 Introduction/Background Hypertension is a common condition, affecting approximately 20% of adults. Secondary hypertension (ie, hypertension with a demonstrable cause) accounts for only 5% to 10% of all cases of hypertension, with the remaining cases considered primary hypertension or essential hypertension. Renovascular hypertension is the most common type of secondary hypertension and is estimated to have a prevalence between 0.5% and 5% of the general hypertensive population, and it has an even higher prevalence among patients with severe hypertension and end-stage renal disease, approaching 25% in elderly dialysis patients [1]. There are varied causes of reduced renal perfusion with resultant renovascular hypertension, the most common being renal artery stenosis (RAS) secondary to either atherosclerotic disease (90%) or fibromuscular dysplasia (10%) [2]. Less common etiologies include vasculitis, embolic disease, dissection, post-traumatic occlusion, and extrinsic compression of a renal artery or of a kidney [3]. Clinical features associated with an increased likelihood of renovascular hypertension include an abdominal bruit, malignant or accelerated hypertension, significant (diastolic pressure >110 mm Hg) hypertension in a young adult (<35 years of age), new onset after 50 years of age, sudden development or worsening of hypertension, refractory hypertension, deterioration of renal function in response to angiotensin- converting enzyme inhibitors, and generalized arteriosclerotic occlusive disease with hypertension. A critical problem in diagnosing renovascular hypertension is the selection of an appropriate end point against which to judge the accuracy of new tests. Calculations of the sensitivity, specificity, and accuracy of these examinations are normally based on a comparison with a standard such as conventional angiography. However, the definition of a significant RAS has varied.
Renovascular Hypertension.  Introduction/Background Hypertension is a common condition, affecting approximately 20% of adults. Secondary hypertension (ie, hypertension with a demonstrable cause) accounts for only 5% to 10% of all cases of hypertension, with the remaining cases considered primary hypertension or essential hypertension. Renovascular hypertension is the most common type of secondary hypertension and is estimated to have a prevalence between 0.5% and 5% of the general hypertensive population, and it has an even higher prevalence among patients with severe hypertension and end-stage renal disease, approaching 25% in elderly dialysis patients [1]. There are varied causes of reduced renal perfusion with resultant renovascular hypertension, the most common being renal artery stenosis (RAS) secondary to either atherosclerotic disease (90%) or fibromuscular dysplasia (10%) [2]. Less common etiologies include vasculitis, embolic disease, dissection, post-traumatic occlusion, and extrinsic compression of a renal artery or of a kidney [3]. Clinical features associated with an increased likelihood of renovascular hypertension include an abdominal bruit, malignant or accelerated hypertension, significant (diastolic pressure >110 mm Hg) hypertension in a young adult (<35 years of age), new onset after 50 years of age, sudden development or worsening of hypertension, refractory hypertension, deterioration of renal function in response to angiotensin- converting enzyme inhibitors, and generalized arteriosclerotic occlusive disease with hypertension. A critical problem in diagnosing renovascular hypertension is the selection of an appropriate end point against which to judge the accuracy of new tests. Calculations of the sensitivity, specificity, and accuracy of these examinations are normally based on a comparison with a standard such as conventional angiography. However, the definition of a significant RAS has varied.