Renal artery stenosis is produced predominantly by atherosclerotic occlusive disease (80-90% of patients) or fibromuscular dysplasia (10-15% of patients). Characteristically, patients with occlusive disease have common risk factors for atherosclerosis, and their lesions are focal proximal or ostial calcific plaques, often described as “spillover” aortic disease. Patients with fibromuscular dysplasia tend to be women 30-50 years of age with distal renal artery disease that often extends into the branch vessels in a classic “string of beads” pattern of alternating stenoses and dilations.
Renal artery stenosis has two important clinical manifestations: renovascular hypertension and ischemic nephropathy. Renovascular hypertension accounts for about 5% of all cases of hypertension. In certain subsets of patients, the incidence is much higher. Seventy percent of patients over 60 years of age with diastolic blood pressure greater than 105 mm Hg and serum creatinine greater than 2 mg/dL have renovascular hypertension.

In hypertensive children the incidence of this disease approaches 80%. Evaluation should be considered in patients with poorly controlled or acutely worsening hypertension that was previously well controlled by drug therapy (three or more antihypertensive medications), particularly when presenting in conjunction with renal insufficiency, lateral abdominal bruit, or noncardiogenic “flash” pulmonary edema. A history of acute renal failure when starting an angiotensin-converting enzyme inhibitor is highly suggestive.

An incidental finding of renal artery stenosis greater than 50% is noted in as many as 45% of patients undergoing angiography for aortoiliac occlusive disease. Infrequently, it is associated with progressive renal insufficiency. High-grade (over 70%) bilateral stenoses or stenosis in a solitary kidney warrant close follow-up. Renal artery occlusive disease is suspected in patients with rapidly progressive renal insufficiency and no evidence of obstructive uropathy or intrinsic renal disease (no proteinuria on urinalysis, no polycystic disease on ultrasound).

Initial screening tests include duplex ultrasound, captopril renal scintigraphy, and MRA. Sensitivity and specificity of detecting renal artery stenosis greater than 60% are over 90% for each of these modalities, but the tests are highly operator dependent and equipment dependent -  the most reliable examination varies by institution. An assessment should also be made of the kidney parenchyma: renal length, cortical thickness, and presence of infarcts. One pitfall of these modalities is failure to identify small accessory renal arteries, which when diseased can contribute to renovascular hypertension.

Indications for treatment include renovascular hypertension refractory to aggressive drug therapy or renal artery stenosis with progressive renal failure or sudden-onset noncardiogenic pulmonary edema. Severe stenosis unaccompanied by renal insufficiency or poorly controlled hypertension may be considered for therapy to prevent loss of renal mass.

Angiography is generally required for planning an operative strategy and in many cases discloses a lesion amenable to angioplasty and stenting. Ideal lesions for endovascular treatment are focal, proximal, nonostial plaques that do not extend into the branch vessels. Primary stenting is advised for stenoses in renal arteries greater than 5 mm in diameter because of improved patency over angioplasty alone. One exception to this rule is fibromuscular dysplasia, in which a durable clinical effect is often produced by angioplasty alone. In patients with renal insufficiency, use of nonionized contrast, preprocedure intravenous hydration, and administration of the antioxidant acetylcysteine, 600 mg orally twice daily for 2 days before and 2 days after examination, are advised. The long-term patency of renal artery stents is yet undefined, but a 20% restenosis rate from intimal hyperplasia is noted at 6-36 months. Overall, 3-13% of initially stented patients ultimately require surgery.

Surgery is indicated for threatened loss of total renal mass (bilateral renal artery stenosis greater than 75%), for treatment of progressive renal failure or uncontrolled renovascular hypertension in patients with lesions refractory to angioplasty, for complex lesions extending into the branch vessels, or for concomitant aortic disease requiring surgical reconstruction. Because of superior long-term patency, surgery may be preferred over angioplasty for primary treatment of renal artery occlusive disease in good-risk younger surgical candidates. Surgical options include transaortic renal endarterectomy, renal artery bypass, or extraanatomic (hepatorenal, splenorenal, or iliorenal) bypass. Mannitol (25 g intravenously) and fenoldopam (0.5-1 ug/kg/min) have been beneficial in the perioperative management of these patients. Nephrectomy is considered for patients with renovascular hypertension and irreversible renal atrophy (kidney length less than 7 cm, severe cortical thinning, less than 10% of total renal function by split function testing). Endarterectomy and aortorenal bypass have 5-year patency greater than 80%, with beneficial blood pressure response in 70-90% of patients and improvement or stabilization in renal function in 70-80%.

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