Urology Textbook
Clinical Essentials
By Dirk Manski, MD

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Renal Artery Stenosis: Diagnosis and Treatment

Definition of Renal Artery Stenosis

Renal artery stenosis is the narrowing of one or both renal arteries, which can lead to renovascular hypertension and ischemic nephropathy (Sarafidis et al., 2023; Bhalla et al., 2022).

Epidemiology of Renal Artery Stenosis

20–40% of patients with atherosclerosis (peripheral arterial disease, aortic aneurysm, or coronary artery disease) have significant renal artery stenosis; the age at presentation is usually over 50 years. Renal artery stenosis with ischemic nephropathy is the cause of dialysis-dependent kidney failure in 14% of patients over 60 years. Fibromuscular dysplasia causes renal artery stenosis in younger patients and is more common in women.

Etiology and Pathology of Renal Artery Stenosis

Renal Artery Stenosis due to Atherosclerosis

Atherosclerosis is the predominant cause (90%) of renal artery stenosis, mainly affecting the proximal part of the renal artery. The obstruction is caused by eccentric plaques, which narrow the lumen and may lead to dissection or thrombosis with complete vessel occlusion.

Risk factors for atherosclerosis: hyperlipidemia, hypertension, smoking, male sex, genetic predisposition (familial clustering), and diabetes mellitus.

Renal Artery Stenosis due to Fibromuscular Dysplasia

The pathological forms of fibromuscular dysplasia include medial and perimedial fibroplasia, particularly in women aged 25–50 years, and intimal involvement, particularly in children. The obstruction usually causes mid- to distal renal artery lesions. Angiography often shows the characteristic appearance of multifocal dysplasia with a "string-of-beads" morphology.

Other Causes of Renal Artery Stenosis

Aneurysm, neurofibromatosis, middle aortic syndrome (a form of Takayasu arteritis), extrinsic obstruction caused by tumors, radiation effects, and inflammation.

Pathophysiology of Renal Artery Stenosis

A hemodynamically significant renal artery stenosis activates the renin-angiotensin-aldosterone system (RAAS) and leads to renovascular hypertension. In addition, chronic hypoperfusion can cause ischemic nephropathy with renal atrophy and progressive loss of function.

Signs and Symptoms of Renal Artery Stenosis

Clinical suspicion should arise particularly in patients with new-onset or resistant hypertension, hypertensive crises, an abdominal bruit, otherwise unexplained deterioration of renal function, an increase in serum creatinine after initiation of ACE inhibitor or angiotensin receptor blocker therapy, asymmetric kidney size, or recurrent flash pulmonary edema or otherwise unexplained episodes of heart failure.

Diagnostic Workup in Renal Artery Stenosis

Laboratory Tests

Creatinine, eGFR, and electrolytes are used to assess renal function. Mild proteinuria may be present on urinalysis.

Renal Doppler Sonography

Duplex sonography of the renal arteries includes measurement of peak systolic velocity (PSV), end-diastolic velocity (EDV), the reno-aortic ratio (RAR), and the resistive index (RI). Indirect intrarenal signs include the tardus-parvus pattern, characterized by a prolonged systolic upstroke (acceleration) and low peak systolic velocity. Advantages of Doppler sonography include its noninvasive nature, low cost, and feasibility while the patient is taking antihypertensive medication. However, its accuracy is operator-dependent and can be limited by obesity, overlying bowel gas, or unfavorable vascular anatomy.

Flow Velocities in the Renal Artery

The normal peak systolic velocity (PSV) is 80–150 cm/s. The end-diastolic velocity (EDV) is 20–50 cm/s. Renal artery stenosis increases PSV and EDV. A PSV above 180 cm/s and an EDV above 80 cm/s suggest renal artery stenosis.

Reno-aortic Ratio (RAR)

The RAR is calculated from the peak systolic velocities (PSV) in the renal artery and aorta [Equation]. A value above 3.5 suggests renal artery stenosis, provided aortic flow is normal.

The reno-aortic ratio (RAR) >3.5 is typical for renal artery stenosis when normal aortic flow is present. See the aorta.

Resistive Index (RI)

An RI below 0.5 suggests significant renal artery stenosis but is not sufficient as the sole diagnostic criterion. An RI >80% predicts severe organ damage; blood pressure improvement after endovascular intervention or revascularization is unlikely.

CT Angiography

CT angiography is a highly reliable noninvasive method for the morphologic diagnosis of renal artery stenosis and also provides good visualization of calcifications, vascular anatomy, and accessory renal arteries. Disadvantages include ionizing radiation and iodinated contrast medium, so the indication should be considered carefully in patients with advanced renal insufficiency.

MRI Angiography

MR angiography is a good alternative to CT angiography, particularly when iodinated contrast medium should be avoided. However, it is limited in the assessment of smaller branch vessels, by motion artifacts, and in patients with certain implants.

Digital Subtraction Angiography (DSA)

DSA is the reference method for definitive anatomic and hemodynamic assessment of renal artery stenosis. It is used when noninvasive findings are inconclusive or before planned revascularization. Its advantage is the ability to measure the pressure gradient and perform an intervention during the same procedure. Disadvantages include its invasive nature, the risk of embolization, dissection, and bleeding, and contrast medium exposure.

Renal Scintigraphy with Captopril Challenge

Captopril scintigraphy plays only a minor role in modern diagnostics. ACE inhibitors must be paused for one week before the test. Renal scintigraphy is performed before and 1 h after administration of captopril 25 mg p.o. or enalapril 0.04 mg/kg body weight i.v. Pathological findings include decreased unilateral or bilateral function compared with baseline, size differences indicating renal atrophy, delayed time to peak secretion (>11 min), and cortical retention of the radionuclide.

Differential Diagnosis of Renal Artery Stenosis

Important differential diagnoses include primary hyperaldosteronism and, less commonly, other causes of renovascular hypertension such as vasculitis, neurofibromatosis, radiation effects, extrinsic vascular compression, or renin-producing renal tumors (renal cell carcinoma, Wilms tumor).

Page Kidney

Compression of the kidney by a retroperitoneal hemorrhage, a constricting retroperitoneal process, or a renal cyst can cause renin release and renal hypertension.

Chronic Pyelonephritis

Parenchymal scars from chronic pyelonephritis can cause segmental ischemia, renin release, and renal hypertension.

Treatment of Renal Artery Stenosis

Medical Therapy

Medical therapy is the cornerstone of treatment for atherosclerotic renal artery stenosis. The goals are control of arterial hypertension, reduction of cardiovascular risk, and stabilization of renal function. Treatment particularly includes ACE inhibitors or angiotensin receptor blockers, calcium channel blockers, diuretics, beta-blockers, statins, and antiplatelet therapy according to the overall vascular risk profile.

Indications for Interventional Therapy

Invasive treatment of renal artery stenosis (percutaneous transluminal angioplasty or open surgical vascular reconstruction) is indicated in patients with ischemic nephropathy requiring intervention or with insufficient medical control of renovascular hypertension. Intervention is particularly indicated in patients with a solitary kidney or bilateral disease because of the high risk of renal insufficiency.

Endovascular Therapy (Percutaneous Transluminal Angioplasty)

Percutaneous transluminal angioplasty (PTA) can be performed directly after angiography (DSA). In fibromuscular dysplasia, a stent is usually not used. In atherosclerotic renal artery stenosis, primary stent placement is recommended.

Results: Randomized trials in atherosclerotic renal artery stenosis have not shown a general benefit of routine stent placement in addition to modern medical therapy with regard to hard renal or cardiovascular endpoints in unselected patients. The decision to intervene should therefore be individualized and based primarily on high-risk clinical constellations.

Complications: Possible complications include access-site complications, contrast-associated deterioration of renal function, cholesterol embolization, dissection, thrombosis, restenosis, and, rarely, renal infarction or retroperitoneal hemorrhage.

Open Surgical Vascular Reconstruction

Open surgical vascular reconstruction is indicated when relevant concomitant disease is present, such as an aneurysm; when PTA is technically not feasible; or in the event of PTA complications.

Aortorenal (Anatomic) Bypass Operation

Endarterectomy or an interposition graft (vascular prosthesis, saphenous vein, or internal iliac artery) is used to replace the renal artery. An aortorenal bypass is not feasible in the presence of significant atherosclerosis or an aneurysm of the abdominal aorta.

Extra-anatomic Bypass Operation

Alternatives to an anatomic bypass include a left splenorenal bypass and a right hepatorenal bypass.

Results

Open surgical revascularization can be durably successful in selected cases, but it is more invasive than endovascular therapy and is associated with a higher perioperative risk. It is therefore used only selectively today.

Prognosis of Renal Artery Stenosis

The prognosis of atherosclerotic renovascular disease is determined largely by systemic atherosclerosis and the overall cardiovascular risk profile. In advanced ischemic nephropathy, the long-term prognosis is poor.


Index: 1–9 A B C D E F G H I J K L M N O P Q R S T U V W X Y Z

References

Bhalla V, Textor SC, Beckman JA, Casanegra AI, Cooper CJ, Kim ESH, Luther JM, Misra S, Oderich GS; American Heart Association Council on the Kidney in Cardiovascular Disease; Council on Hypertension; Council on Peripheral Vascular Disease; and Council on Cardiovascular Radiology and Intervention. Revascularization for Renovascular Disease: A Scientific Statement From the American Heart Association. Hypertension. 2022 Aug;79(8):e128-e143. doi: 10.1161/HYP.0000000000000217.

Gornik HL, Persu A, Adlam D, Aparicio LS, Azizi M, Boulanger M, Bruno RM, De Leeuw P, Fendrikova-Mahlay N, Froehlich J, Ganesh SK, Gray BH, Jamison C, Januszewicz A, Jeunemaitre X, Kadian-Dodov D, Kim ESH, Kovacic JC, Mace P, Morganti A, Sharma A, Southerland AM, Touzé E, Van der Niepen P, Wang J, Weinberg I, Wilson S, Olin JW, Plouin PF; Working Group ‘Hypertension and the Kidney’ of the European Society of Hypertension (ESH) and the Society for Vascular Medicine (SVM). First international consensus on the diagnosis and management of fibromuscular dysplasia. J Hypertens. 2019 Feb;37(2):229-252. doi: 10.1097/HJH.0000000000002019.

Sarafidis PA, Theodorakopoulou M, Ortiz A, Fernandez-Fernández B, Nistor I, Schmieder R, Arici M, Saratzis A, Van der Niepen P, Halimi JM, Kreutz R, Januszewicz A, Persu A, Cozzolino M. Atherosclerotic renovascular disease: a clinical practice document by the European Renal Best Practice (ERBP) board of the European Renal Association (ERA) and the Working Group Hypertension and the Kidney of the European Society of Hypertension (ESH). Nephrol Dial Transplant. 2023 Nov 30;38(12):2835-2850. doi: 10.1093/ndt/gfad095.



  Deutsche Version: Nierenarterienstenose

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