapy revealed normal, bilateral DTPA uptake.

To explain the effects Majd et al observed, a number of mechanisms have been proposed, although none explains the entire observed phenomenon. Normally, a balance maintains glomerular filtration in vascular tone between the preglomerular and postglomerular arterioles. With significant RAS, this balance is disturbed as the pressure in the preglomerular arteriole is decreased and as the filtration pressure can be maintained only by the postglomerular arteriolar vasoconstriction mediated by the renin-angiotensin system.

The administration of ACE such as captopril inhibitors prevents the conversion of angiotensin I to the active vasoconstrictors angiotensin II and angiotensin III. By inhibiting the compensatory increase in vascular tone at the postglomerular arteriole, ACE inhibitors decrease glomerular filtration in the setting of RAS. The administration of ACE inhibitors in conjunction with radionuclide renography provides a noninvasive method for the detection of functionally significant RAS.

Several radiopharmaceuticals with different clearance mechanisms are available, although all show a degree of clearance via glomerular filtration. In particular, DTPA is primarily cleared by means of glomerular filtration. The decreased clearance of DTPA induced by ACE inhibitors in RAS, as Majd et al observed, is readily shown on renograms as decreased function in the affected kidney and deterioration in the renogram curve.

In patients with RAS, effective renal plasma flow (ERPF) is shown to increase after the administration of an ACE inhibitor because of the efferent arteriolar vasodilatation, which increases blood flow through the renal parenchyma and decreases blood flow through the glomerulus. ¹³¹I-labeled OIH also closely estimates ERPF. Recently, technetium-labeled mercaptoacetyltriglycine (MAG3) has also been used to qualitatively assess ERPF.

Since the introduction of captopril renography, various modifications have been made. Some centers only use one agent, either DTPA or MAG3. A positive ACE inhibition radionuclide scan indicates that RVHT is present, and it also implies the existence of hemodynamically significant RAS (>60-75% of the lumen).

It is important to understand that the criteria for a positive study depends upon the tracer used. If DTPA is used, there should be a change in split function if RVHT is present (since DTPA is dependent upon GFR for uptake there will be decreased initial uptake in the affected kidney). If MAG3 is used, split function will usually not change, but there will be increased cortical retention (usually measured as 20 minute to maximum ratio) in the affected kidney. This is because initial MAG3 uptake is primarily dependent upon tubular secretion rather than GFR. However, later clearance of MAG3 is dependent upon GFR (therefore decreased excretion is the primary finding). Rarely, the split function will change when MAG3 is used in cases of severe RVHT.

Recent preliminary data suggests that aspirin renography may be as sensitive as captopril renography for detecting RAS. Considering that aspirin, compared with captopril, reduces renal blood flow and thus tubular tracer delivery in poststenotic kidneys, aspirin renography is expected to be more useful, particularly if tubular tracers are used.

Degree of Confidence

Standard renography with ¹³¹I-labeled OIH has low specificity and low sensitivity in the diagnosis of RAS.

For RAS greater than 50%, Tc-MAG3 captopril renography has a sensitivity of 90%, a specificity of 91%, a positive predictive value of 70%, and a negative predictive value of 97%.

Recent data from Imanishi et al suggests that iodine-123 OIH or MAG3 renography is more sensitive for the diagnosis of unilateral RVHT when aspirin is given. Although Maini et al found that aspirin renography is superior to captopril renography, results from van de Ven et al show that, for the identification of RAS, the usefulness of aspirin renography equals but does not surpass that of captopril renography.

False Positives/Negatives

With standard, ¹³¹I-labeled OIH radionuclide renography, false-positive studies may result from all conditions that cause unilateral reduction in blood flow. These conditions include chronic pyelonephritis, renal outlet obstruction, renal vein thrombosis, compression of the renal hilum, perirenal abscess, perirenal hematoma, and ptosis of the kidney.

Patients with RVHT may have a false-negative captopril renogram after the chronic administration of captopril despite adequately maintained blood pressure. Therefore, where possible, ACE inhibitors should be discontinued prior to captopril renography. Overhydration may result in false-negative result, and underhydration may result in a false-positive test result. Bilateral RAS may be difficult to diagnose. Poor renal function more often results in a nondiagnostic examination. An asymmetric, small kidney with poor function is often unresponsive to a captopril renogram.

ANGIOGRAPHY

Section 9 of 12  

• Authors and Editors
• Introduction
• Differentials
• Radiograph
• CT SCAN
• MRI
• Ultrasound
• Nuclear Medicine
• Angiography
• Intervention
• Multimedia
• References

Findings

Conventional angiography remains the criterion standard for the detection of RAS, although CTA and MRA are challenging it. The severity of the stenosis and the presence of collateral circulation to the kidney may be assessed to determine the hemodynamic significance of RAS. Lesions occluding more than 50% of the diameter of the artery are considered significant. Both the angiographic and the nephrographic phases can be studied because the latter may better depict ischemic changes.

Epinephrine may further restrict blood flow to the kidneys and make the collateral circulation more obvious. Generally, flush aortography suffices for mainstem RAS, but if branch stenosis is suspected, selective renal angiography may better define the lesion. DSA does not address the hemodynamic significance of RAS.

RAS due to AD generally affects the middle and distal renal artery in 79% of the patients, it affects a branch renal artery in 4%, or a combination of the 2 in 17%. MFP is bilateral approximately in 65%; the left-to-right ratio is 4:1.

Degree of Confidence

Renal angiography remains the criterion standard in the diagnosis of RAS. Angiography is essential when renovascular intervention is contemplated. The angiographic measurement of the size of RAS, an important parameter in assessing the significance of RAS, is inaccurate. Angiography provides only anatomic information, and it does not enable the assessment of blood flow through the stenosis.

False Positives/Negatives

On DSA images, artifact from moving structures such as peristalsis may be mistaken for RAS. Standing waves may be confused with RAS.

INTERVENTION

Section 10 of 12  

• Authors and Editors
• Introduction
• Differentials
• Radiograph
• CT SCAN
• MRI
• Ultrasound
• Nuclear Medicine
• Angiography
• Intervention
• Multimedia
• References

Interventions appropriate for patients with RAS/RVHT may include medical therapy, percutaneous transluminal angioplasty (PTA), vascular stent placement, intravascular ultrasonography-guided atherectomy, and surgical revascularization.

Medical therapy

Treatment with antihypertensive drugs is indicated and optimal blood pressure control is essential. ACE inhibitors should be avoided. Other risk factors that should be addressed include atherosclerosis, smoking, and hyperlipidemia. Definitive therapy for the underlying cause should always be considered to prevent the development of ischemic nephropathy. In patients with diffuse atherosclerosis, the complication rate with both surgery and angioplasty is relatively high. Medical therapy may be preferred to other treatments.

Percutaneous transluminal angioplasty

PTA has become the procedure of choice for treatment of symptomatic stenoses. Patency rates after PTA are strongly dependent on the size of the vessel treated and the quality of inflow and outflow through the vessel. RAS is an established cause of either RVHT or chronic renal insufficiency. Because of the excellent results obtained with renal angioplasty, it is the most commonly performed procedure in symptomatic RAS.

Previously, angioplasty was considered a contraindication in patients with a solitary or transplanted kidney. This is no longer the case and, angioplasty is now considered the procedure of choice for treatment of RAS in these patients.

Technical success is achieved in more than 90% of patients, and patency rates are 90-95% at 2 years for MFP and 80-85% for atherosclerosis. Restenosis requiring repeat angioplasty has been reported in fewer than 10% of patients with AD and in 8-30% with atherosclerotic stenosis. Improvement in blood pressure control with fewer antihypertensive medications is achieved in 30-35% of fibromuscular lesions and in 50-60% of atherosclerotic lesions. A success rate of 83% has been reported with PTA in RAS associated with renal transplantation.

Vascular stent placement

Vascular stenting is considered complementary to PTA.

Many vascular stents are now available. Some stents are metallic devices, which are either self-expanding or balloon expandable. The US Food and Drug Administration (FDA) has approved a few of these for peripheral coronary work and transjugular intrahepatic portosystemic shunt (TIPS) procedures.

The ultimate role of stents in the treatment of vascular disease is not yet established, but these devices have already had a dramatic impact on the practice of interventional radiology. In studies from both the US and Europe, stenting of smaller vessels has resulted in an unacceptably high incidence of thrombosis. These problems are being addressed in the development of new stent materials and coatings.

Intravascular stents placed during angioplasty may be helpful in the prevention of restenosis and the management of RAS. Early results suggest that stenting may prove useful in patients with ostial disease, in those in whom restenosis occurs after PTA, or in those with complications (eg, renal artery dissection) resulting from PTA. Primary renal artery stenting in patients with atherosclerotic RAS has a high technical success rate and a low complication rate.

Intravascular ultrasonography-guided atherectomy

In a single reported case, hypertension secondary to AD was successfully diagnosed with intravascular sonography, and intravascular sonography-guided renal atherectomy was curative.

Surgical revascularization

Currently, surgical revascularization is reserved for patients in whom the main renal artery appears completely occluded and in whom the surviving renal parenchyma is vascularized by collaterals. Surgical revascularization might also be used when an ostial stenosis is present with a buttressing atheroma on either side of the ostium. Some of these lesions may also be amenable to percutaneous vascular stent placement.

Several surgical options are available. The stenotic segment may be excised and the artery resutured directly onto either the aorta or surviving stump. A vein graft may be transplanted or the kidney resected and reimplanted in the iliac fossa with the renal artery anastomosed to the iliac artery. Another novel method involves a splenectomy and anastomoses of the splenic artery to the renal artery when RAS involves the left kidney. The underlying diagnosis determines the results of this surgery. With advanced diffuse atherosclerosis, surgery may become less feasible because the certainty that the RAS is the cause of the hypertension is less and the prognosis may be determined by comorbidities.

A potential complication is the release of cholesterol emboli during the surgery; however, 80-90% of patients undergoing operation for atherosclerotic RAS benefit with cure or improvement. The perioperative mortality rate is less than 5%. In patients with AD, the cure rate is as high as 80%, and morbidity rates are low. However, similar results can be achieved with the minimally invasive renal angioplasty technique, at a considerably less morbidity, mortality, and expense. In patients with diffuse atherosclerosis, the complication rate with both surgery and angioplasty is relatively high.

Measurement of renin activity

Antihypertensive therapy may increase or decrease plasma renin levels. Nonsteroidal anti-inflammatory drugs can also decrease plasma renin levels. The baseline plasma renin activity is elevated in 50-80% of patients with RVHT. Measuring the increase in the baseline plasma renin activity 1 hour after the administration of 25-50 mg of the ACE inhibitor captopril can increase the predictive value of baseline plasma renin activity. Patients with RAS have an exaggerated increase in baseline plasma renin activity, perhaps due to the removal of the normal suppressive effect of high angiotensin II levels on renin secretion in the ischemic kidney.

The sensitivity and specificity of studies of the captopril renin test are 75-100% and 60-95%, respectively. A major limitation is the need to discontinue antihypertensive therapy, including the use of ACE inhibitors, beta-blockers, and diuretics, as they can affect the baseline plasma renin activity. The sensitivity of the test is also low, and its predictive value is lower than that of a captopril renogram.

Ischemic kidneys release higher levels of renin in their veins. Renal venous sampling for measuring renin levels to compare the venous drainage from each kidney can be used to predict the degree of renal ischemia and the potential success of surgical revascularization. A 1.5-fold increase in renin level in the ischemic kidney indicates a positive result and suggests that revascularization may be successful in the treatment of elevated blood pressure.

Renin secretion in the contralateral kidney is suppressed, as evidenced by the similar levels of renin measured in the renal artery, infrarenal inferior vena cava and renal vein. Approximately 10% of healthy patients have a ratio above 1.5, and fewer than 20% have a ratio below 1.1. The accuracy of the measurements may improve by prior administration of an ACE inhibitor, which increases renin secretion on the affected side.

False-negative and false-positive results are frequent. Although more than 90% of patients with unilateral RAS and increased renin levels in the affected renal vein have a positive response to angioplasty or surgery, approximately 50% patients with nondiagnostic findings also benefit from revascularization. As a result, most clinicians rely on the clinical index of suspicion rather than renin measurements in the renal vein to estimate the physiologic significance of RAS. However, these renin measurements may still be useful in patients with bilateral RAS, in whom measurements may determine the side that most contributes to the hypertension.

Medical/Legal Pitfalls

• Patients with a moderate-to-severe renal insufficiency are at a significant risk of contrast material–induced acute tubular necrosis and atheroembolic renal failure, which could result in permanent or temporary dialysis. These complications must be discussed with the patient and put into perspective before any invasive procedures (eg, surgery, angiography, or angioplasty) is performed.
• Contrast nephropathy typically manifests as a transient increase in the serum creatinine level 3-6 days after the administration of iodinated contrast material.
• • Contrast nephropathy is reported in as many as 40% of patients with underlying renal failure.
  • Most patients with contrast nephropathy ultimately recover renal function.
  • Porter reviewed results from nearly 300 patients with contrast nephropathy and concluded that fewer than 10% required permanent dialysis.

See also the Medscape topic Medical Malpractice and Legal Issues.

MULTIMEDIA

Section 11 of 12  

• Authors and Editors
• Introduction
• Differentials
• Radiograph
• CT SCAN
• MRI
• Ultrasound
• Nuclear Medicine
• Angiography
• Intervention
• Multimedia
• References

Media file 1:  Renal artery stenosis/renovascular hypertension. Left, Sonograms of the kidneys on a 57-year-old woman with difficult-to-control hypertension shows kidneys of uneven sizes: The left kidney is 96 mm, and the right kidney is 63 mm. Top right, Isotopic renogram (obtained with technetium mercaptoacetyltriglycine [MAG3]) after captopril shows a markedly depressed renal function in the right kidney. Bottom right, Analogous images show negligible activity in the right kidney. Note that this pattern is more typical for DTPA than MAG3 (as DTPA depends on the glomerular filtration rate for uptake which is decreased after captopril in renovascular hypertension [RVHT]). In severe cases of RVHT, MAG3 uptake can be decreased, as in this case. However, typically, uptake is preserved with decreased cortical excretion.
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Media type:  Image

Media file 2:  Renal artery stenosis/renovascular hypertension: Sonograms of the kidneys on a 46-year old woman with difficult to control hypertension showing uneven sizes of the kidneys the right kidney is 2.5 cm smaller in size. An isotope renogram obtained with technetium mercaptoacetyltriglycine (Tc-MAG3) shows a markedly depressed renal function in the right kidney (purple).
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Media type:  CT

Media file 3:  Renal artery stenosis/renovascular hypertension. Left, Flush aortogram in a 63-year-old man with hypertension shows marked stenosis of the right renal artery and complete occlusion of the left renal artery. Note the extensive atheroma in the aorta and iliac arteries. Right, nephrogram-phase image shows a significantly smaller left kidney with a faint nephrogram. Some blood supply to the left kidney is retained via collaterals (see image on the left).
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Media type:  X-RAY

Media file 4:  Renal artery stenosis/renovascular hypertension. Digital subtraction flush aortogram in a 77-year-old normotensive man shows marked left renal artery stenosis and diffuse aortic atheroma. The patient presented with lower-limb claudication.
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Media type:  X-RAY

Media file 5:  Renal artery stenosis/renovascular hypertension. Digital subtraction flush aortogram in an 83-year-old mildly hypertensive man shows complete occlusion of the left renal artery; only a stub of the artery is visualized. Note the diffuse aortic atheroma. The patient presented with lower-limb claudication.
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Media type:  X-RAY

Media file 6:  Renal artery stenosis/renovascular hypertension. Three-dimensional phase-contrast magnetic resonance angiographic (MRA) images of normal renal arteries.
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Media type:  MRI

Media file 7:  Renal artery stenosis/renovascular hypertension. Dynamic gadolinium-enhanced magnetic resonance angiogram (MRA) shows normal renal arteries.
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Media type:  MRI

Media file 8:  Renal artery stenosis/renovascular hypertension. Flush aortogram in a 32-year-old man with familial hypercholesterolemia and difficult-to-control hypertension. Radiograph shows a complete occlusion of the right renal artery and marked stenosis of the left renal artery.
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Media type:  X-RAY

Media file 9:  Renal artery stenosis/renovascular hypertension. Left, A balloon angioplasty catheter is seen in situ across the left renal artery stenosis in the same patient as in Image 7. Right, After angioplasty, an excellent anatomic (and functional) result was achieved.
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Media type:  X-RAY

Media file 10:  Renal artery stenosis/renovascular hypertension. Technetium mercaptoacetyltriglycine (Tc-MAG3) isotopic renogram in the same patient as in Images 8-9 shows curves before and after angioplasty.
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Media type:  Image

Media file 11:  Renal artery stenosis/renovascular hypertension. Digital subtraction flush aortogram in a patient with a right iliac fossa transplanted kidney. Image shows stenosis at the anastomotic site associated with post-stenotic dilatation.
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Media type:  Image

Media file 12:  Renal artery stenosis/renovascular hypertension. Digital subtraction flush aortogram in a patient with a left iliac fossa transplanted kidney. Image shows an intrarenal branch stenosis associated with post-stenotic dilatation.
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Media type:  Image

Media file 13:  Renal artery stenosis/renovascular hypertension. Differential diagnosis. Selective right renal angiogram shows standing waves in an intralobar artery. Standing waves in the renal arteries show as multiple serrated indentations that are symmetrically distributed at evenly spaced intervals. These of no pathologic significance and may represent arterial spasm. They may also affect intrarenal branches, as in this case.
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Media type:  Image

REFERENCES

Section 12 of 12

• Authors and Editors
• Introduction
• Differentials
• Radiograph
• CT SCAN
• MRI
• Ultrasound
• Nuclear Medicine
• Angiography
• Intervention
• Multimedia
• References

• Andreoni KA, Weeks SM, Gerber DA, et al. Incidence of donor renal fibromuscular dysplasia: does it justify routine angiography?. Transplantation. Apr 15 2002;73(7):1112-6. [Medline].
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• Birrer M, Do DD, Mahler F, et al. Treatment of renal artery fibromuscular dysplasia with balloon angioplasty: a prospective follow-up study. Eur J Vasc Endovasc Surg. Feb 2002;23(2):146-52. [Medline].
• Broekhuizen-de Gast HS, Tiel-van Buul MM, Van Beek EJ. Severe hypertension in children with renovascular disease. Clin Nucl Med. Jul 2001;26(7):606-9. [Medline].
• Courtel JV, Soto B, Niaudet P, et al. Percutaneous transluminal angioplasty of renal artery stenosis in children. Pediatr Radiol. Jan 1998;28(1):59-63. [Medline].
• Ergun EL, Caglar M, Erdem Y, et al. Tc-99m DTPA acetylsalicylic acid (aspirin) renography in the detection of renovascular hypertension. Clin Nucl Med. Sep 2000;25(9):682-90. [Medline].
• Estepa R, Gallego N, Orte L, et al. Renovascular hypertension in children. Scand J Urol Nephrol. Oct 2001;35(5):388-92. [Medline].
• Fine EJ. Diuretic renography and angiotensin converting enzyme inhibitor renography. Radiol Clin North Am. Sep 2001;39(5):979-95. [Medline].
• Goto A, Kawauchi N. Images in clinical medicine. Captopril-augmented renal scan. N Engl J Med. Feb 8 2001;344(6):430. [Medline].
• Hoshino Y, Nakamura T, Nakano A, et al. Successful treatment of renovascular hypertension due to fibromuscular dysplasia by intravascular ultrasound-guided atherectomy. Nephron. Jul 2002;91(3):521-5. [Medline].
• Huang X, Song L, Ma AQ. A malignant phenotype of hypertrophic cardiomyopathy caused by Arg719Gln cardiac beta-myosin heavy-chain mutation in a Chinese family. Clin Chim Acta. Aug 20 2001;310(2):131-9. [Medline].
• Imanishi M, Yano M, Okumura M, et al. Aspirin renography in diagnosis of unilateral renovascular hyp