More than 900 million people have hypertension, and renovascular disease is a causative factor in 2–7% of cases. Atherosclerosis of the aorta and renal artery and fibromuscular dysplasia account for nearly all cases. Less common causes of hypertension include renal artery emboli, renal artery aneurysms, renal artery dissection, hypoplasia of the renal arteries, and stenosis of the suprarenal aorta.
Atherosclerosis characteristically produces stenosis at the orifice of the main renal artery. The lesion usually consists of an atheroma that originates in the aorta and extends into the renal artery. Less commonly, the atheroma arises in the renal artery itself. Renovascular hypertension is more common in males and is bilateral in about 95% of cases.
Fibromuscular dysplasia usually involves the distal thirds of the main renal artery. Medial fibroplasia is the most common variety of FMD, accounting for 85% of these lesions. It is bilateral in 50% of cases. The arterial stenoses are caused by concentric rings of hyperplasia that project into the arterial lumen. Renal artery aneurysms frequently coexist. FMD occurs mainly in women, with onset of hypertension usually occurring before age 45 years. It is the causative disorder in 10% of children with hypertension. Developmental renal artery hypoplasia, coarctation of the aorta, Takayasu’s aortitis are other vascular causes of hypertension in childhood.
Symptoms and Signs of Renovascular Hypertension
Most patients with renovascular hypertension are asymptomatic, but irritability, headache, and emotional depression are seen in a few. Persistent elevation of the diastolic pressure is usually the only abnormal physical finding. A bruit is frequently audible to one or both sides of the abdomen.
Other clues include absence of a history of hypertension; early onset of hypertension (particularly during childhood or during early adulthood); marked acceleration of the degree of hypertension; resistance to control with antihypertensive drugs; and rapid deterioration of renal function. One should suspect renovascular hypertension if initial diastolic pressure is greater than 115 mm Hg, or if renal function deteriorates while a patient is being given ACE inhibitors. Sudden onset of pulmonary edema with hypertension also is highly suggestive.
In the past, there have been several diagnostic tests devised to diagnose renovascular hypertension. Divided urinary excretion studies, selective renin determinations from renal vein samples, and captopril renal scintigraphy are now rarely used.
In experienced hands, duplex ultrasound scanning has an overall agreement with angiography of over 90%. Renal artery stenosis is characterized by peak systolic velocities in the range of 180–200 cm/s, and the ratio of these velocities to those in the aorta approaches 3.5. Magnetic resonance angiography, especially with gadolinium enhancement, may provide high-resolution images of diseased renal arteries.
Renal arteriography is the most precise method for delineating the obstructive lesion. Since atherosclerotic disease most often involves the origins of the renal arteries, a midstream aortogram should be obtained in addition to selective renal artery catheterization.
Nonionic contrast agents should be used. Administration of N-acetylcysteine and periprocedural sodium bicarbonate infusion dramatically reduces the incidence of acute tubular necrosis with angiography and should used routinely.
Treatment of Renovascular Hypertension
Surgical repair is reserved for failed angioplasty and stenting, renal revascularization during a procedure on the aorta, and lesions that are in branch vessels. As with any operation, the indications for arterial reconstruction are influenced by the extent of disease and the anticipated morbidity associated with operation. Nephrectomy may be considered when arterial repair is impossible or especially hazardous and the disease is unilateral.
Options include endarterectomy, which is most easily accomplished through an incision into the adjacent aorta, or bypass using prosthetic or autogenous conduits. An alternative is “nonanatomic” bypass such as a hepatorenal or splenorenal procedure. The celiac and splenic arteries often have coexistent occlusive atherosclerotic disease that mandates preoperative arteriographic assessment of these vessels.
Extracorporeal techniques have been developed for distal branch aneurysms or extensive FMD. These require removal of the kidney, continuous cold perfusion of its vascular tree, and microvascular techniques for arterial replacement. The kidney is then either returned to a site near its original position or transplanted to the ipsilateral iliac fossa.
Procedures for revascularization are successful in over 90% of patients with fibromuscular hyperplasia. Operation for atherosclerotic stenosis results in improvement or cure of hypertension in about 60%. The results for angioplasty and stenting are not as good. There is atheroembolization to the kidney during angioplasty, and current trials with protection devices to catch emboli, as done during carotid stenting, are evaluating whether this will improve the results.
The results of intervention for salvage of renal function are even better. Results are better in patients whose only clinical manifestation of atherosclerosis is secondary hypertension than in those with clinically overt systemic atherosclerosis. The operative mortality of renovascular surgery in children is almost nil, whereas it increases to 2–8% in adults with diffuse atherosclerosis.