Renal Artery Angioplasty 

Updated: Jul 23, 2020
Author: Vibhuti N Singh, MD, MPH, FACC, FSCAI; Chief Editor: Kyung J Cho, MD, FACR, FSIR 

Overview

Background

Percutaneous transluminal angioplasty (PTA) of the renal artery has become an increasingly widespread peripheral vascular intervention for the treatment of renovascular hypertension (HTN). Catheter-based procedures began in 1964 when Charles Dotter initially developed PTA for treating peripheral vascular atherosclerosis. Andreas Grüntzig revolutionized the technique in 1974 when he developed a soft, flexible, double-lumen balloon catheter for use in coronary arteries.

PTA has since rapidly evolved into a widely used, versatile, and dependable vascular interventional technique. Excellent results may be achieved in the renal arteries if patients are well selected and if experienced clinicians perform the procedure. (See the images below.)

Percutaneous transluminal angioplasty. Percutaneous transluminal angioplasty.
Renal arteriogram obtained after renal percutaneou Renal arteriogram obtained after renal percutaneous transluminal angioplasty.

Renovascular HTN and renal PTA

In the United States, renovascular HTN is present in approximately 4% of the total population of persons with HTN. It is associated with increased morbidity because patients with severe HTN who have renovascular HTN are at increased risk for renal insufficiency.

Traditional therapeutic modalities that include drug therapy and surgical revascularization have too many shortcomings. Medicines frequently fail to adequately control the patient's blood pressure (BP) adequately despite polypharmacy; medicines may cause undesirable adverse effects; and patients may be noncompliant. Moreover, lowering BP in the presence of severe renal stenosis may lead to ischemic renal atrophy.

Surgery imparts considerable morbidity, and results vary. The associated need for general anesthesia may cause complications in patients, who are often poor candidates because of diffuse atherosclerosis or renal insufficiency. Nonetheless, the correction of renal stenosis is considered the treatment of choice whenever feasible.

Since its introduction in 1978, percutaneous transluminal renal angioplasty (PTRA) has emerged as a highly effective technique for the correction of renal artery stenosis (RAS). Renal angioplasty has notable physiologic, psychological, and economic advantages over other treatment modalities, and it should be considered the therapy of choice for renovascular HTN.[1, 2, 3, 4, 5, 6, 7, 8, 9, 10, 11]

Alone or in combination with stent implantation, PTRA is increasingly used as an alternative to surgical revascularization for the treatment of RAS, which may cause HTN or jeopardize renal function. Technical success is usually achieved in more than 85% of cases; the failure rate is 10%.

PTRA-related complications occur in 7% of patients (see Technique). An overall benefit on BP control is observed in 20-40% of patients with atherosclerotic RAS (ARAS) and 60-70% of those with fibromuscular dysplasia (FMD; see Outcomes). Independent of etiology, PTRA appears to be technically effective in correcting RAS. However, its position with respect to medical or surgical treatment must be better defined through randomized, controlled studies aimed at comparing the clinical efficacies of these approaches.[12, 13, 14]

Etiology of renal artery stenosis

RAS has multiple causes, but most lesions are the result of atherosclerosis. FMD is the second most common etiology.[15] (See the image below.)

Renal artery stenosis in patient with medically re Renal artery stenosis in patient with medically refractory renovascular hypertension.

The incidence of RAS in patients undergoing cardiac catheterization is as follows:

  • RAS occurs in 62% of patients with peripheral vascular disease (PVD) and HTN [16]
  • RAS is found in 33% of patients with coronary artery disease (CAD)
  • About 18% of patients with CAD have stenoses of greater than 50% [17]
  • Both CAD and renal insufficiency are independent predictors for RAS
  • The incidence of bilateral RAS is approximately 46% [18]

Regarding asymptomatic RAS, as many as 50% of patients with RAS do not have HTN. The incidence of progression of RAS is variable, but progression occurs in most patients. The overall progression rate is 49%, with 14% of patients developing total occlusion. Serum creatinine values do not adequately mirror progressive anatomic disease, and control of HTN does not thwart progression of RAS. The absence of HTN after PTRA does not preclude restenosis.

RAS is frequently underdiagnosed.

Atherosclerotic RAS (ARAS) is a common condition that is often but not necessarily associated with HTN. Because of its progressive nature, ARAS is becoming one of the leading causes of end-stage renal disease (ESRD). Indeed, ARAS is reported to progress within 5 years in 51% of patients, and renal atrophy develops in 21% of patients in whom ARAS is initially greater than 60% of the caliber of the vessel.

RAS may occur in the setting of a transplant (transplant RAS, or TRAS) and is often treated with endovascular techniques.[19] A study by Chen et al found stenting to be superior to angioplasty alone for treating TRAS.[20]

Indications

Indications for PTRA

The indications for renal angioplasty are evolving. The common indications are as follows[21] :

  • Sudden onset of HTN
  • HTN in a patient without a positive family history
  • HTN in a patient without a medical history of factors known to cause HTN
  • Malignant HTN
  • HTN refractory to pharmacotherapy
  • Patient noncompliance with medications
  • HTN in a patient with abdominal bruit suggestive of renal artery narrowing
  • HTN in a patient who develops renal failure while taking captopril
  • Sudden-onset HTN in a young woman not taking oral contraceptives (for patients in this group, the likelihood of FMD is increased)

Indications for PTRA or renal stenting

Indications for PTRA or renal stenting include the following:

  • Progressive decline in renal function
  • Accelerated or difficult-to-control HTN - Presence of greater than 75% RAS and one of the following: (1) HTN requiring three or more medications for control, (2) HTN on treatment with mean BP greater than 110 mm Hg, (3) chronic renal insufficiency with creatinine below 3 mg/dL, or (4) acute renal failure with preserved renal size and echogenicity on ultrasonography (US)

Other expanding indications include the following:

  • Congestive heart failure (CHF)
  • Unstable angina
  • Recent development of ESRD that is partly the result of RAS (the patient may be able to avoid dialysis)
  • Angiographic lesion in the absence of HTN or renal insufficiency [22]
  • Patients with unstable angina or CHF and refractory HTN and up to 70% stenosis of one or both renal arteries (in one study, renal stenting resulted in dramatic improvement independent of coronary angioplasty [23] )
  • High-grade RAS in patients undergoing infrarenal abdominal aortic aneurysm repair [24]

Renovascular disease: clinical indicators

Clinical indicators of renovascular disease are as follows:

  • HTN - Onset before age 30 years or after age 50 years; abrupt onset; history of CAD; history of tobacco abuse; absence of family history of HTN; presence of abdominal bruit 4-5 cm lateral to midline
  • Pulmonary edema or renal insufficiency - Bilateral renal artery disease; RAS in a single kidney; treatment with an angiotensin-converting enzyme (ACE) inhibitor (may cause sudden azotemia)

These epidemiologic data emphasize the need for an aggressive diagnostic approach and treatment of ARAS, for the treatment of HTN, and for the prevention of ischemic nephropathy. These goals may be achieved, to some extent, with PTRA.

Contraindications

Contraindications for PTRA or renal stenting include the following:

  • Advanced disease - Creatinine level greater than 3-4 mg/dL (recommendations vary); kidney length less than 8 cm
  • Limited life expectancy
  • Generally poor surgical or PTRA candidate - Bleeding diathesis; recent myocardial infarction (MI)
  • Pregnancy

Outcomes

Clinical success rates

Several published series have reported clinical results obtained with angioplasty.[25, 26] (See Table 1 below.)

Table 1. Success Rates of Percutaneous Transluminal Renal Angioplasty (PTRA) in Renal Artery Stenosis (RAS) Caused by Atherosclerosis (80% of RAS) and Fibromuscular Dysplasia (FMD; 20% of RAS) [25, 26] (Open Table in a new window)

Outcome

Atherosclerotic RAS, %

RAS Due to FMD, %

Primary success

85

89

Hypertension cured

19

41

Hypertension improved

61

44

Restenosis

50

15

*Ostial location is an independent predictor of poor outcome. Clinical success rates are 54% at 3 years, with high restenosis rates.

Fibromuscular dysplasia

When the cause of renal stenosis is FMD, the results of PTRA are uniformly good, with cure in about 58% of patients, improvement in 35%, and failure in 7%. These results are comparable to those obtained with surgery. Restenosis is uncommon in patients with this condition, and follow-up angiograms (< 5 years after angioplasty) often show no trace of stenosis.

Chen et al assessed the safety and efficacy of PTA with selective stenting in 105 patients (mean age, 26.7 ± 8.2 years; 49.5% female) who had RAS due to FMD.[27]  The technical success rate for endovascular therapy was 95.2% without severe complications. During 1-year follow-up, mean systolic and diastolic BP decreased from 157.6 ± 17.5 and 102.3 ± 14.2 mm Hg, respectively, to 129.6 ± 12.3 and 81.3 ± 11.1 mm Hg, respectively. The number of antihypertensive medications decreased from 2.2 ± 1.2 to 0.8 ± 1.0. The cure rate was 49.0%, and improved BP rate was 40.0%. Serum creatinine levels remained stable. The primary and secondary restenosis rates were 13.4% and 5.8%, respectively. 

Atherosclerosis

When atheroma causes the stenosis, the results of revascularization are not as good, with cure in 22% of patients, improvement in 57%, and failure in 21%, whichever modality (angioplasty or surgery) is used. Furthermore, in patients with diffuse atheromatous disease, the complication rate is relatively high with both surgery and angioplasty; for these patients, medical therapy may be preferred. The common indications for renal stenting include the following:

  • Ostial stenosis
  • Flow-limiting dissection of the renal artery after PTA
  • Persistent significant gradient after PTA
  • Restenosis after balloon angioplasty

Short balloon-expandable stents are usually used for renal stenting.

Clinical outcomes

Early decrease in blood pressure

In patients in whom PTRA is technically successful, a prompt decrease in BP is usually observed. The mechanism of this early decrease is not understood. Plasma renin activity, norepinephrine, and muscle sympathetic nerve activity all increase in the first or second hour, despite the falling BP. This finding raises the possibility that some vasodilator substance is released.

In the atheromatous patients with unilateral stenoses, the eventual benefit rate (defined as improvement or cure of HTN 3 months after angioplasty) was 87%; in the FMD patients, it was 92%.

Patients with stenosis and a solitary kidney are excellent candidates; one series showed a benefit rate of 92% for such patients.

Effect on blood pressure in ARAS

Differences in the criteria used to select patients, in defining an improvement in BP, in the duration and modalities used for follow-up, and in medical treatment hamper any comparison of studies addressing the effects of PTRA on BP. Despite these limitations, authorities have generally agreed that for patients with ARAS, PTRA rarely leads to a reduction in BP.

In a review of the experience in 10 centers, 691 patients were treated with PTRA. About 19% were cured; BP improved in 51%; and BP was unchanged in 30%. In other reviews, the effects on BP were even less encouraging. For instance, 8% of several hundreds of patients with HTN were cured with PTRA. In a study by the present authors, 66 patients were followed up for at least 6 months; the patency of the dilated artery was confirmed mostly by means of echographic Doppler velocimetry. In these patients, the rate of cure was 3%, with a 38% rate of improvement.

The introduction of stents has not improved the outcome of PTRA with regard to BP. A 4-year follow-up study of 163 patients who were successfully treated with stent implantation showed that only one was cured; improvement was seen in 42%. These negative results are not surprising in consideration of the fact that the great majority of patients with ARAS have been exposed to the deleterious effects of high BP for years. Their HTN results in extensive renal and vascular damage, which prevents BP from returning to normal levels, even after the stenotic artery is dilated.

This conclusion obviously stresses the need for the careful selection of the few patients who may benefit from dilation procedures. For patients who do not fulfill the diagnostic criteria for real renovascular HTN and those in whom even PTRA is considered too risky, medical treatment permits the same degree of BP control achievable with dilation. Indeed, three major studies that compared the effects of PTRA and medical treatment in patients with ARAS showed that the BP reductions obtained with the two approaches were similar (see Table 2 below).[21, 28, 29] The only advantage for patients treated with PTRA was diminution of their drug regimen.

Table 2. Success Rates of Percutaneous Transluminal Renal Angioplasty (PTRA) in Renal Artery Stenosis (RAS) Caused by Atherosclerosis (80% of RAS) [21, 28, 29] (Open Table in a new window)

Intervention

Success Rate, %

Restenosis Rate, %

PTRA

85

50

Renal stenting

100

25

In a retrospective study analyzing 224 patients treated with PTRA for primary symptomatic RAS at four tertiary centers, Zachrisson et al found that treatment led to significant reductions in mean systolic pressure (168 to 146 mmHg), diastolic pressure (84 to 76 mmHg), number of antihypertensive drugs (3.54 to 3.05), and antihypertensive treatment index (21.75 to 16.92).[30]  These improvements were maintained at 1 year and at the last clinical evaluation after a mean follow-up of 4.31 years. Renal function increased transiently without sustained improvement, or deterioration, during later follow-up.

Effect on renal function

Theoretically, PTRA should be used more for preserving renal function than for reducing BP. Given the progressive nature of ARAS, PTRA should be performed before ischemic damage to a kidney has occurred. Renal outcome with PTRA is better when renal function is still normal than when it is altered. In general, the overall cardiovascular risk for patients undergoing PTRA with a baseline serum creatinine level greater than 1.5 mg/dL is 5 times higher than that of patients with a creatinine level below that value.

So far, no medications have been shown to retard the progression of ARAS. On the other hand, no evidence supports the theory that PTRA improves renal function in patients with ARAS.[31] (See Table 3 below.)

Table 3. Natural History: Progression of Medically Treated Renal Artery Stenosis [31] (Open Table in a new window)

Outcome

Rate, %

Decrease in glomerular filtration rate

37

Increase in creatinine level

20

Decrease in renal size

35

In a large meta-analysis, 25-53% of patients who underwent PTRA had some improvement in renal function. In another review of 215 patients with ARAS and mild renal insufficiency treated with stent implantation, 35% had improvement in renal function, as estimated by assessment of changes in serum creatinine level or creatinine clearance. In 35% of these patients, the condition was stabilized with the procedure.

Bax et al found that in patients with atherosclerotic renal artery stenosis, renal artery stenting had no clear effect on renal function impairment and led to significant complications in some patients.[32] The multicenter trial included 140 patients with creatinine clearance less than 80 mL/min/1.73 m2 and renal artery stenosis of 50% or greater. All patients received medical treatment with antihypertensive agents, a statin, and aspirin.

Although 64 patients were randomized to stent placement, only 46 had the procedure; in many patients, assessment of RAS by noninvasive imaging was inaccurate, and stenting was in fact not indicated.[32] Progression of renal dysfunction, as indicated by a decrease in creatinine clearance of 20% or greater, occurred in 16% of patients in the stent placement group and in 22% of patients in the medication group. Serious complications in the stent group included two procedure-related deaths.

In a retrospective single-center study of long-term renal function, morbidity, and mortality, Zachrisson et al assessed 57 patients with symptomatic RAS who were treated with PTRA and followed for a median of 11 years and 7 months.[33]  The main indications for PTRA were therapy-resistant HTN and declining renal function. Patients were angiographically evaluated for restenosis at 1 year.

Over the course of follow-up, 36 patients (60%) died, mostly as a consequence of cardiovascular events (54%).[33]  At 1 year, 21 patients (37%) had angiographically documented restenosis. Control of HTN was stable over the follow-up period, with an ongoing need for antihypertensive medication. Renal function continued to be moderately reduced and did not differ between patients who had restenosis and those who did not.

Apparently, even for preserving renal function, PTRA should be performed only in patients who have been rigorously selected.[26] Patients who might benefit from PTRA should be evaluated to the same extent as those chosen for a possible antihypertensive effect. (See Table 4 below.)

Table 4. Effect of Renal Stenting on Serum Creatinine Level [26] (Open Table in a new window)

Change in Creatinine Level

Rate, %

Improved

29

None

67

Worsened

4

Markers of outcome

Unfortunately, there is no consensus regarding valid markers of a favorable renal outcome with PTRA.

One may use the radioisotopic technique, which allows an accurate evaluation of the split function of the two kidneys. This method may avoid the limitations inherent to assessments based on creatinine and creatinine clearance.

The preservation of renal function depends not only on the restoration of renal blood flow but also on the wearing off of other ischemia-induced mechanisms of renal damage that may fully regress only after a long period.

PTRA may affect the glomerular filtration rate (GFR) of the dilated kidney, as well as baseline values of peripheral plasma renin activity and angiotensin II (Ang II). These changes may suggest that the degree of activation of the renin system could be a predictor of the functional recovery of the kidney.

From a mechanistic point of view, this finding fits well with the notion that Ang II is essential for the maintenance of GFR. Indeed, if renin is released in proportion to the reduction in renal blood flow, it is entirely plausible that the ischemic kidneys exposed to the highest concentration of Ang II are also those in which the GFR may increase when the renal blood flow is restored with successful PTRA.[29, 34, 35, 36, 37]

 

Periprocedural Care

Preprocedural Planning

Patient selection

Renovascular disease is present in 10-40% of patients with end-stage renal disease (ESRD); these constitute the fastest-growing group of patients with ESRD. Nonselective correction of renal artery stenosis (RAS) has led to disappointing results. Most groups that compared conservative treatment with angioplasty found only modest or no beneficial effects of angioplasty on renal function and blood pressure (BP).

The CORAL (Cardiovascular Outcomes in Renal Artery Lesions) trial included 947 participants who had atherosclerotic RAS (ARAS) and either (a) systolic hypertension (HTN) while on two or more antihypertensive drugs or (b) chronic kidney disease; the participants were randomly assigned to medical therapy plus renal artery stenting or medical therapy alone.[38, 13] The investigators did not find stenting to provide significant added benefit with regard to preventing clinical events in this setting.

Patients with a high likelihood of a favorable response should be identified.[14, 39, 40] Factors that affect outcome include the following:

  • Severity of RAS
  • Procedure used to treat RAS (eg, antihypertensive drugs, angioplasty with or without stents, surgery)
  • Nephrotoxicity to radiologic contrast materials
  • Atheroembolism [41]
  • Underlying renal disease forestalling a favorable response in renal function or BP, even after the successful correction of RAS (most important)

Renal resistance may be evaluated by using Doppler ultrasonography (US) or captopril scintigraphy to determine whether patients may or may not respond to intervention. Each factor must be considered before the correction of RAS to achieve satisfactory results in improving renal function and BP.

Preprocedural evaluation

Diagnostic studies for renovascular disease include the following:

  • Rapid-sequence intravenous pyelography (IVP) - This test has a sensitivity of 74.5% and a specificity of 86.2%, but limited sensitivity for bilateral or branch RAS; the false-positive rate of 12% in patients with essential HTN [42]
  • Test of the renin ratio in the renal vein - This test has a sensitivity of 80% and a specificity of 62%; use of sodium depletion, hydralazine, nifedipine, and captopril may enhance asymmetric response and increase sensitivity without affecting specificity; renal cysts, pyelonephritis, and ureteral obstruction may increase the asymmetry of renin secretion [43]
  • Radionuclide imaging - This test has a sensitivity and specificity of approximately 95% with use of captopril; addition of furosemide may increase sensitivity; severe renal insufficiency and the presence of bilateral RAS reduce its accuracy [44]
  • Renal artery duplex US (RADUS) - This test has a sensitivity of approximately 98% (as compared with arteriography) and a specificity of 98%, as well as a positive predictive value of 99% and a negative predictive value of 97% [45] ; drawbacks are that it is technician-dependent, that it is not universally available, and that as many as 10% of patients cannot be imaged because of body habitus
  • Magnetic resonance angiography (MRA) - This is likely to be the test of choice, with a sensitivity of nearly 100% and a specificity of nearly 90% [46] ; drawbacks are that it is nonportable and that it cannot be used in patients with implanted devices, metal artifacts, or claustrophobia or in patients of certain size and weight
  • Spiral (multisection) computed tomography (CT) - Sensitivity and specificity are not yet determined
 

Technique

Renal Artery Angioplasty and Stenting

For a percutaneous transluminal renal angioplasty (PTRA), the patient is sterilely prepared and draped, conscious sedation is employed, a local anesthetic (lidocaine 1% or 2% solution) is infiltrated at the femoral access site, an arterial sheath is placed in the femoral artery, and the renal guide catheter is advanced over a 0.035-in. guide wire under fluoroscopic guidance. After the tip of the guide catheter is positioned at the ostium of the renal artery, an angiogram (see the images below) is obtained.

Percutaneous transluminal renal angioplasty in mid Percutaneous transluminal renal angioplasty in middle-aged woman with malignant renovascular hypertension. Preprocedural right renal arteriogram was obtained after sterile preparation and draping of patient, conscious sedation, infiltration of local anesthetic (lidocaine 1% or 2% solution) at femoral access site, placement of arterial sheath in femoral artery, and advancement of renal guide catheter over 0.035-in. guide wire under fluoroscopic guidance. After tip of guide catheter is positioned at ostium of renal artery, angiogram (as shown here) is obtained. After guide wire is removed, proximal end of catheter is connected to manifold, and 4-8 mL of contrast is manually injected during cineangiographic recording. Once obtained, image may be played over and over in loop, or particular frame may be saved for review during angioplasty. Intravenous antithrombotic agent, usually heparin, is administered before clinician proceeds with angioplasty. Patient's activated clotting time is monitored.
Preangioplasty angiogram obtained in young woman w Preangioplasty angiogram obtained in young woman with malignant hypertension shows tight stenosis in middle segment of right renal artery. Its appearance is consistent with that of fibromuscular dysplasia (FMD), for which angioplasty is procedure of choice and for which stenting is usually not indicated. Intra-arterial nitroglycerin, 300 mcg, was given without any change in appearance of stenosis (which differentiates it from spasm). In general, intra-arterial nitroglycerin injection is not necessary to differentiate it from FMD that has been demonstrated on prior abdominal aortogram.

After the guide wire is removed, the proximal end of the catheter is connected to a manifold, and 4-8 mL of contrast is manually injected during cineangiographic recording. Once an image is obtained, it may be played over and over in a loop, or a particular frame may be saved for review during angioplasty. An intravenous (IV) antithrombotic agent, usually heparin, is administered before the clinician proceeds with angioplasty. The patient's activated clotting time is monitored.

A 0.018-in. guide wire is advanced through the 6-French renal guide across the renal stenosis. A small torque device is used over the proximal segment of the guide wire for steering, while a small terminal bend is created by hand over the distal end of the guide wire before it is introduced into the guide catheter. Passage of the guide wire is monitored by using fluoroscopy and injections of small amounts of contrast agent. Occasionally, a combination of torque and forward pressure is required to cross the lesion. In addition, in tight lesions, the balloon catheter is sometimes advanced and used as a support for passage of the guide wire. (See the image below.)

Guide wire (0.018-in.) is advanced through 6F rena Guide wire (0.018-in.) is advanced through 6F renal guide across ostial right renal stenosis. Small torque device is used over proximal segment of guide wire for steering, while small terminal bend is created by hand over distal end of guide wire before it is introduced into guide catheter. Passage of guide wire is monitored by using fluoroscopy and injections of small amounts of contrast agent. Occasionally, combination of torque and forward pressure is required to cross lesion. In addition, in tight lesions, balloon catheter is sometimes advanced and used as support for passage of guide wire.

A 6-mm × 18-mm balloon is positioned across the lesion by carefully advancing it over the guide wire. The balloon is prepared before it is loaded over the wire by connecting its proximal balloon port to an inflating device that contains a 50:50 solution of contrast agent and sterile saline and then by drawing negative pressure to extrude any air bubbles. The inflating device is left in negative pressure while the balloon is advanced with one hand and the guide wire is held with the other.

The balloon is advanced beyond the distal end of the guide catheter, which is gently pulled back, and the balloon is straddled across the stenosed segment. A small amount of contrast agent is injected to confirm proper positioning of the balloon. (See the image below.)

Balloon (6 mm × 18 mm) is positioned across lesion Balloon (6 mm × 18 mm) is positioned across lesion by carefully advancing it over guide wire. Balloon is prepared before it is loaded over guide wire by connecting its proximal balloon port to inflating device that contains half-and-half solution of contrast agent and sterile saline and then by drawing negative pressure to extrude any air bubbles. Inflating device is left in negative pressure while balloon is advanced with one hand and guide wire is held with the other. Balloon is advanced beyond distal end of guide catheter, which is gently pulled back, and balloon is straddled across stenosed segment. Small amount of contrast agent is injected to confirm proper positioning of balloon.

The balloon is inflated by increasing the pressure with the inflation device to several atmospheres of pressure (usually 4-8 bars). The mixed solution of contrast agent and saline in the inflation device gradually moves into the balloon. As the balloon expands, it becomes visible under fluoroscopy (see the images below). The balloon is held up for several seconds to apply circumferential pressure on the stenosed arterial segment and then deflated and gradually pulled back into the guide catheter.

Balloon is inflated by increasing pressure with in Balloon is inflated by increasing pressure with inflation device to several atmospheres of pressure (usually 4-8 bars). Mixed solution of contrast agent and saline in inflation device gradually moves into balloon. As balloon expands, it becomes visible under fluoroscopy, as shown. Balloon is held up for several seconds to apply circumferential pressure on stenosed arterial segment, then deflated and gradually pulled back into guide catheter.
Fluoroscopic image shows inflated percutaneous tra Fluoroscopic image shows inflated percutaneous transluminal angioplasty (PTA) balloon in midright renal artery over guide wire. In this case, Judkins right 4 (JR4) guide was used to access right renal artery via right femoral approach. Balloon was left inflated for several seconds, then deflated and pulled out. Additional intra-arterial nitroglycerin was infused.

After PTRA and after the balloon catheter is removed but while the guide wire is still retained, angiography is performed to evaluate the success of the procedure (see the images below).

Angiogram obtained after percutaneous transluminal Angiogram obtained after percutaneous transluminal angioplasty and after balloon catheter is removed, but while guide wire is still retained, shows increased luminal diameter at stenotic segment. However, segment appears to be at least 50% narrowed. Flow into renal artery from aorta is increased. Vascular wall shows no clear dissection. No filling defect (which may represent clot) is visible. Distal flow into branches of right renal artery is brisk, with good nephrogram.
Angiogram obtained after percutaneous transluminal Angiogram obtained after percutaneous transluminal angioplasty and after balloon catheter was removed shows good result with residual stenosis of < 20% at previously stenosed site. Flow into renal artery from aorta is increased. Vascular wall shows no clear dissection. No filling defect (which may represent clot) is visible. Distal flow into branches of right renal artery is brisk, with good nephrogram.

Preparation of a stent-balloon catheter is similar to that of a balloon catheter; however, no negative pressure is created for insertion into the guide catheter. The stent-balloon catheter is advanced over the guide wire through the guide catheter beyond the distal opening and across the lesion. The stent is positioned over the lesion; placement is confirmed with the injection of a small amount of contrast material through the guide. The guide catheter is pulled back on the wire a little to allow the proximal edge of the stent to be slightly in the aorta. Before the stent balloon is inflated, the guide catheter is pushed upward to straighten the stent and wire in the proximal portion of the renal artery. (See the image below.)

Stent-balloon catheter is prepared in manner simil Stent-balloon catheter is prepared in manner similar to balloon catheter; however, before it is inserted into guide catheter, no negative pressure is created. Stent-balloon catheter is then advanced over guide wire through guide catheter beyond distal opening and across lesion. Stent is positioned over lesion by confirming its placement with injection of small amount of contrast material through guide. Guide catheter is pulled back on wire slightly to allow proximal edge of stent to be slightly in aorta. Before stent balloon is inflated, guide catheter is pushed upward to straighten stent and wire in proximal portion of renal artery. Stent is then deployed by first creating negative pressure in stent balloon and then inflating it by injecting contrast agent–saline solution through inflation device. Stent is left inflated for several seconds at 5-10 bars of pressure. Balloon is then deflated and withdrawn while guide wire is retained across lesion, and guide catheter is slightly advanced into stent.

Next, the stent is deployed by first creating negative pressure in the stent balloon and then inflating it by injecting the contrast agent–saline solution through the inflation device. The stent is left inflated for several seconds at 5-10 bars of pressure. The balloon is then deflated and withdrawn while the guide wire is retained across the lesion, and the guide catheter is slightly advanced into the stent. (See the image below.)

Fluoroscopic image shows guide wire still lying ac Fluoroscopic image shows guide wire still lying across stented segment. Stent shadow is visible in proximal portion of right renal artery, and it appears well expanded.

Next, after the absence of a flap, dissection, or filling defect is confirmed, the guide wire is withdrawn. Poststenting angiography is performed to look for any residual stenosis in the proximal renal artery. Finally, the guide catheter is withdrawn.

Last, guide wire is withdrawn after absence of fla Last, guide wire is withdrawn after absence of flap, dissection, or filling defect is confirmed. Poststenting angiogram shows 0% residual stenosis in proximal renal artery. Guide catheter is finally withdrawn.

Complications

The rate of restenosis in patients with atheromatous disease has been reported to be 19% after 9 months and 35% if the lesion is ostial. The latter rate may be an underestimate.

In the randomized study by Weibull,[29] the 1-year rate of restenosis was 25%. Losinno et al reported a 5-year patency rate of 82%, though this percentage was based on an incomplete sample of patients.[47]

Other complications of angioplasty include the following:

  • Hematoma at the puncture site
  • Azotemia, caused by the dye load
  • Cholesterol emboli

These complications tend to be more common in old patients with diffuse atheromatous disease than in others.

When PTRA is performed in patients with elevated creatinine levels, alternative contrast agents such as carbon dioxide and gadolinium-based contrast agents (eg, gadopentetate dimeglumine, gadobenate dimeglumine, gadodiamide, gadoversetamide, and gadoteridol) may be used to minimize the risk of azotemia as a complication of renal angioplasty. Findings from early clinical experience suggested that distal protection devices used during stenting of carotid arteries may effectively filter debris produced during renal angioplasty and stenting, preventing renal failure.

However, gadolinium-based contrast agents have been linked to the development of nephrogenic systemic fibrosis (NSF) or nephrogenic fibrosing dermopathy (NFD). NSF/NFD is a debilitating and sometimes fatal disease. Characteristics include the following:

  • 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
  • Muscle weakness

The disease has occurred in patients with moderate to end-stage renal disease after a gadolinium-based contrast agent was given to enhance magnetic resonance imaging (MRI) or magnetic resonance angiography (MRA) scans. For more information, see the FDA Drug Warning or this article.

Dissection or occlusion of the renal artery may also occur, but this is rare. When this complication occurs, renal stenting may restore renal blood flow. Acute pulmonary edema as a complication of angioplasty has been reported in a patient with bilateral RAS.

In one large series, the 30-day mortality was 2.2%; all deaths occurred in patients with atheroma.