To view the figures and tables related to this article, please refer to the print version of our November/December issue, page 44.

Renovascular hypertension, especially if due to unilateral disease, is usually easily controlled using modern antihypertensive medications. Ischemic nephropathy—one of the few reversible causes of renal failure in adults—is the most appropriate indication for intervention in renal artery occlusive disease. Selection for intervention must consider and integrate the clinical, anatomic, and physiologic status of the patient to yield the best possible risk-benefit (Table 1). Intervention must be performed with special attention toward limiting nephrotoxic iodinated contrast and unnecessary manipulation in the diseased aorta and renal artery, especially in patients with ischemic nephropathy.

The potential benefits of intervention must be weighed against the potential risks and the natural history of the disease. Most natural history studies exaggerate the progression of atheromatous renal artery disease. Much of these data were gathered prior to effective and specific medications for control of renin-dependent hypertension and are prior to major lifestyle modifications, such as smoking cessation and lipid control.

The potential risks of renal artery interventions, especially cholesterol embolization, are underrecognized and underreported.1 Physicians performing renal artery interventions must understand the nonlinear relationship of renal functional reserve (GFR) and serum creatinine (SCr) and its implications for the margin of safety (Figure 1).

Severe iatrogenic renal parenchymal damage due to diagnostic and therapeutic intravascular procedures can be masked in patients with normal preintervention global SCr values. Thus, 50% of total renal mass, or one of the kidneys, can be destroyed without any change in global renal function, as measured by SCr values, although the creatinine clearance and ipsilateral renal function will be reduced. Patients with elevated SCr whose renal function is at the ?knee? of this curve have very diminished renal reserve and are at much greater risk. An additional 10% loss of renal parenchyma can put such a patient on dialysis. There can be extensive damage to the kidneys that, in many patients with normal preintervention renal function, may not be apparent during or after renal artery intervention. Thus, it is imperative not to intervene for anatomic renal artery stenosis without adequate indications, particularly not in incidentally discovered renal artery stenosis without previous clinical evaluation. Therefore, prior to renal artery interventions the physiological significance of a stenosis should be confirmed by demonstrating a hemodynamically significant transstenotic pressure gradient, in addition to appropriate clinical and anatomic indications (Figure 2A,B).

A complete description of associated complications can be found on page 50 in the article entitled Tips and Tricks for High-Risk Patients.

At New York Presbyterian Hospital Weill Cornell Center, we attempted to place Palmaz stents in 94 renal arteries in 84 patients between May 1992 and January 1997. Eighty-seven stents were placed for ostial lesions; 77% were placed primarily in ostial lesions or total occlusions and 28% were placed after previously failed angioplasties. Indications for intervention were hypertension in 96%; renal failure (Cr &Mac179;1.5 mg/dL in 60%, and &Mac179;2 mg/dL in 45%) in 60% ; and recurrent flash pulmonary edema in 30% of patients. Many patients had multiple indications.

Ninety-eight percent of procedures were technically successful. There were seven procedural complications: two thrombosed branch renal arteries partially lysed with urokinase; two puncture site pseudoaneurysms; one puncture site hematoma requiring a transfusion; and three cases of cholesterol embolization, one with permanent renal failure and two with transient renal failure. Angiographic follow-up was performed in 36% of implanted stents. Seventy-eight percent of stents were widely patent, 22% of stents showed &Mac179;60% restenosis. One patient died prior to follow-up from an unrelated cause. Clinical follow-up was available in all 89 patients at a mean of 19 months (range, 0-57 months), and was available in 40 patients at more than 15 months.

The mean blood pressure prior to stenting was 183/91 mm Hg; mean blood pressure at latest clinical follow-up was 149/78 mm Hg (P<.001). The number of antihypertensives was reduced from a mean of 2.93 ± 1.4 to 2.63 ± 1.3.

Table 2 summarizes changes in renal function of our patients. Eleven of 13 patients with recurrent flash pulmonary edema and bilateral renal artery stenosis were cured after stenting of one or both renal arteries. Our results are similar to other series (Table 3).2-8

Imaging Follow-up
Visualization of the intrastent lumen with MRA is not possible in ferrous stainless-steel stents. The OmniFlex (AngioDynamics, Queensbury, NY) stent is constructed from a platinum alloy, a nonferromagnetic metal, which produces little artifact and is the only balloon-expandable MR-transparent stent (Figure 3). This is clearly very important when restenosis is suspected and must be evaluated. Ultrasound gives only indirect measures of patency. CTA is limited by the need for iodinated contrast and stent artifacts in evaluating restenosis. DSA is invasive and also requires iodinated contrast.

Renal artery stenting is the treatment of choice for renal dysfunction, poorly controlled hypertension, or recurrent pulmonary edema in patients with physiologically significant renal artery stenosis. The intermediate term results are similar to open surgical repair.

Thomas A. Sos, MD, is Professor and Vice Chair of Radiology at the New York Presbyterian Weill Cornell Center, in New York. He has a financial interest in AngioDynamics. Dr. Sos may be reached at (212) 746-2601;

David W. Trost, MD, is Associate Professor of Radiology and Chief of the Division of Interventional Radiology at the Weill Cornell Center, New York Presbyterian Hospital, in New York. He holds no financial interest in any product or manufacturer mentioned herein. Dr. Trost may be reached at (212) 746-2601;

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