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

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 .

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 ).

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.

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.

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.