Stenosis of the renal artery(RAS) may be due to atherosclerotic disease or fibromuscular dysplasia (seen in young women). Findings that suggest renal artery stenosis include refractory hypertension, hypertensive retinopathy, hypokalemia, an abdominal or flank bruit, erythrocytosis or ptosis of a kidney. Other factors which implicate renal artery stenosis include hypertension occurring before age 20 or after age 50, and the combination of severe hypertension and unexplained renal insufficiency. Renal duplex scansare an effective way to assess stenosis. Renal artery angiography is the gold standard diagnostic test. CT or MR angiography are effective studies also. The diagnosis may also be suspected in patients whose IVP shows a difference in renal size of two centimeters and a unilateral delay in opacification or a hyperconcentration of dye. Patients who develop an increase in their serum BUN and creatinine values after beginning treatment with ACE inhibitors should be suspected of having bilateral renal artery stenosis and evaluated accordingly.

Renal vein renin assays are useful to demonstrate the functional significance of a discovered stenosis. The renin level assayed from a vein with a functionally significant stenosis should exceed the renin level from the unaffected side by 50% or greater.

Treatment may consist of medical management, surgical intervention, or angioplasty. If fibromuscular dysplasia is the underlying cause, then angioplasty is a reasonable initial option as it may prove curative of the hypertension.  With atherosclerotic stenosis, the benefits of angioplasty are less clear as the hypertension usually persists despite treatment of the obstructed renal artery or arteries. Therefore, the intial therapy of atherosclerotic RAS is medical management of the patient's blood pressure. As the resultant hypertension in patients with RAS is renin dependent, ACEI's, ARB's, or aldosterone therapy may prove effective; however, since many of these patients have refractory hypertension, multidrug therapy is often necessary to control blood pressure to adequate levels. Since atherosclerotic RAS is a form of peripheral arterial disease (PAD), and since PAD is a coronary artery disease equivalent, therapy with a statin to control lipids aggressively and an antiplatelet agent are indicated. Other risk factors for atherosclerosis (aggressive diabetes mellitus management and smoking cessation) should be addressed. As mentioned above, ACEI"s or ARB's may be associated with an elevation in the serum creatinine in patients with RAS. Close monitoring of the serum BUN and creatinine is recommended when starting ACEI or ARB therapy, and if renal function worsens significantly, then therapy should be discontinued and a trial with another class of antihypertensive initiated.