Percutaneous Arterial Dilation and Stenting for Arteriosclerotic Renovascular Hypertension and Ischemic Nephropathy



Percutaneous Arterial Dilation and Stenting for Arteriosclerotic Renovascular Hypertension and Ischemic Nephropathy



Thomas A. Sos


Anecdotal experience and many retrospective studies support the utility of renal artery stenting in carefully selected patients, yet Level 1 evidence has been lacking. Several multicenter prospective randomized studies have been conducted to determine whether renal artery stenting was superior to medical therapy for treatment of ischemic nephropathy. The negative conclusions of the widely quoted Angioplasty and STenting for Renal Artery Lesions (ASTRAL) trial, a large European trial, the Stent Placement in Patients with Atherosclerotic Renal Artery Stenosis and Impaired Renal Function (STAR) trial, a much smaller Dutch trial, and the Cardiovascular Outcomes in Renal Atherosclerotic Lesions (CORAL), a large, primarily US-based trial have all been reported, who results were published in January 2014. Based on the conclusions of these studies, many clinicians no longer consider renal artery stenting a reasonable option for their patients with renal artery stenosis, renal dysfunction, and hypertension.



Patient Selection


Hypertension, renal dysfunction, and atheromatous renal artery stenosis can occur independently or can be causally linked (Figure 1). There are unfortunately no foolproof and universally agreed upon criteria to identify patients in whom hemodynamically and physiologically significant anatomic renal artery stenosis is the cause of the clinical manifestations of potentially reversible ischemic nephropathy and renal vascular hypertension. A summary of the author’s selection criteria are shown in Boxes 1 and 2 and Table 1.



BOX 1   Clinical Criteria for Renal Vascular Hypertension and Ischemic Nephropathy





BOX 2   Anatomic Criteria for Diagnosis of Hemodynamically Significant Renal Artery Stenosis





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FIGURE 1 The complex relationship of renal artery stenosis, hypertension, and renal insufficiency and their clinical presentation.

In the CORAL, ASTRAL and STAR trials, most of these selection criteria were not met by the patients who were included, and there were also serious problems associated with the interventional treatment in the ASTRAL and STAR trials; these flaws are critical in understanding the failure of stenting to show superiority to medical therapy, as is discussed in detail later.



Techniques of Renal Artery Stenting


Almost all atheromatous renal artery stenoses occur at the aortic ostium. Extreme care must be taken during all catheter and wire manipulations in the juxtarenal abdominal aorta to minimize manipulations and iodinated contrast use to decrease the chances of microcholesterol embolization or contrast-induced nephropathy. As suggested by logarithmic glomerular filtration rate (GFR) curves (Figure 2), the likelihood of deterioration of kidney function following an equal insult during renal artery stenting is related to the preprocedure kidney function. The author advocates performing the procedure in the obliquity where the lesion is best seen on prior imaging and where the catheter tip is en face to the stenosis (Figures 3 to 5).


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FIGURE 2 Renal functional reserve (GFR) and serum creatinine (SCr) concentration. Note: SCr increases logarithmically only after 50% or more of renal parenchyma is lost. Int, Intermediate.

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FIGURE 3 The right renal artery (RRA) origin is 30 degrees ventral and the left renal artery (LRA) is 7 degrees dorsal to the mid coronal plain of the aorta (0 degrees). (From Kim PA, Khilnani NM, Trost DW, et al: Fluoroscopic landmarks for optimal visualization of the proximal renal arteries, J Vasc Interv Radiol 10:37–39, 1999.)

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FIGURE 4 Magnetic resonance arteriography (MRA) with gadolinium. There is a severe focal ostial right renal artery stenosis (arrows) and a viable 8.8 cm right kidney, a very severe left renal artery stenosis with an atrophic 7.1 cm left kidney, and severe aortic atheroma.

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FIGURE 5 A, Intraarterial digital subtraction aortogram (DSA). B, Selective right renal arteriogram. Each DSA sequence was obtained at 7.5 frames per second using 1艠3 dilution of low-osmolar contrast medium. The aortogram was made with 10 mL injected at 10 mL/second, and the selective renal arteriogram was made with 4 mL injected at 4 mL/second. DSA confirms the severe right ostial renal artery stenosis (black arrow) and severe left renal artery stenosis and also shows severe and extensive aortic atheroma and heavy wall calcification seen as subtraction artifacts.

The Sos flick technique (Figure 6) is used with the Sos Omni Selective (AngioDynamics, Queensbury, NY) recurve-type catheter and a soft-tipped Bentson-type wire for approaching and crossing renal artery stenoses.


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FIGURE 6 The Sos flick technique of selective renal artery catheterization for ostial renal artery stenosis using the Sos Omni Selective (AngioDynam Queensbury, NY) recurve-type catheter. A, The catheter in the aorta. B to D, As the catheter and wire are advanced cephalad, the wire tip (arrow) flicks laterally (D) when it reaches the nubbin of the stenotic or occluded renal artery. E, The wire enters the artery.

The Sos flick usually results in renal artery entry on one pass and almost never requires contrast injection. The author only 10 mL of half or third dilution of full-strength low-osmolar iodinated contrast by saline for aortography (Figures 6 and 7) and prehydrate patients before renal artery stenting, especially those with preexisting renal insufficiency or those at high risk for it. The evidence for using renal artery protection devices is lacking. They all are potentially dangerous and, most importantly, most cholesterol embolization has already occurred by extended fishing in the diseased juxtarenal aorta.


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FIGURE 7 Digital subtraction aortogram (DSA) obtained using 5 mL of 1艠3 dilute contrast after successful stenting (black arrow). Note the branch stenosis (white arrow), which was not treated.

After the stenosis is crossed, pressure measurements are obtained through a long 5-Fr vascular sheath in the aorta and at the tip of the selective catheter to measure the gradient. A 0.014-in. or 0.018-in. stiff shaft and very floppy tipped guidewire is advanced into a proximal renal artery branch for good purchase. In some cases the stent can be advanced bareback into the stenosis; however, in very severely stenotic and or heavily calcified stenoses it is preferred to first advance the 5-Fr sheath with its introducer through the stenosis over the 0.014-in. or 0.018-in. guidewire, which prevents heaving to deal with a stent that will not cross the lesion and is then difficult to retract back into the sheath. This technique is preferred to balloon predilation, which is another option in these types of cases. The stent should be deployed extending a few millimeters into the aorta and a few millimeters beyond the distal margin of the lesion; attempts to deploy a shorter stent more accurately often results in having to deploy additional overlapping stents to cover the lesion adequately, with a greater likelihood of restenosis.



Illustrative Case


In contrast to the STAR and ASTRAL trials, Patient A presented with clinically, anatomically, and hemodynamically (physiologically) significant renal artery stenosis and the serious clinical sequelae of chronic renal insufficiency as a result of ischemic nephropathy and renovascular hypertension. This patient was 84 years old and had an at least 10-year history of hypertension that had recently become uncontrolled (239/99 mm Hg) on three medications. On five antihypertensive medications BP was 160–180/60–70 mm Hg. She had a 10-year history of Sjögren’s syndrome and progressive chronic renal insufficiency (serum creatinine [SCr] increased from 1.5 mg/dL to 2.7 mg/dL over the previous 6 months). Magnetic resonance angiography (MRA) with gadolinium (see Figure 5) was performed, recognizing that there was a slight risk of nephrogenic systemic fibrosis. MRA demonstrated severe bilateral ostial renal artery stenosis, left renal atrophy, and severe aortic atheroma in the region of the renal arteries. Aortography, selective right renal arteriography, and pressure gradient measurement confirmed these findings and the hemodynamic significance of the right renal artery stenosis.


We do not routinely perform a selective renal arteriogram prior to stenting. In this case, following the Sos flick, which successfully engaged the renal artery ostium, the wire could not be advanced through the stenosis into the distal renal artery. An ostial arteriogram was performed with a nontraumatic technique using 4 mL of 1艠3 dilute contrast injected at 4 mL/sec to guide further wire manipulation.


The patient in this case had many of the most important criteria for intervention outlined in BOX 3. Several treatment options are available including medical therapy, surgical revascularization, and percutaneous stenting. In this case, she had already clearly failed medical therapy. For surgical revascularization, hepatorenal bypass is an extra-anatomic reconstruction that has little risk of cholesterol embolization, but the patient had a moderately high anesthesia and surgical risk as a result of her age, diffuse vascular disease, and Sjögren’s syndrome. For percutaneous stenting, the irregular atheroma of the aortic wall and the intraluminal atheroma increased the chances of cholesterol embolization to 3% to 5%, but there was a low technical procedural and sedation risk.



BOX 3   Criteria for Intervention


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Aug 25, 2016 | Posted by in CARDIOLOGY | Comments Off on Percutaneous Arterial Dilation and Stenting for Arteriosclerotic Renovascular Hypertension and Ischemic Nephropathy

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