Renovascular hypertension is BP elevation due to partial or complete occlusion of one or more renal arteries or their branches. It is usually asymptomatic unless long-standing. A bruit can be heard over one or both renal arteries in < 50% of patients. Diagnosis is by physical examination and renal imaging with duplex ultrasonography, radionuclide imaging, or magnetic resonance angiography. Angiography is done before definitive treatment with surgery or angioplasty.
Renovascular disease is one of the most common causes of curable hypertension but accounts for < 2% of all cases of hypertension. Stenosis or occlusion of one or both main renal arteries, an accessory renal artery, or any of their branches can cause hypertension by stimulating release of renin from juxtaglomerular cells of the affected kidney. The area of the arterial lumen must be decreased by ≥ 70% and a significant poststenotic gradient must also be present before stenosis is likely to contribute to BP elevation. For unknown reasons, renovascular hypertension is much less common among blacks than among whites.
Overall, about 80% of cases are caused by atherosclerosis and 20% by fibromuscular dysplasia. Atherosclerosis is more common among men > 50 and affects mainly the proximal one third of the renal artery. Fibromuscular dysplasia is more common among younger patients (usually women) and usually affects the distal two third of the main renal artery and the branches of the renal arteries. Rarer causes include emboli, trauma, inadvertent ligation during surgery, and extrinsic compression of the renal pedicle by tumors.
Renovascular hypertension is characterized by high cardiac output and high peripheral resistance.
Symptoms and Signs
Renovascular hypertension is usually asymptomatic. A systolic-diastolic bruit in the epigastrium, usually transmitted to one or both upper quadrants and sometimes to the back, is almost pathognomonic, but it is present in only about 50% of patients with fibromuscular dysplasia and is rare in patients with renal atherosclerosis.
Renovascular hypertension should be suspected if
A history of trauma to the back or flank or acute pain in this region with or without hematuria suggests renovascular hypertension (possibly due to arterial injury), but these findings are rare. Asymmetric renal size (> 1 cm difference) discovered incidentally during imaging tests, and recurrent episodes of unexplained acute pulmonary edema or heart failure also suggest renovascular hypertension.
If renovascular hypertension is suspected, ultrasonography, magnetic resonance angiography (MRA), or radionuclide imaging may be done to identify patients who should have renal angiography, the definitive test.
Duplex Doppler ultrasonography can assess renal blood flow and is a reliable noninvasive method for identifying significant stenosis (eg, > 60%) in the main renal arteries. Sensitivity and specificity approach 90% when experienced technicians do the test. It is less accurate in patients with branch stenosis.
MRA is a more accurate and specific noninvasive test to assess the renal arteries.
Radionuclide imaging is often done before and after an oral dose of captopril 50 mg. The ACE inhibitor causes the affected artery to narrow, decreasing perfusion on the scintiscan. Narrowing also causes an increase in serum renin, which is measured before and after captopril administration. This test may be less reliable in blacks and in patients with decreased renal function.
Renal angiography is done if MRA indicates a lesion amenable to angioplasty or stenting or if other screening tests are positive. Digital subtraction angiography with selective injection of the renal arteries can also confirm the diagnosis, but angioplasty or stent placement cannot be done in the same procedure.
Measurements of renal vein renin activity are sometimes misleading and, unless surgery is being considered, are not necessary. However, in unilateral disease, a renal vein renin activity ratio of > 1.5 (affected to unaffected side) usually predicts a good outcome with revascularization. The test is done when patients are depleted of Na, stimulating the release of renin.
Without treatment, the prognosis is similar to that for patients with untreated primary hypertension.
All patients should have aggressive medical management of their hypertension (see General Treatment).
For patients with atherosclerotic renal artery stenosis, angioplasty with stent placement was previously considered beneficial for many patients. However, data from a recent large, randomized, controlled trial (the cardiovascular outcomes in renal atherosclerotic lesions [CORAL]) showed that stent placement did not improve outcomes compared to medical management alone. Although stent placement did provide a small (-2 mm Hg), statistically significant decrease in systolic BP, there was no significant clinical benefit for prevention of stroke, MI, heart failure, death due to cardiovascular or renal disease, or progression of kidney disease (including the need for renal replacement therapy). Importantly, all patients in the CORAL study received aggressive medical management of their hypertension and any diabetes, along with antiplatelet drugs and a statin to manage atherosclerosis. Thus, the decision to eschew angioplasty must be accompanied by strict adherence to current medical management guidelines.
For most patients with fibromuscular dysplasia of the renal artery, percutaneous transluminal angioplasty (PTA) is recommended. Placement of a stent reduces the risk of restenosis; antiplatelet drugs (aspirin, clopidogrel) are given afterward. Saphenous vein bypass grafting is recommended only when extensive disease in the renal artery branches makes PTA technically unfeasible. Sometimes complete surgical revascularization requires microvascular techniques that can only be done ex vivo with autotransplantation of the kidney. Cure rate is 90% in appropriately selected patients; surgical mortality rate is < 1%. Medical treatment is always preferable to nephrectomy in young patients whose kidneys cannot be revascularized for technical reasons.
Last full review/revision May 2014 by George L. Bakris, MD
Content last modified May 2014