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Table 2. Indicators of renovascular disease

• Abrupt or severe hypertension

• Hypertension resistant to optimal medical therapy

• Onset of hypertension under age 30 or over age 55

• Bruits in the abdomen or flank

• Unexplained renal failure in an elderly hypertensive

• Worsening renal function during therapy with ACE inhibitors

• Hypertensive retinopathy (grade 3 or 4)

• Hypertension with asymmetric renal size, atherosclerotic heart or peripheral vascular disease

A Normal

Figure 15. Principle of ACE inhibition (captopril) renography. In a normal patient (A), blood is delivered to the glomerulus via the afferent arteriole and leaves by the efferent arteriole. Normally, there is a sufficiently high glomerular pressure to allow for renal physiology (represented by arrows) across the capillary membrane and Bowman's capsule. In a patient with renal artery stenosis and renovascular hypertension (B), the initial drop in blood pressure in the glomerulus is counteracted with angiotensin II-mediated vasoconstriction of the efferent arteriole (arrow). Glomerular pressure and hence renal physiology is maintained. If captopril is administered (C), the efferent arteriole relaxes with a subsequent drop in glomerular pressure and filtration. This decrease in renal physiology can be detected with renal scanning. (Figure provided by Dr. I.D. Greenberg.)

Figure 15. Principle of ACE inhibition (captopril) renography. In a normal patient (A), blood is delivered to the glomerulus via the afferent arteriole and leaves by the efferent arteriole. Normally, there is a sufficiently high glomerular pressure to allow for renal physiology (represented by arrows) across the capillary membrane and Bowman's capsule. In a patient with renal artery stenosis and renovascular hypertension (B), the initial drop in blood pressure in the glomerulus is counteracted with angiotensin II-mediated vasoconstriction of the efferent arteriole (arrow). Glomerular pressure and hence renal physiology is maintained. If captopril is administered (C), the efferent arteriole relaxes with a subsequent drop in glomerular pressure and filtration. This decrease in renal physiology can be detected with renal scanning. (Figure provided by Dr. I.D. Greenberg.)

secondary to atherosclerosis or, in the younger patient, fibromuscular dysplasia. Clinical indications to pursue renovascular hypertension are summarized in Table 2.

Renovascular disease is also the most difficult secondary cause of hypertension to detect non-invasively. The gold standard for diagnosing renal artery stenosis is the conventional renal angiogram. Renal artery stenosis can also be demonstrated by MRI and duplex ultrasonography. However, the demonstration of renal artery stenosis does not guarantee that the stenosis is causing renovascular hypertension. Furthermore angiography is associated with a risk of making renal failure worse secondary to iodinated radiographic contrast or cholesterol emboli.

Because of the low incidence of renovascular hypertension, a highly sensitive screening test is necessary. The captopril renal scan is the most useful test for detecting

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