Residency · Residency · Interventional Radiology

Renal Artery Stenosis and Revascularization

Anatomy

The renal arteries arise from the abdominal aorta at the L1-L2 level, just below the SMA. The right renal artery passes posterior to the inferior vena cava. Accessory renal arteries are present in 25 to 30 percent of patients, most commonly as inferior polar arteries. At the hilum, the renal artery divides into segmental branches through anterior and posterior divisions. These are end arteries with no significant collateral connections between segmental branches, meaning that embolization leads to segmental infarction.

Etiologies of Renal Artery Stenosis

Atherosclerotic Renal Artery Stenosis (ARAS)

Atherosclerotic disease accounts for 90 percent of all renal artery stenosis cases. The stenosis is predominantly ostial or proximal, within 1 cm of the aortic origin. It typically affects patients older than 55 with cardiovascular risk factors and is part of a systemic atherosclerotic process associated with coronary, cerebrovascular, and peripheral artery disease. The disease is progressive and can lead to ischemic nephropathy and renal atrophy.

Fibromuscular Dysplasia (FMD)

Fibromuscular dysplasia accounts for the remaining 10 percent of cases and predominantly affects young to middle-aged women, with a female-to-male ratio of 9 to 1. The most common type is medial fibroplasia, comprising more than 80 percent of FMD cases and producing the classic "string of beads" appearance on angiography. FMD affects the mid and distal renal artery rather than the ostium and is bilateral in 35 to 60 percent of cases. It may also affect the carotid, vertebral, and iliac arteries.

Other Causes

Less common causes include neurofibromatosis type 1 in children, vasculitis such as Takayasu arteritis and polyarteritis nodosa, renal artery dissection, radiation-induced stenosis, and extrinsic compression from tumors or retroperitoneal fibrosis.

Clinical Presentation

Renovascular hypertension presents as refractory hypertension despite three or more antihypertensive agents, sudden onset or worsening of hypertension, or hypertension in a young patient (suggesting FMD). Ischemic nephropathy manifests as progressive renal insufficiency in the setting of bilateral renal artery stenosis or stenosis to a solitary kidney. Flash pulmonary edema, also known as Pickering syndrome, consists of recurrent episodes of acute pulmonary edema out of proportion to cardiac function and is a classic indication for revascularization. Renal asymmetry, with a size discrepancy greater than 1.5 cm on imaging, suggests chronic ischemia to the smaller kidney.

Diagnostic Workup

Screening Tests

Duplex ultrasound is the first-line screening test. A peak systolic velocity greater than 180 to 200 cm/s suggests more than 60 percent stenosis, and a renal-to-aortic ratio greater than 3.5 is also significant. A resistive index greater than 0.80 suggests underlying parenchymal disease that is unlikely to benefit from revascularization. CTA provides excellent anatomic detail and identifies ostial calcification, accessory arteries, and renal parenchymal perfusion. MRA, either gadolinium-enhanced or non-contrast using arterial spin labeling or phase contrast, avoids iodinated contrast but may overestimate stenosis severity; gadolinium should be avoided in severe chronic kidney disease due to the risk of nephrogenic systemic fibrosis.

Confirmatory and Functional Tests

Catheter angiography remains the gold standard and allows simultaneous pressure measurements and intervention. A translesional pressure gradient with a mean gradient greater than 10 mmHg or systolic gradient greater than 20 mmHg is considered hemodynamically significant. Renal frame count or parenchymal blush provides indirect assessment of renal perfusion. Captopril renography, a nuclear medicine test, has been largely replaced by cross-sectional imaging.

Landmark Clinical Trials

CORAL Trial (2014)

The CORAL trial randomized 947 patients with atherosclerotic renal artery stenosis to medical therapy alone versus medical therapy plus renal artery stenting. There was no significant difference in the composite cardiovascular and renal endpoint. Stenting did not provide additional benefit for blood pressure control or renal function preservation. However, the trial has been criticized for potentially enrolling patients without hemodynamically significant stenosis, excluding complete occlusions, and optimizing medical therapy in the control arm.

ASTRAL Trial (2009)

The ASTRAL trial randomized 806 patients and found no benefit of revascularization for renal function, blood pressure, or cardiovascular events. Criticisms include the inclusion of patients with mild stenosis below 50 percent, underpowering for severe disease subgroups, and varied operator experience.

STAR Trial (2009)

The STAR trial enrolled 140 patients and similarly found no benefit of stenting over medical therapy for renal function. It was limited by a small sample size and inclusion of patients with non-significant stenosis.

Interpretation

These trials shifted practice away from routine stenting for atherosclerotic renal artery stenosis. They likely enrolled many patients who did not have hemodynamically significant stenosis or whose kidneys were no longer salvageable. Select patients with severe, hemodynamically significant disease and preserved renal parenchyma may still benefit from intervention.

Current Indications for Renal Artery Revascularization

Generally Accepted Indications

Flash pulmonary edema (Pickering syndrome) with bilateral renal artery stenosis or stenosis to a solitary kidney is the strongest indication. Refractory hypertension, defined as failure of three or more optimal-dose antihypertensives including a diuretic, with proven hemodynamically significant stenosis is another accepted indication. Progressive renal insufficiency attributable to renal artery stenosis with preserved renal parenchyma (kidney larger than 7 cm and resistive index below 0.80) and unstable angina with significant renal artery stenosis, where afterload reduction improves cardiac function, are also recognized.

FMD

PTA alone, without stenting, is the treatment of choice for fibromuscular dysplasia. Technical and clinical success rates are excellent, with more than 85 percent of patients experiencing cure or improvement of hypertension. Stenting is rarely needed and is reserved for cases complicated by dissection or recoil. Cure of hypertension is possible in young patients with short-duration disease.

Atherosclerotic RAS

Balloon-expandable stent placement is the technique of choice because ostial lesions require precise deployment. Embolic protection devices may reduce atheroembolic complications, though this remains debated. A typical stent measures 5 to 7 mm in diameter and 12 to 18 mm in length, with 1 to 2 mm of protrusion into the aorta.

Endovascular Technique

Access

The transfemoral approach is standard. A guide catheter or guiding sheath provides support, with renal double-curve, hockey stick, or IMA-shaped configurations available. A transradial or transbrachial approach is useful for downward-pointing renal arteries.

Procedure Steps

The procedure begins with selective renal artery catheterization and diagnostic angiography in multiple projections. A translesional pressure gradient is measured, with significance defined as a mean gradient greater than 10 mmHg. Predilation with an undersized balloon is performed if needed. A balloon-expandable stent is deployed across the ostium with 1 to 2 mm protruding into the aorta to cover the ostial plaque. The stent is post-dilated to its nominal diameter, and completion angiography with pressure measurement confirms a good result.

Complications

Potential complications include renal artery dissection or perforation, atheroemboli to the kidney causing cholesterol crystal embolization, contrast-induced nephropathy, access site complications, and in-stent restenosis, which occurs in 10 to 20 percent of cases at one to two years.

<image>Angiographic comparison of atherosclerotic renal artery stenosis and fibromuscular dysplasia. Two panels: Left panel shows a selective renal arteriogram with a high-grade ostial stenosis of the right renal artery due to atherosclerotic plaque, with calcification visible at the aortic origin and a poststenotic dilation. Right panel shows a selective renal arteriogram with the classic "string of beads" appearance of medial fibroplasia in the mid-to-distal renal artery, with alternating stenoses and dilations. Labels indicate the ostial versus mid-vessel location, and the different treatment approaches (stenting for ARAS, PTA alone for FMD).</image>

<image>Step-by-step illustration of renal artery stenting for ostial atherosclerotic stenosis. Four panels: (1) Guide catheter engaged in the renal artery origin with a guidewire across the stenosis; (2) Balloon-expandable stent positioned across the ostium with 1-2 mm protruding into the aortic lumen; (3) Stent deployment by balloon inflation with the stent flaring slightly at the ostium; (4) Completion angiogram showing a widely patent stent with restored renal perfusion and no residual stenosis. Insets show translesional pressure measurements before (gradient >20 mmHg) and after (<5 mmHg) stenting.</image>

<image>Flowchart for the evaluation and management of suspected renovascular hypertension. Starting with clinical suspicion (refractory HTN, young patient with HTN, flash pulmonary edema, asymmetric kidneys), leading to screening with duplex ultrasound or CTA/MRA. If positive, branches into ARAS (leads to assessment of hemodynamic significance and parenchymal viability before deciding on medical therapy alone vs. revascularization) and FMD (leads to PTA as first-line treatment). Decision nodes include kidney size, resistive index, translesional gradient, and clinical syndrome (flash pulmonary edema, refractory HTN, declining GFR).</image>

Clinical Pearls

The CORAL and ASTRAL trials shifted the paradigm: routine stenting for atherosclerotic renal artery stenosis is not beneficial, and patient selection is everything. Flash pulmonary edema (Pickering syndrome) remains the strongest indication for renal artery stenting and has the best outcomes. FMD is treated with PTA alone without stenting, and cure of hypertension is achievable, especially in young patients with short-duration disease. Translesional pressure gradients should always be measured before stenting because anatomic stenosis alone does not equal hemodynamic significance. Balloon-expandable stents are mandatory for ostial renal artery lesions, and the stent must protrude 1 to 2 mm into the aorta. A small kidney (less than 7 cm) with an elevated resistive index (greater than 0.80) is unlikely to recover function after revascularization. FMD patients should be screened for stenosis in other vascular beds, including the carotid, vertebral, and iliac arteries.

References

• Cooper CJ et al. Stenting and medical therapy for atherosclerotic renal-artery stenosis (CORAL trial). N Engl J Med 2014
• ASTRAL Investigators. Revascularization versus medical therapy for renal-artery stenosis. N Engl J Med 2009
• Defined by the AHA/ACC Renal Artery Stenosis Clinical Practice Guidelines. Circulation 2006
• Defined by the Defined by the ACR Appropriateness Criteria for Renal Artery Stenosis. Radiology 2017
• Defined by the Defined by the ESC/ESVS Guidelines on Peripheral Arterial Diseases 2024

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