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Clinical Evaluation of Renal Artery Disease
Approximately 46% of individuals age 20 and older have high blood pressure. In those age 75 and older, 79% of men and 85% of women have hypertension. Most have primary (essential) hypertension; however, there are a number of different causes of secondary hypertension, including those related to lifestyle or medications, such as obesity, excess alcohol ingestion, drug abuse, and oral contraceptive agents. Among other secondary causes, renovascular disease and renal parenchymal disease are the most common. Notably, there is a difference between hypertension that is associated with atherosclerotic renal artery stenosis (RAS) and hypertension caused by RAS (renovascular hypertension). Incidentally discovered RAS is quite common, whereas atherosclerotic renovascular hypertension occurs much less frequently. More than 90% of all renovascular disease is caused by atherosclerosis. Fibromuscular dysplasia (FMD) is the second most common cause of RAS. Patients with atherosclerotic RAS are typically older than age 65 and have the usual risk factors for atherosclerosis. FMD predominately occurs in women (94%) with a mean age at diagnosis of 54, but it may occur at any age. The most common clinical manifestation of FMD is hypertension, whereas atherosclerotic RAS may present with hypertension, acute and chronic kidney disease (CKD), and/or recurrent episodes of heart failure and “flash” pulmonary edema. FMD and atherosclerotic RAS may also be incidental findings when imaging is performed for another reason. Atherosclerotic RAS most often occurs at the ostium or proximal portion of the renal artery, while FMD usually occurs in the mid- to distal renal artery and its primary branches ( Figs. 23.1 and 23.2 ).
(A) and (B) Digital subtraction angiogram showing typical features of atherosclerotic renal artery stenosis (RAS). There is severe bilateral ostial RAS. (C) Angiogram after stents were placed in right and left renal arteries.
(A) Digital subtraction angiogram demonstrating multifocal fibromuscular dysplasia located in the mid to distal part of the left renal artery. Note “beading,” with beads larger than the normal caliber of the artery, typical of multifocal fibromuscular dysplasia. (B) Angiogram of the left renal artery after percutaneous balloon angioplasty. Angiographic appearance is improved, and there was resolution of the pressure gradient.
In addition to the sequelae of RAS (hypertension, CKD), patients with atherosclerotic RAS succumb prematurely from myocardial infarction (MI) and stroke. It is therefore important to treat patients with atherosclerotic RAS with optimal medical therapy similar to those with coronary and carotid artery disease (antiplatelet agent, statin, and management of other cardiovascular [CV] risk factors).
When considering the diagnosis of RAS, it is useful to think in terms of the circumstances in which RAS is likely to occur ( Box 23.1 ).
Box 23.1
Clinical Clues That Suggest Presence of Renal Artery Stenosis
Hypertension
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Hypertension onset age < 30 or > 65 years
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Malignant or accelerated hypertension
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Resistant hypertension (blood pressure > 140/90 mm Hg despite appropriate three-drug regimen, including a diuretic)
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Loss of blood pressure control in a previously well-controlled patient
Renal Abnormalities
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Acute renal failure precipitated by an angiotensin-converting enzyme (ACE) inhibitor or angiotensin receptor blocking (ARB) agent
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Unexplained azotemia
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Patient receiving renal replacement therapy (dialysis) without a definite known cause of end-stage renal disease (ESRD)
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Atrophic or small kidney
Cardiac Disease
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Recurrent congestive heart failure (CHF) or flash pulmonary edema
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Angina disproportionate to coronary anatomy
Presence of Atherosclerosis in Other Vascular Beds
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Peripheral artery disease (PAD)
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Aortoiliac occlusive disease
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Aortic aneurysm
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Multivessel coronary artery disease (CAD)
Consequences of renal artery stenosis
Hypertension
Individuals who develop hypertension between the ages of 30 and 64 usually have primary hypertension. If the initial diagnosis of hypertension is made before the age of 30, it is usually due to FMD if other known secondary causes (obesity, oral contraceptive use, drug abuse, and parenchymal renal disease) have been excluded. Because atherosclerosis occurs in older individuals, it is usually the cause of RAS in individuals aged 65 or older. There is no recent data regarding the prevalence of RAS in patients older than 65 years. In an older population-based study of Medicare patients aged 65 or older, the prevalence of atherosclerotic RAS was 6.8%. In this cohort, RAS was found in nearly twice as many men as women (9.1% vs. 5.5%); no significant differences were identified between Caucasian and African American subjects (6.9% vs. 6.7%). It is not uncommon for patients to have primary hypertension for many years, and as they age, develop atherosclerotic RAS. Under those circumstances, the patient may have had well-controlled blood pressure that suddenly becomes more difficult to control.
Patients may have anatomically significant RAS and no hypertension at all. In a systematic review of 40 studies that evaluated a total of 15,879 patients, the mean prevalence of RAS among patients with suspected renovascular hypertension was 14.1%. On further analysis of the patients who were incidentally found to have RAS on imaging studies, 65.5% were hypertensive and 27.5% had renal failure. Therefore the mere presence of RAS and hypertension does not necessarily mean that one is causing the other. Accelerated or malignant hypertension has also been associated with a very high prevalence of RAS. Resistant hypertension is defined as the failure to normalize blood pressure to less than 140/90 mm Hg despite an optimal medical regimen consisting of at least three drugs with different mechanisms of action, including a diuretic. The diagnosis of renovascular disease should be strongly considered in patients with true drug-resistant hypertension.
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