Renal Artery Stenosis

Renal artery stenosis (RAS) is the narrowing of one or both of the renal arteries, most often caused by atherosclerosis or fibromuscular dysplasia. This narrowing of the renal artery can impede blood flow to the target kidney, resulting in renovascular hypertension – a secondary type of high blood pressure. Possible complications of renal artery stenosis are chronic kidney disease and coronary artery disease.

Signs and symptoms

Most cases of renal artery stenosis are asymptomatic, and the main problem is high blood pressure that cannot be controlled with medication. Decreased kidney function may develop if both kidneys do not receive adequate blood flow, furthermore some people with renal artery stenosis present with episodes of flash pulmonary edema.

Cause

Renal artery stenosis is most often caused by atherosclerosis which causes the renal arteries to harden and narrow due to the build-up of plaque. This is known as atherosclerotic renovascular disease, which accounts for about 90% of cases. This narrowing of renal arteries due to plaque build-up leads to higher blood pressure within the artery and decreased blood flow to the kidney. This decreased blood flow leads to decreased blood pressure in the kidney, which leads to the activation of the Renin-Angiotensin-Aldosterone (RAA) system. Juxtaglomerular cells secrete renin, which converts angiotensinogen to angiotensin I, which is then converted to angiotensin II by angiotensin converting enzyme (ACE). Angiotensin II then acts on the adrenal cortex to increase secretion of the hormone aldosterone. Aldosterone causes sodium and water retention, leading to an increase in blood volume and blood pressure. Therefore, people with RAS have chronic high blood pressure because their RAA system is hyperactivated.

Pathophysiology

The pathophysiology of renal artery stenosis leads to changes in the structure of the kidney that are most noticeable in the tubular tissue.

Changes include:
* Fibrosis
* Tubular cell size (decrease)
* Thickening of Bowman capsule
* Tubulosclerosis
* Glomerular capillary tuft (atrophy)

Diagnosis

The diagnosis of renal artery stenosis can use many techniques to determine if the condition is present, a clinical prediction rule is available to guide diagnosis.

Among the diagnostic techniques are:
* Doppler ultrasound study of the kidneys
* Refractory hypertension
* Auscultation (with stethoscope) - bruit ("rushing" sound)
* Captopril challenge test
* Captopril test dose effect on the differential renal function as measured by MAG3 scan.
* Renal artery arteriogram.

The specific criteria for renal artery stenosis on Doppler are an acceleration time of greater than 70 milliseconds, an acceleration index of less than 300 cm/sec² and a velocity ratio of the renal artery to aorta of greater than 3.5.

Treatment

Atherosclerotic renal artery stenosis

It is initially treated with medications, including diuretics, and medications for blood pressure control. When high-grade renal artery stenosis is documented and blood pressure cannot be controlled with medication, or if renal function deteriorates, surgery may be resorted to. The most commonly used procedure is a minimally-invasive angioplasty with or without stenting. It is unclear if this approach yields better results than the use of medications alone. It is a relatively safe procedure. If all else fails and the kidney is thought to be worsening hypertension and revascularization with angioplasty or surgery does not work, then surgical removal of the affected kidney (nephrectomy) may significantly improve high blood pressure.

Stenting v.s. Medical Treatment

Historically, balloon dilation of vascular lesions was first performed in 1964. The first treatment of renovascular lesions by percutaneous catheter angioplasty (PTA) was performed in 1978 by Andreas Roland Grüntzig. Stenting became the standard of endovascular care for ostial stenoses because of the poor technical success of PTA. The use of renal artery stents, particularly for ostial lesions, has further improved long-term patency rates. Further research into the efficacy of renal artery stenting has since been conducted, including the ASTRAL and CORAL trials, and research is ongoing as to whether there is clear benefit to stenting over more conservative management such as by medications alone.

The ASTRAL trial randomized 806 patients to renal artery revascularization via stenting versus medical therapy, with the following results:
* No survival advantage in the stented group
* No benefit for renal function in the stented group
* Serious complications with stenting (2 deaths, 3 amputations, others)

The CORAL study randomized 947 patients to stenting versus medical therapy, with a primary endpoint of major cardiovascular or renal events. Similarly, this study also found there was no benefit to stenting over medical treatment alone.

Collectively, the evidence so far does not support renal artery stenting as a proper mainstay treatment for stenosis because it conveys no survival benefit, no true renoprotection, and does not decrease the need for antihypertensive medications. A debate remains about whether or not it is beneficial to stent for purely ostial lesions, and comparing the success in treating with angioplasty (such as ballon dilatation) versus stenting. Smoking cessation and thoughtful blood pressure control, via lifestyle/dietary changes and medication, are the current mainstays of managing renovascular hypertension.

Fibromuscular dysplasia

Angioplasty alone is preferred in fibromuscular dysplasia, with stenting reserved for unsuccessful angioplasty or complications such as dissection.

References

Further reading

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External links

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