CHAPTER 10 Renal arteries and veins

Arteriography and venography (online videos 10-1 and 10-2)

Evaluation of the renal arteries begins with abdominal aortography to detect renal artery ostial disease and accessory arteries before selective catheterization is done. A 4- or 5-French (Fr) pigtail catheter (or similar configuration) is positioned with the side holes at the level of the main renal arteries (approximately the L1 or L2 vertebral body). Images are routinely obtained in an anteroposterior or slight right posterior oblique views.¹ If computed tomography (CT) or magnetic resonance (MR) angiograms are available, they will guide selection of an optimal projection to place the renal artery origins in profile or may replace the catheter aortogram.

Selective renal arteriography is performed with a 4- or 5-Fr cobra or reverse curve (e.g., Sos or Simmons) catheter. The average flow rate in a normal renal artery is 5 to 6 mL/sec. More distal catheterization is done with coaxial microcatheters and microwires. Because the renal artery and its branches are prone to vasospasm and dissection, guidewires and catheters should be manipulated with extreme care.

Renal venography is accomplished with a straight catheter (e.g., cobra shape) or reverse curve catheter (e.g., Simmons 2). Valves at the origin of the veins may cause resistance to catheter passage. The valves can always be crossed with gentle guidewire probing. A wire may be required to seat the catheter well within the vein.

In patients with renal dysfunction (serum creatinine level greater than 1.2 to 1.5 mg/dL), various measures are taken to minimize the risk of contrast-induced nephropathy ²^–⁶ (see Chapter 2).

Anatomy

Development

In the fetus, the kidneys lie in the pelvis and receive blood from neighboring vessels, including the median sacral and common iliac arteries.⁷ With time, lateral splanchnic branches of the aorta begin to perfuse structures arising from the mesonephric ridge: adrenal glands, gonads, and kidneys. With the ascent of the kidneys to the midabdomen, they are ultimately supplied by the more caudal of these lateral splanchnic arteries. Anomalies in the location and number of renal arteries can be explained by incomplete regression of some of these primitive vessels.

Normal anatomy

The renal arteries arise from the lateral surface of the aorta at about the L1-L2 vertebral level.⁸^,⁹ The right renal artery runs posterior to the inferior vena cava (IVC) and right renal vein to enter the renal hilum. The left renal artery passes behind the left renal vein. The proximal renal arteries have small inferior adrenal, ureteric, and capsular branches, which often are not seen on imaging studies. At the renal hilum, the artery bifurcates into dorsal and ventral rami (Fig. 10-1). These trunks separate into segmental branches, which then further divide into lobar branches supplying the renal pyramids. The vessels successively branch into the interlobar, arcuate, and interlobular arteries. In the renal cortex, the interlobular arteries divide into afferent arterioles that supply the glomeruli.

Figure 10-1 Arteriogram of a normal right kidney.

The renal venous system follows a branching pattern similar to that of the renal arteries. However, wide anastomoses exist among the intrarenal veins (Fig. 10-2). Both main renal veins run in front of their corresponding arteries. The right renal vein passes behind the duodenum and enters the right lateral surface of the IVC.¹⁰ The left renal vein, which is about three times as long, runs between the aorta and superior mesenteric artery and then drains into the left lateral wall of the IVC. The left gonadal vein enters the left renal vein along its undersurface just to the left of the spine (Fig. 10-3). The left adrenal vein enters the left renal vein on its superior surface usually in a combined trunk with the left inferior phrenic vein. The right adrenal and gonadal veins typically have separate entrances into the IVC at or near the origin of the right renal vein (see Figs. 13-8, 13-9, and 13-13). In most patients, branches of the ascending lumbar and hemiazygous venous systems enter the left renal and left gonadal veins (see Fig. 16-4). Some patients have valves in the renal veins between the hilum and the IVC.

Figure 10-2 Normal right renal venograms.

Figure 10-3 Normal left renal venogram with partial filling of the left phrenicoadrenal trunk (thick arrow) and gonadal vein to the level of the first valve (thin arrow).

Variant anatomy (online cases 4 and 31)

Accessory renal arteries supply one or both kidneys in about 25% to 35% of the general population.¹¹^–¹⁵ Most accessory renal arteries supply the lower pole of the kidney but may originate anywhere from the suprarenal aorta to the iliac artery (Figs. 10-4 through 10-6). Anomalies of position (i.e., ectopia), fusion, or rotation of the kidney are associated with variations in the origin and number of renal arteries. The horseshoe kidney usually is fed by three or more arteries arising from the aorta, iliac arteries, or both.

Figure 10-4 A, Accessory right and left renal arteries (arrows).B, In another patient, a small artery above the left renal artery is noted. C, Selective injection indicates an accessory renal artery feeding the lower pole.

Figure 10-5 Accessory right renal artery. A, Contrast-enhanced computed tomography shows main right renal artery (arrow).B, An accessory right renal artery exits the aorta above the main vessel (arrow).

Figure 10-6 Accessory right renal artery. A, Injection of the main artery demonstrates the beaded appearance of fibromuscular dysplasia (arrowhead). In addition, it shows no crossing of vessels in the hilum and indistinct nephrogram in mid and lower pole, suggesting the presence of an additional artery feeding the dorsal aspect of the kidney (B). Also note prominent capsular arteries (arrow).

Several renal vein anomalies may be encountered ¹⁶^–¹⁹ (Table 10-1 and Figs. 10-7 through 10-9). That close to one third of the population has multiple (especially right) renal veins is not well appreciated by many interventionalists. The circumaortic left renal vein consists of a “preaortic” segment that enters the IVC in the usual location and a “retroaortic” segment between the kidney and the low IVC. The two veins may or may not communicate in the renal hilum. The solitary retroaortic left renal vein is a less common variant.¹⁵

Table 10-1 Renal Venous Anomalies

Type	Reported Frequency (%)
Multiple right renal veins	8 to 24
Circumaortic left renal vein	2 to 10
Retroaortic left renal vein	2 to 7
Right gonadal vein enters right renal vein	<10

Figure 10-7 Two right renal veins communicate in the renal hilum.

Figure 10-8 Circumaortic left renal vein. A, Gadolinium-enhanced magnetic resonance angiogram shows main left renal vein (arrow) entering the inferior vena cava (IVC). B, Circumaortic component passes behind the aorta to join the IVC (arrow).C, Maximum intensity projection demonstrates the orthotopic and circumaortic (C) left renal veins.

Figure 10-9 Retroaortic left renal vein. Axial and reformatted coronal computed tomography scans show the solitary left renal vein (arrow) passing behind the aorta well below the expected position of the vessel.

Collateral circulation

With renal artery stenosis or occlusion, an extensive collateral circulation maintains blood flow to the kidney. Although renal arteries have been described as end arteries, communications between extrarenal arteries and segmental, interlobar, and arcuate vessels do exist. The classic description of collateral arterial flow in the kidney was made by Abrams and Cornell.²⁰ The intrarenal vessels are primarily supplied by three collateral networks: the capsular, peripelvic, and periureteric arteries. These three systems are ultimately fed by the lumbar arteries, aorta, internal iliac artery, inferior adrenal artery, and other vessels (Fig. 10-10).

Figure 10-10 Significant left renal artery stenosis from intimal or perimedial fibroplasia type fibromuscular dysplasia. A, Pretreatment arteriogram shows typical weblike appearance of lesion in the distal left renal artery. B, Following angioplasty, inreased flow in the main artery causes antegrade flow in ureteric branches beyond the stenosis, which provided retrograde collateral circulation into the kidney before treatment.

In main renal vein obstruction, venous outflow occurs through ureteral, gonadal, adrenal, ascending lumbar, and capsular venous pathways (Fig. 10-11).

Figure 10-11 Venous collaterals with chronic left renal vein stenosis caused by impingement between the superior mesenteric artery and aorta (“nutcracker phenomenon”).

Major disorders

Atherosclerotic renovascular disease (online case 18)

Etiology and natural history

The renal arterial system plays a critical role in many patients with hypertension and chronic kidney disease. More commonly, long-standing or inadequately treated high blood pressure (from any cause) leads to progressive thickening and luminal narrowing of the small arteries of the kidneys. This nephrosclerosis is characterized by global damage of distal intrarenal vessels, which become irregular, tortuous, and pruned (Fig. 10-12). Less commonly, main, accessory, or branch renal artery obstruction (stenosis or occlusion) leads to so-called renovascular hypertension (RVH). The consequent reduction in intrarenal arterial pressure is sensed by the juxtaglomerular apparatus of the afferent arterioles. The renin-angiotensin-aldosterone system is triggered, leading to increased renin production, vasoconstriction of systemic arteries, sodium and water retention, and systemic hypertension. Other factors that sustain hypertension include endothelin release and upregulation of the sympathetic nervous system.²¹ Over time, untreated RVH will also cause nephrosclerosis that in and of itself contributes to elevated blood pressure. RVH is reported in about 3% to 5% of cases of hypertension in the general population, although this figure is hotly debated.²²

Figure 10-12 Nephrosclerosis of the left kidney. Note irregularity and pruning of distal intrarenal branches (compare with Fig. 10-1).

Ischemic nephropathy is generally defined as loss of renal function related to hypoperfusion from renal artery disease.²³ Atherosclerotic renal artery disease affecting both renal arteries or the artery to a solitary kidney is a common cause of ischemic nephropathy. Bilateral occlusions may eventually cause end-stage kidney disease. However, diminished central blood flow may be a minor factor in development of chronic kidney disease compared with microvascular changes caused by diabetes, hyperlipidemia, or hypertension itself.²⁴ Finally, the magnitude of renal artery stenosis has no direct correlation with the severity of kidney disease, unless the artery is completely occluded.²⁵^,²⁶

Atherosclerosis is responsible for at least two thirds of cases of clinically significant renal artery stenosis.²¹ Obstruction usually results from aortic plaque engulfing the renal artery ostium (i.e., within 5 to 10 mm of the aortic lumen). Less frequently, plaque develops independently in the truncal portion of the renal artery. In several studies, atherosclerotic renal artery stenosis was found to be progressive in more than one third of cases.²⁷^,²⁸ However, conversion to frank thrombosis is uncommon. Atherosclerotic renal artery disease must be distinguished from other causes of renal artery obstruction, particularly fibromuscular dysplasia (FMD; see later) (Box 10-1). Other kidney-related conditions that occasionally lead to chronic hypertension include trauma (e.g., Page kidney), cystic disease, renal cell carcinoma (RCC) or pheochromocytoma, renal artery aneurysm, reninoma, and renal infarction.

Clinical features

Most patients with atherosclerotic RVH or ischemic nephropathy are middle aged or older adults and have one or more risk factors for atherosclerosis. Younger patients are more likely to suffer from one of the less common causes of RVH (see later discussion). Although African Americans suffer from essential hypertension more frequently than do whites, RVH is relatively more common in whites.²⁹ Patients with thrombosis superimposed on underlying disease often are asymptomatic. However, worsening of hypertension or loss of renal function may occur when there is occlusion of the artery to a solitary functioning kidney.

In the United States, the prevalence of significant renovascular disease (detected by duplex sonography) among individuals older than 65 years is about 7%.³⁰ Significant atherosclerotic renal artery stenosis is associated with particularly high rates of chronic kidney disease (about 25%), coronary artery disease, peripheral arterial disease, and stroke.³¹

Imaging

Because hypertension is common but RVH is not, screening should be reserved for patients at moderate to high risk for RVH. Box 10-2 lists the criteria proposed by the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure.³² Revised guidelines are currently in preparation.

Several metabolic screening tests may be first performed to exclude other uncommon causes of hypertension (e.g., pheochromocytoma, aldosteronoma). Noninvasive imaging procedures are then used to further screen patients. Catheter arteriography is employed only when results are equivocal or endovascular therapy is being considered. No single screening procedure has emerged as the ideal technique.

Color doppler sonography

Ultrasound is one of the principal tools for detecting RVH because it is quick, relatively inexpensive, and completely safe (Fig. 10-13). If the aorta and main renal artery can be imaged, criteria for significant renal artery stenosis include intrastenotic peak systolic velocity (PSV) of greater than 180 cm/sec and PSV renal/aortic ratio of greater than 3.0 to 3.5³³^,³⁴ (Fig. 10-14). If these vessels cannot be seen because of technical factors, the intrarenal arteries are interrogated. With significant renal artery stenosis, damping and slowing of the time to peak systole (“parvus et tardus” waveform) is typical.³⁵ In addition, flow acceleration is diminished and the acceleration time prolonged (<300 to 390 cm/sec² and >0.06 to 0.07 sec, respectively).³³^,³⁶ The resistive index([PSV − diastolic velocity]/PSV) usually is less than 0.45.³⁴ However, duplex sonography is highly operator dependent, and some studies have failed to confirm the touted accuracy of this technique.³⁷^,³⁸

Figure 10-13 Normal renal artery duplex ultrasound with sampling of intrarenal branches.

Figure 10-14 Severe left renal artery stenosis. A, Color Doppler ultrasound shows high peak systolic velocity (417 cm/sec) in the proximal renal artery. B, Spectral waveforms of intrarenal arteries depict the “tardus et parvus” waveform expected with a significant upstream stenosis. C and D, Aortography defines the tight truncal renal artery stenosis (arrow). The left kidney is small. E, The lesion is crossed with a guidewire, and a balloon expandable stent placed. F, Post-stent arteriography shows a widely patent lumen, but embolization of atheroma or thrombus into lower pole vessels is evident.

Computed tomography and magnetic resonance angiography

Many centers rely on gadolinium-enhanced MR angiography for screening patients with suspected RVH if renal function is close to normal. Patients with preexisting renal insufficiency are at risk for nephrogenic systemic fibrosis after receiving some gadolinium-based contrast agents. With current techniques, MR angiography can detect main renal artery stenoses with up to 90% to 100% sensitivity and 75% to 100% specificity ³⁸^–⁴⁵ (Figs. 10-15 and 10-16). Weaknesses of the method include identification of disease in accessory and segmental renal arteries and artifacts related to metallic clips, intravascular stents, or patient motion. However, isolated significant stenoses of accessory arteries in this population are uncommon (<2%).⁴⁶

Figure 10-15 Tight ostial left renal artery stenosis. A, Magnetic resonance angiography depicts the lesion well (arrow).B, Catheter arteriography confirms the stenosis, which was treated successfully with a balloon-expandable stent (C). Note slight extension of stent into the aorta.

Figure 10-16 Medial fibroplasia type of fibromuscular dysplasia of the right renal artery. A, Magnetic resonance angiogram shows classic “string of beads” appearance of distal portion of the artery. B, Catheter angiogram confirms these findings. Mild changes of fibromuscular dysplasia are noted beyond the main artery. A systolic pressure gradient of 50 mm Hg was found. C, Following angioplasty with a 6-mm balloon, the gradient was reduced to 5 mm Hg.

Multidetector row CT angiography achieves comparable sensitivity and specificity to MR angiography in depicting renal artery stenosis ³⁹^,⁴⁰^,⁴⁴^,⁴⁷ (Fig. 10-17). Sixty-four–detector row CT is almost equivalent to catheter angiography in uncovering in-stent restenosis (which is obscured in MR angiography).⁴⁸ Its major disadvantage is the need for iodinated contrast in a population at increased risk for contrast nephropathy.

Figure 10-17 Transverse image from contrast-enhanced computed tomography scan shows a mild to moderate stenosis of the proximal right renal artery.

Captopril renal scintigraphy

To a great extent, this functional rather than anatomic imaging modality has fallen out of favor in routine evaluation of patients with suspected RVH.⁴⁰^,⁴⁹

Renal vein renin sampling

Normally, the ratio of renin activity in the renal vein versus the IVC is about 1.24.⁵⁰ In a patient with RVH and two functioning kidneys, the affected kidney overproduces renin, and renin secretion from the contralateral kidney is suppressed. Several criteria have been used to diagnose RVH based on renal vein renin values, including a renal vein renin ratio between the involved and uninvolved kidney of greater than 1.5 and a ratio of (renal renin–IVC renin)/IVC renin of greater than 0.48 (Vaughan formula).⁵¹ While renal vein renin sampling was once a mainstay of RVH diagnosis, it is seldom used by interventionalists (Fig. 10-18).

Figure 10-18 Renal vein renin analysis in patient with severe uncontrolled hypertension. A and B, Abdominal aortography shows two left renal arteries, the more inferior of which has an origin stenosis (arrow). The right kidney is very small, and there is only minimal flow through a highly diseased artery (arrow,C). Right (D), lower pole left (E), and upper pole left (not shown) renal vein renins were obtained. Markedly elevated levels from the right kidney prompted right nephrectomy. Blood pressure was then easily controlled.

Catheter angiography

Catheter angiography is still the gold standard for the diagnosis of RVH. Initial abdominal aortography may not be necessary if high-quality CT or MR angiography studies clearly depict the renal artery ostia and identify all renal arteries. Narrowing of accessory renal arteries or intrarenal branches can cause RVH and should be carefully sought; intrarenal stenoses are particularly common in children with RVH (Figs. 10-19 and 10-20). Stenoses may go undetected for several reasons, including oblique origin of the renal artery from the aorta and superimposition of intrarenal branches. Multiple angiographic views may be necessary to identify such hidden lesions.

Figure 10-19 Intrarenal renal artery stenosis. Stenosis at the origin of a segmental branch (arrow) produced renovascular hypertension in this child. The upper pole of the kidney is not filled because of injection into the dorsal ramus of the renal artery.

Figure 10-20 Neurofibromatosis in an 11-year-old boy with hypertension. A, Aneurysms and an intrarenal branch stenosis (arrow) are noted. B, There is some improvement in the intrarenal obstruction after balloon angioplasty.

Atherosclerosis produces irregular narrowing of the renal ostium or proximal renal artery (see Figs. 10-14 and 10-15). Bilateral disease is common, and infrarenal aortic atherosclerosis usually is present. After a stenosis has been identified, its hemodynamic significance must be proved by one of the following criteria²¹^,⁵²:

• Reduction in luminal diameter of greater than 75%

• Systolic pressure gradient across stenosis in the main renal artery greater than 10 to 20 mm Hg or greater than 20% of aortic systolic pressure

A stenosis with a 50% to 75% reduction in the luminal diameter may be hemodynamically significant, but in such cases, pressures should be measured.

Treatment

Selection of patients with RVH or ischemic nephropathy for endovascular or operative therapy is highly controversial ²¹^,⁵³ (Box 10-3). Recent improvements in anti-hypertensive medications and routine lifelong treatment of this population with lipid-lowering “statins” and oral antiplatelet agents may allow many people with RVH and normal or mild renal insufficiency to be treated medically. The mere presence of a significant renal artery stenosis does not by itself warrant treatment, because not all such patients will have a positive clinical outcome from arterial recanalization. In addition, the procedure itself may worsen renal function by contrast nephropathy, atheroembolization, or, rarely, complete vessel occlusion.

Renal artery stent placement

Over the past two decades, endovascular treatment of renal artery disease has been embraced by interventionalists of all kinds.⁵⁴ Advocates point to numerous large historical series that support the value of renal artery stents in treating hypertension or stabilizing (or even reversing) renal insufficiency.⁵⁵^–⁵⁸ However, this enthusiasm has been tempered by several recent randomized trials that have failed to show significant benefit, particularly in light of nontrivial adverse events (see later discussion). Although some of these studies are fraught with important drawbacks, many physicians outside the interventional community are skeptical of routine application of this aggressive approach.

Patient selection

In patients with hypertension, renal artery revascularization is of no proven value for the following:

• Nonsignificant renal artery stenosis

• Incidental finding of significant disease in the absence of hypertension or renal insufficiency

• Significant renal artery stenosis with severe bilateral nephrosclerosis that may be responsible for hypertension

Box 10-3 lists the primary indications for intervention in patients with atherosclerotic RVH or ischemic nephropathy.²¹^,⁵⁹ Angioplasty alone is rarely employed in this setting, with the possible exception of focal truncal stenoses.⁶⁰ Stents significantly improve the technical success of renal artery angioplasty for atherosclerotic disease, particularly for ostial lesions (from 55% to 70% to more than 95%).⁵⁶^,⁶⁰^–⁶⁵ This improvement alone may largely explain the better long-term patency rates associated with stent placement. Use of stents in renal arteries with nominal diameter of less than 5 mm usually is avoided because of the relatively higher rates of clinically significant restenosis in this setting.⁶⁶

Revascularization for renal salvage is considered in patients with significant bilateral renal artery disease or disease in a solitary functioning kidney with some functional reserve. Even when the main renal artery is completely occluded, collateral circulation has often developed over time to keep the kidney viable, even up to 6 months or more after occlusion. There is usually no benefit to revascularizing a minimally functioning kidney.

Technique (see fig. 10-14)

Most interventionalists continue the patient’s blood pressure medication until the procedure is completed. The dose of iodinated contrast material should be kept to an absolute minimum. In patients with preexisting renal dysfunction, various measures are taken to protect the kidneys including use of carbon dioxide angiography and administration of N-acetyl cysteine and intravenous bicarbonate infusion (see Chapter 2 and Fig. 3-20). All patients should receive aspirin (325 mg orally) or clopidogrel (300 mg oral loading dose) beforehand. If there are no contraindications, the former is continued for the patient’s lifetime or the latter for at least 3 to 6 months afterward. Parenteral platelet inhibition may be helpful in minimizing deleterious effects to the kidney from atheroemboli or contrast.⁶⁷^,⁶⁸ Full anticoagulation with heparin (or a direct thrombin inhibitor if heparin allergy history exists) is instituted before crossing the obstructive lesion. An intraarterial dose of nitroglycerin (150 to 200 mg) may help prevent guidewire or catheter-induced vasospasm.

The diagnostic catheter is replaced with a 5- or 6-Fr guiding sheath or catheter with distal curve appropriate for the renal artery origin. Traditionally, the stenosis was crossed with a floppy 0.035” guidewire, a 5-Fr catheter advanced beyond the lesion, and the balloon or stent inserted over a stiff 0.035” Rosen or TAD exchange wire. Most practitioners now favor low-profile platforms.⁶⁹ Thus the stenosis is crossed with a steerable 0.014” to 0.018” microwire followed by a microcatheter. If difficulty is encountered traversing the lesion, several maneuvers should be tried. Changes in the patient’s respiration can dramatically alter the aortorenal artery angle. Stiffer (or sometimes less stiff) guidewires may be helpful.

A heavy-duty microwire with a floppy tip is positioned to give support for the balloon-mounted stent delivery catheter but avoid damage to the distal renal artery branches. Monorail systems that circumvent the need for a long exchange wire are popular. Great care must be taken with wire manipulations because even a small-caliber floppy-tipped nitinol wire can dissect the main vessel or perforate small renal artery branches, leading to occlusion or hemorrhage.

Recent data prove that endovascular renal procedures reliably cause showers of atheroembolic particles into the distal vasculature.⁷⁰^,⁷¹ This embolic burden may negate any positive effect expected from the intervention. Distal embolic protective devices (occlusion balloons or permeable filters) that trap this material may prevent microembolic injury to the treated kidney. These filters are strongly advocated by some experts.

If the lumen is initially so narrow that passage of the guiding sheath or stent device is impossible, predilation of the stenosis with an undersized balloon may be required. Off-label use of a variety of stents is standard practice but is not condoned by the U.S. Food and Drug Administration. The device is usually a nitinol stent that is factory-mounted on a slightly oversized diameter angioplasty balloon. It is chosen by measuring the luminal diameter of the normal portion of the renal artery or contralateral artery on the diagnostic arteriogram. In adults, the usual balloon diameter is 5 to 7 mm. The shortest available stent length is selected to entirely cover the diseased area. The stent may be inserted into the artery within the guiding sheath or directly over the guidewire without sheath protection (“bareback”). The stent is exposed by withdrawing the guiding catheter from the renal artery.

For ostial lesions, the stent is positioned with the proximal end about 1 mm inside the aortic lumen to completely cover the overhanging plaque. Angiograms are obtained through the guiding sheath to ensure precise positioning. The stent is deployed by expansion of the balloon with an inflation device. Additional stents are placed if needed, which is rare. Care should be taken to avoid placing stents into the distal renal artery, which could preclude later surgical revascularization or damage branch vessels. In the event of vessel rupture, an angioplasty balloon of appropriate size is quickly reinflated within the stent. Placement of a covered stent is usually required. The procedure ends with a completion angiogram and pressure measurements to document satisfactory result.

Results

Success in renal artery revascularization for RVH is judged by blood pressure response, with clinical benefit defined as cure (i.e., blood pressure lower than 140/90 mm Hg without medication) or improvement (i.e., reduced number of medications required to maintain blood pressure below 140/90 mm Hg or a 15-mm Hg reduction in blood pressure on the same or reduced number of medications).²² In ischemic nephropathy, clinical benefit is defined as reduction or stabilization in serum creatinine or flattening of the renal dysfunction curve (1/creatinine versus time).

A widely patent artery can be created with a metallic stent in greater than 95% of cases.²⁴^,⁶¹^,⁶³^,⁷²^,⁷³ In atherosclerotic RVH, actual cure of hypertension is achieved in less than 10% to 20% of individuals whether stents are used or not. Blood pressure control is better in about 50% to 80% of patients. Based on historical series, angioplasty and stent placement lead to improvement or stabilization of renal insufficiency in about 70% of cases; however, in some (but not all) series, that benefit diminished over time.⁶⁴^,⁶⁶^,⁷²^,⁷⁴ The value of embolic protection is unproven despite some encouraging nonrandomized series.⁶⁷^,⁶⁸^,⁷⁵

The reported angiographic restenosis rate for atherosclerotic lesions is about 20%.⁶³^,⁶⁶^,⁷⁶^,⁷⁷ However, the reported Doppler sonographic restenosis rate at 9 to 12 months has ranged from 21% to 50%.⁷⁸^,⁷⁹ Luminal compromise seems to increase slowly over time. One important predictor of clinically significant restenosis is small initial vessel diameter (<5 mm). Preliminary trials suggest that drug-eluting stents may be of added value in such small caliber arteries.⁸⁰^,⁸¹ Restenosis is treated by repeated balloon angioplasty without or with additional stent placement⁸²^,⁸³ (see Fig. 1-10).

Despite encouraging results from retrospective studies and registries, controlled randomized trials of stent placement versus best medical therapy for patients with atherosclerotic renal artery stenosis have not supported routine endovascular therapy for management of RVH or ischemic nephropathy.²⁴^,⁵³^,⁷³^,⁸⁴^,⁸⁵ Critics are quick to note the frequency of major adverse events associated with stent insertion, including loss of renal function after revascularization in 10% to 20% of individuals.²¹ These studies had numerous deficiencies, including inclusion of a substantial number of patients with nonsignificant renal artery stenosis and lack of standardization of stent insertion techniques. Nonetheless, the cumulative burden of these recent trials is sobering. There is hope that the ongoing multicenter CORAL and RADAR trials will satisfy both proponents and skeptics of renal artery stent placement.⁸⁷^,⁸⁸

Complications

Major complications occur in about 8% to 15% of procedures ²²^,⁸⁹ (see Fig. 10-14). Permanent decline in renal function is noted in about 6% of cases and usually is caused by contrast nephropathy and/or microembolization. Periodic surveillance CT angiography or duplex ultrasound is advisable to detect restenosis and the need for further treatment.⁴⁸^,⁷⁹

Surgical therapy

In patients with RVH or ischemic nephropathy, surgery is reserved for failures of endovascular treatment, cases with associated aortic disease that require open operation, and most renal artery occlusions.⁹⁰ If minimal aortic disease is present, the standard procedure is aortorenal bypass grafting with autologous vein. In patients with severe aortic atherosclerosis or an aortic aneurysm, the hepatic or splenic artery may be used as a bypass conduit for the right or left renal artery, respectively.⁹¹^,⁹² If the main renal artery is occluded but the distal artery reconstitutes through collaterals, bypass is sometimes done to improve function or treat RVH. Otherwise, hypertension may be treated by excision of the renin-producing kidney (see Fig. 10-18).

Renal artery fibromuscular dysplasia (online case 76)

Etiology and clinical features

Fibromuscular dysplasia (FMD) is a group of related noninflammatory disorders of unknown etiology in which affected arteries become narrowed, aneurysmal, or dissected.⁹³ FMD is not rare; it is found in about 3% to 5% of preoperative imaging studies of potential kidney donors.⁹⁴^,⁹⁵ Six types of FMD are described in one traditional classification scheme; the most common type is medial fibroplasia⁹³^,⁹⁶ (Table 10-2). In this form of the disease, the normal media is replaced by fibrous tissue and extracellular matrix. The thickened segments alternate with sites of medial thinning, which produces the classic “string-of-beads” appearance of the lumen on imaging studies. The less common types of FMD cause luminal beading, smooth and tapered stenosis, focal bandlike narrowing, dissection, or aneurysm without stenosis.

Table 10-2 Classification of Subtypes of Renal Artery Fibromuscular Dysplasia

Type	Frequency (%)	Morphology
Medial fibroplasia	60 to 70	Alternating narrowing and aneurysms (“string of beads”)
Perimedial fibroplasia	15 to 25	Irregular, beaded narrowing
Medial hyperplasia	5 to 15	Tubular, smooth narrowing
Medial dissection	5	False channel in media
Intimal fibroplasia	1 to 2	Focal, smooth narrowing
Periarterial fibroplasia	<1	Tubular, smooth narrowing

FMD is largely a disease of young or middle-aged women. However, it may be seen in men and young children. The disorder is often asymptomatic and only detected on imaging studies obtained for other reasons. Difficult to control hypertension and onset at a younger age should suggest the diagnosis. Renal FMD rarely results in ischemic nephropathy.