Renal artery stenosis in older people

Learning points

Renal artery stenosis (RAS) is a vascular disease characterised by narrowing of one or more main renal arteries or its branches.
Atherosclerosis and fibromuscular dysplasia are two major causes of unilateral RAS.
Atherosclerotic RAS (ARAS) is the leading cause of RAS and usually affects the renal artery ostia, proximal one-third of the main renal artery and the adjacent aorta.
The gold standard for diagnosing RAS is renal arteriography. However, a variety of less invasive tests are being employed for evaluation for testing purposes.
There is a consensus that all with ARAS should be on medical therapy to control hypertension.
Antiplatelet medications and statins should be considered as these patients have a high risk of adverse cardiovascular events.
The indications for revascularisation are less clear and available RCTs have their limitations. Further studies are needed to clearly identify those who will benefit from revascularisation.

Introduction

Renal artery stenosis (RAS) is a vascular disease characterised by narrowing of one or more main renal arteries or its branches. It is a major cause of hypertension, particularly among older people.
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Aetiology

Atherosclerosis and fibromuscular dysplasia are two major causes of unilateral RAS. Atherosclerosis is the leading cause and accounts for more than 90% of cases and fibromuscular dysplasia is the second commonest cause (10% to 30%).¹ Other causes (less than 10%) may include vasculitis (Takayasu arteritis, Buerger’s disease, polyarteritis nodosa), neurofibromatosis type 1, post radiation, and external compression of the renal artery in retroperitoneal fibrosis.²

Atherosclerosis primarily affects patients over the age of 45 years, men in particular, and usually involve the aortic orifice or the proximal 2cm of the main renal artery. Risk factors for atherosclerosis include dyslipidaemia, cigarette smoking, viral infection, immune injury, and increased homocysteine levels.

Fibromuscular dysplasia, in contrast to atherosclerosis, most often affects women younger than the age of 50 years and typically involves the middle and distal main renal artery or the intrarenal branches.²

Pathophysiology

Atherosclerotic RAS (ARAS) is the leading cause of RAS and usually affects the renal artery ostia, proximal one-third of the main renal artery and the adjacent aorta. This contrasts with RAS associated with fibro-muscular dysplasia where the distal two-thirds of the renal arteries tend to be involved.²In advanced cases of ARAS, intra-renal branch arteries can be affected as well. In 20% of patients with ARAS, bilateral renal artery involvement or involvement of a single functioning kidney will be seen.³

Reduction in renal perfusion due to RAS activates the renin–angiotensin system and leads to increased production of angiotensin II. Angiotensin II is a powerful vasoconstrictor and potentiates the vasoconstrictor effects of noradrenaline. It stimulates the production of aldosterone, which increases the circulating blood volume by promoting fluid retention. Hypertension in RAS is attributed to these effects of vasoconstriction and increased circulatory volume. Thus, changes relating to the increased production of angiotensin II could result in secondary hypertension or renovascular hypertension.⁴

When the hypertension is long-lasting, plasma renin activity decreases. Hence plasma renin levels cannot be used as a sensitive indicator to rule out renovascular hypertension.²

The exact contribution of atherosclerotic RAS as a cause for end-stage kidney disease is unknown, but according to Mailloux et al, 12% of patients who were referred for dialysis had ARAS as the predisposing cause for the renal failure.⁵

Ischemic nephropathy or loss in renal mass and deterioration of renal function is a well-known sequel of atherosclerotic RAS. Glomerular filtration rate (GFR) is autoregulated by angiotensin II and other modulators between the afferent and efferent arteries. The maintenance of GFR fails when renal perfusion pressure falls below 70mmHg to – 85mmHg. Therefore, significant functional impairment of autoregulation, leading to a decrease in the GFR, is only likely to be observed until arterial luminal narrowing exceeds 50%. Studies demonstrate that a moderate reduction in renal perfusion pressure (up to 40%) and renal blood flow (mean 30%) cause reduction in glomerular filtration, however, tissue oxygenation within the kidney cortex and medulla can adapt without the development of severe hypoxia.

It is reported that more advanced stenosis corresponding to a 70% to 80% of vascular occlusion leads to demonstrable cortical hypoxia, and it is proposed that this hypoxia produce rarefaction of micro-vessels, as well as activation of inflammatory and oxidative pathways that cause interstitial fibrosis.⁶

Therefore, loss of renal function in renovascular disease in addition to being a usually reversible consequence of antihypertensive therapy can reflect a progressive narrowing of the renal arteries and/or progressive intrinsic renal disease. Eventually, long-standing parenchymal injury becomes an irreversible process. At this point, restoring renal blood flow provides no recovery of renal function or clinical benefit.⁶

It was reported that 19% of patients with ≥60% stenosis of the renal arteries had a more than 1cm loss in renal length at the end of first year. High-grade stenosis, elevated systolic blood pressure, and low velocity flow in the renal cortex on duplex were identified as risk factors for reduction of renal mass.⁷

Epidemiology

The exact incidence of atherosclerotic renal artery stenosis (ARAS) in the general population is unknown as the majority with this condition will remain asymptomatic.¹There seems to be a substantial risk of ARAS in those with atherosclerosis-related vascular disease elsewhere in the body. In patients with coronary artery disease, the prevalence of ARAS is estimated to be 11 to 23%.⁸In a cohort of patients who underwent digital subtraction angiography (DSA) for lower limb claudication or tissue loss, 44.9% had concomitant RAS.⁹

As diabetes is a well-known risk factor for accelerated atherosclerosis, the incidence of ARAS is expected to be high in those with diabetes. In addition, those with ARAS had a significantly higher risk of atherosclerotic heart disease, heart failure, cerebrovascular events, and chronic kidney disease.¹⁰

The prevalence of RAS is probably less than 1% of patients with mild hypertension but can increase to as high as 10 % to 40% in patients with acute (even if superimposed on a pre-existing elevation in blood pressure), severe, or refractory hypertension. Several studies report the prevalence of unilateral stenosis (compared with bilateral stenosis) approximately from 53 % to 80%. Studies suggest that ischaemic nephropathy may be the cause of 5% to 22% of advanced renal disease in all patients older than 50 years.

Patients with fibromuscular dysplasia have involvement of the renal arteries in proximately 75% to 80% of cases. Roughly two-thirds of patients have involvement of multiple renal arteries. Fibromuscular dysplasia is more common in females than in males.¹¹

Clinical presentation

Hypokalaemia, presence of an abdominal bruit, and diagnosis of hypertension at an unusually young age are some classic features associated with RAS.²

Acute onset decompensated heart failure, also known as “flash pulmonary oedema”, is also a presentation that is usually associated with bilateral RAS or RAS affecting a solitary functioning kidney.¹²

ARAS caused by atherosclerosis is a progressive disease. In the study done by Zierler et al, 23% of those with <60% stenosis had progressed to 60% or more by end of the first year. This proportion increased to 42% by two years. Some 5% of those with more than 60% stenosis at diagnosis progressed to complete occlusions by one year. This was 11% at the end of two years.¹³

Life expectancy is reduced in those with ARAS when compared with the general population. This seems to be true when patients with ARAS are compared with well-matched patients with essential hypertension.⁸ Death is usually due to cardiovascular events. The mortality is even higher when ARAS is associated with end-stage renal failure.³

The American Heart Association (AHA) guidelines describe several clinical scenarios where RAS should be suspected and excluded, among them are six possible scenarios^14:

Onset of hypertension before 30 years of age.
Onset of severe hypertension after 55 years of age.
Accelerated hypertension (sudden, persistent worsening of previously controlled hypertension), resistant hypertension (hypertension not controlled with a three-drug regimen which includes a diuretic), and malignant hypertension (hypertension with acute end organ damage).
New onset renal dysfunction or worsening of renal function after starting therapy with an angiotensin-converting enzyme inhibitor (ACEI) or angiotensin receptor blocker (ARB).
Unexplained atrophic kidney or discrepancy in the size of the two kidneys >1.5cm.
Sudden, unexplained pulmonary oedema (especially in patients with azotaemia).

Patients with reno-vascular disease frequently have severe retinopathy, peripheral or coronary vascular disease.^15,16 RAS can complicate pre-existing hypertension. In this presentation, the concern is for patients for whom RAS is complicating the management of their hypertension.

Diagnosis

Laboratory tests

Laboratory tests in patients with possible RAS may comprise:

Blood tests: renal function tests to assess the degree of renal dysfunction
Urinary tests: a 24-hour urine collection or a protein-creatinine ratio on a random void urine specimen, to assess the level of renal dysfunction more accurately and for measuring the degree of proteinuria. The renal vascular disease is more often associated with minimal-to-moderate degrees of proteinuria, which are usually not in the nephrotic range. Urinalysis for seeing red blood cells or red blood cell casts; a hallmark feature of glomerulonephritis.

Serologic tests

Serologic tests for systemic lupus erythematosus or vasculitis if these conditions are suggested, including antinuclear antibodies, C3, C4, antinuclear cytoplasmic antibodies.

Imaging techniques

Imaging tests for the reno-vascular disease is warranted in those who fulfil the following criteria:

The clinical – as well as laboratory- findings suggest a cause of secondary hypertension rather than primary hypertension.
Other causes of secondary hypertension such as primary kidney disease, primary aldosteronism, or pheochromocytoma have been excluded before investigating for renal artery stenosis.
A corrective intervention is planned if a clinically significant stenotic lesion is found.

The gold standard for diagnosing RAS is renal arteriography. However, a variety of less invasive tests are being employed for evaluation for testing purposes. Duplex, computed tomography angiography (CTA) and magnetic resonance angiography (MRA) are non-invasive imaging modalities.¹⁷

The choice of test should be based upon institutional expertise and patient factors. If the non-invasive test is inconclusive and the clinical suspicion remains high, conventional renal arteriography is recommended. Once RAS is suspected, imaging studies should be done to confirm the diagnosis.

Duplex Doppler ultrasonography (Duplex)

Duplex ultrasound is a reliable, cost-effective, readily available, and free of radiation. It is also a non-invasive, relatively inexpensive technique that can be used in patients with any level of renal function However, operator dependency is a disadvantage. Obesity and overlying bowel gas may interfere with proper image acquisition. There is a chance that accessory renal artery may be missed on duplex.¹⁸

When compared against DSA, duplex has a sensitivity of 84 to 92% of and a specificity of 64 to 99% for detecting RAS. It is useful for follow-up imaging after intervention as well.¹⁴

Spectral broadening and increased velocities are indicators of hemodynamically significant stenoses on duplex. When the ratio between renal artery peak systolic velocity (PSV) and aortic PSV (reno-aortic velocity ratio) is above 3.5, it indicates a 60% stenosis. Renal artery PSVs of >150 and 180cm/s are suggestive of 50 and 60% stenoses, respectively.¹⁸

Renal artery resistive index (RI; PSV − end diastolic velocity/PSV) can be calculated using duplex, and a high RI is indicative of renal microvascular disease.¹⁸ There are two approaches are used to detect RAS with Doppler Ultrasound:

Direct visualization of the renal arteries: this approach involves direct scanning of the main renal arteries with colour or power Doppler US followed by spectral analysis of renal artery flow using an anterior or anterolateral approach. Owing to various factors essentially as gas interposition and the anatomy of the left renal artery, a complete examination of both renal arteries can be achieved in only 50%–90% of cases.
Analysis of intra-renal Doppler waveforms: The different segments of kidneys are scanned via trans-lumbar approach systematically to detect a stenosis of a segmental or accessory renal artery.¹⁹

Computed tomography angiography

Computed tomography angiography (CTA) involves exposure to radiation and iodinated contrast material. There is a risk of allergic reactions and contrast-induced nephropathy associated with intravascular contrast injection. It is a useful technique as it avoids arterial catheterisation and puncture and thus the risk of athero-embolism, but it has associated risk of contrast associated nephropathy, particularly in patients with pre-existing chronic kidney disease.

CTA has the ability to acquire excellent images of the renal arteries, especially after three-dimensional reconstruction. The three-dimensional reconstruction of the renal vascular tree is a sensitive and specific method of visualising the whole vasculature including the presence of accessory renal arteries.

Compared to Digital Subtraction Angiography (DSA), it has a sensitivity of 59 to 96% and a specificity of 82 to 99% for detection of RAS.¹⁸

Magnetic Resonance Angiography (MRA)

MR imaging (MRI) does not expose the patient to radiation or iodinated contrast. Gadolinium-based contrast material is used for image enhancement, and those with impaired renal function have a risk of nephrogenic systemic fibrosis when exposed to gadolinium. Claustrophobia and certain MRI incompatible, implantable devices may preclude MRA.¹⁸

Compared with DSA, MRA has a sensitivity of 90 to 100% of and a specificity of 76 to 94% for diagnosing RAS. Different imaging methods can be used:

Time of flight (TOF) in which the high velocity of the blood jet at the level of stenosis appears as signal void or simply black
Phase contrast technique
Gadolinium-enhanced MR angiography: capable of performing breath-hold three-dimensional spoiled gradient-echo imaging with short repetition times and echo times. The angiographic contrast is the result of the T1-shortening effect of the intravenously administered paramagnetic contrast agent.

According to several case studies, MRA has been justified only for diagnosing stenosis situated in the proximal 3 cm to 3.5cm of renal arteries with the limitation to reveal distal renal artery stenosis, segmental renal artery stenosis and the presence of the metallic stent¹⁷. In some cases, renal impairment does not permit the use of contrast, in which case TOF imaging is beneficial.

Digital subtraction angiography

DSA is invasive, and arterial puncture can be associated with risks such as bleeding, dissection, distal embolism, and pseudoaneurysm formation. Additionally, it exposes the patient to radiation and iodinated contrast as well. Considered the gold standard of imaging in RAS, particularly for the confirmation and identification of renal artery occlusion, DSA is rarely used as the preferred first line imaging modality due to the availability and advances in non-invasive techniques.

Other tests

ACE inhibitor scintigraphy, selective renal vein renin studies by “renal venous sampling”, plasma renin activity, and the captopril test are not recommended as diagnostic tests for RAS due to their poor sensitivity and specificity.¹⁴ These tests, such as ‘renal venous sampling’, are used to measure renal renin secretion in order to select hypertensive patients with renal artery blockages who may benefit from renal artery dilation or surgery.

Management

Initial treatment for RAS is observation instead of revascularisation when either stenosis is 50% to 80%, and imaging findings are negative, or the degree of stenosis is less than 50%.

Management would involve serial control every six months with duplex scanning, accurate correction of dyslipidaemia, use of drugs that block platelet aggregation, and drugs to control hypertension.²⁰

The degree of RAS that would justify any intervention attempt is greater than 80% in patients with bilateral stenosis or stenosis in a solitary functioning kidney regardless of whether they have renal insufficiency or not.

When renal function is normal or nearly normal, revascularisation is recommended for prevention of renal insufficiency in certain cases, such as those with renal artery stenosis greater than 80% and up to 85%.²¹

Medical therapy

There is a consensus that all with ARAS should be on medical therapy to control hypertension. Blood pressure in this group of patients is difficult to control and they usually require multiple antihypertensives from different drug classes.¹

As the hypertension is mediated by activation of renin–angiotensin axis, ACEIs or ARBs are frequently used. Starting therapy with these drugs in the setting of bilateral severe RAS, stenosis affecting a single kidney, stenosis with a contralateral atrophic kidney, or stenosis with advanced chronic kidney disease can precipitate acute deterioration of renal function. Caution should be administered in such instances with regular monitoring of renal function, as early withdrawal of the ACEIS/ARBs can halt and reverse the acute kidney injury.¹⁸

ACEIs/ARBs have a mortality benefit in patients with ARAS probably due to mitigation of adverse cardiovascular effects of elevated angiotensin II.^3,18 Beta blockers, calcium channel blockers, and diuretics are other antihypertensive drug classes are often combined with ACEIs/ARBs.

The aim should be to achieve reasonable blood pressure control with the fewest number of drugs and minimum adverse effects.¹⁶ Those with ARAS should be advised to stop smoking, and they are usually started on antiplatelet agents and statins to combat the high risk of adverse cardiovascular events.^14,18

Revascularisation

Non-randomised studies done in the 1990s claimed that there was a benefit in revascularisation for ARAS in terms of improving blood pressure control and stabilisation of renal function.¹⁵ More recent randomised clinical trials (RCTs) have produced evidence that contradict these findings. This had led to a more restricted approach for revascularisation in patients with ARAS.

The CORAL investigators randomised 947 patients with ARAS and hypertension or chronic kidney disease to angioplasty and stenting with medical therapy or medical therapy alone and studied the effects of revascularisation on adverse cardiovascular and renal events. The conclusion of the investigators was that renal artery stenting did not have a significant benefit over medical therapy alone with regard to the clinical end points evaluated.²²

According to the RCT done by the Newcastle Renal Artery Stenosis Collaborative Group, who compared balloon angioplasty with medical therapy versus medical therapy alone for the control of hypertension in patients with ARAS, only a modest improvement of blood pressure was noted by the addition of angioplasty. This effect was only seen in a subgroup of patients with bilateral RAS at the cost of significant periprocedural complications. No patient was cured of hypertension after balloon angioplasty.²³

The expected outcome after revascularisation for ARAS is better control of hypertension or a “cure” of hypertension. However, according to the current evidence from RCTS these outcomes are not achieved despite successful revascularisation. Probably, a majority with RAS and hypertension have essential hypertension and all with RAS and hypertension should not be lumped as having “renovascular hypertension”.²⁴ So, recognition of those with true hypertension caused by atherosclerotic narrowing of their renal arteries and selective revascularisation of these patients would be the key.

At the present, the standard investigations used for diagnosis of RAS do not accurately identify the functional significance of these lesions or predict the response to revascularisation.²⁵The solution to this problem would be a shift in focus that concentrates on the physiological significance of the stenosis rather than its anatomy.

Pressure gradients across the lesion have been studied but they do not correlate well with the severity of hypertension or the serum creatinine level. Novel techniques, such as the use of hyperaemic pressure gradients and calculation of fractional flow reserve, may be better predictors of the hemodynamic significance of the stenosis and the response to revascularisation. The evidence available for the use of these techniques in ARAS is very limited at present, and none of the large scale RCTs that are available have utilised these methods.²⁶

Indications for revascularisation

According to the 2017 guidelines published by the European Society of Cardiology, revascularisation can be considered in patients with ARAS and sudden, unexplained pulmonary oedema or heart failure. This is given as a class-IIb recommendation.³

The indications for revascularisation are much wider according to the AHA guidelines published in 2006:¹⁴

Hemodynamically significant ARAS is associated with resistant hypertension, malignant hypertension, accelerated hypertension, and hypertension associated with an unexplained unilateral small kidney, when the patient is intolerant of antihypertensive medication (Class IIa).
Bilateral ARAS or ARAS in a single functioning kidney accompanied by progressive chronic renal impairment (class IIa).
Unilateral ARAS and chronic renal impairment (class IIb).
Hemodynamically significant RAS with recurrent, unexplained congestive heart failure, or episodes of flash pulmonary oedema (class IIa).
Patients with hemodynamically significant RAS and unstable angina (class IIb).
Hemodynamically significant bilateral ARAS or ARAS in a single functioning kidney in an asymptomatic patient (class IIb).

The lesion is defined as hemodynamically significant when the stenosis is more than 70%, or when 50-70% stenosis accompanies a peak trans-lesional pressure gradient of ≥20 mmHg or a mean pressure gradient of ≥10 mmHg¹⁴.

Options for revascularisation

Angioplasty and stenting

Renal artery angioplasty and stenting is the preferred modality of revascularisation over open revascularisation at present. Stenting is associated with better technical success and lower restenosis compared with balloon angioplasty alone.³ Endovascular techniques are rapidly evolving and studies using drug-eluting stents have reported lower restenosis rates when compared with bare metal stents.²⁷

Open revascularisation

In the current endovascular era, open surgery is reserved when percutaneous intervention fails, for patients with complex renal artery anatomy, and for those who need concomitant open surgery for aortic pathologies such as an aneurysm.³

Conclusion

Renal artery stenosis (RAS) is commonly caused by atherosclerosis, less commonly by fibromuscular dysplasia or other less common causes. Renal artery disease in older people is primarily associated with atherosclerotic reno-vascular disease, and RAS is a major cause of hypertension. Ischemic nephropathy and deterioration of renal function are well-known sequels of atherosclerotic RAS.

Hypertensive patients with clinical as well as laboratory findings suggestive of a secondary cause of hypertension should be considered for imaging tests for reno-vascular disease. Among then those with onset of hypertension before 30 years of age and patients with an onset of severe hypertension after 55 years of age.

Less invasive imaging tests are preferred to establish the diagnosis, and these include Duplex, CTA and MRA. However, if the non-invasive test is inconclusive and the clinical suspicion remains high, conventional renal arteriography is recommended.

All patients with ARAS should be on medical therapy to control the blood pressure. Antiplatelet medications and statins should be considered, as these patients have a high risk of adverse cardiovascular events.

The indications for revascularisation are less clear and available RCTs have their limitations. Further studies are needed to clearly identify those who will benefit from revascularisation. Until more robust evidence emerges, it is rational to follow existing guidelines

Dr Nabil Aly, Consultant physician, Royal Liverpool University Hospital, Liverpool

[email protected]

Mr Hussein Rabee, Consultant vascular surgeon, Countess of Chester Hospital, Chester, Visiting Professor, Chester Medical School, University of Chester

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