RAS & RVH

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Overview

Renal artery stenosis (RAS) is the narrowing of the lining of the main artery that supplies the kidney. Depending on the degree of narrowing, patients can develop hypertension called renal vascular hypertension (RVH). This form of hypertension is the most common cause of secondary hypertension.

RVH occurs when RAS produces a critical narrowing of the artery that supplies one of the kidneys. Critical RAS is defined as at least 70% narrowing of the renal artery, based on angiographic (blood vessel x-ray) evaluation.

Reduced blood flow through the renal artery causes the kidney to release increased amounts of the hormone renin. Renin, a powerful blood pressure regulator, initiates a series of chemical events that result in hypertension. Renal vascular hypertension can be very severe and difficult to control.

The kidney with RAS suffers from the decreased blood flow and often shrinks in size (atrophies). This process is called ischemic nephropathy. The other kidney is at risk for developing damage from the hypertension. Often developing hypertensive nephrosclerosis. The persistent elevated blood pressures in this non-stenotic kidney can cause progressive scarring (sclerosis) leading to progressive loss of filtering function in this kidney as well. Both unilateral RAS and bilateral RAS can ultimately lead to chronic renal failure.

Atherosclerotic Renal Artery Stenosis (AS-RAS) and Fibromuscular Dysplasia (FMD)
AS-RAS is due to the build-up of cholesterol on the inner lining of the renal artery. It is exceedingly more common then the unusual case of FMD-RAS.

FMD-RAS
FMD-RAS occurs almost exclusively in women aged 30 to 40 and rarely affects African Americans or Asians. FMD-RAS is due to an abnormality in the muscular lining of the renal artery.

FMD-RAS is often not as well detected on MRA as it is on other non-invasive studies such as, renal scan with ACE-inhibitor challenge, or ultrasound with Doppler interrogation. FMD responds well to angioplasty and stenting. After plasty long-term patency of the lesion is typically seen.

Incidence and Prevalence
Renal vascular disease accounts for less than 1% of all hypertension in people who have moderately increased blood pressure. But in certain high-risk groups, renal vascular disease may be the cause of 10% to 40 % of all hypertension. FMD RAS occurs almost exclusively in women aged 30 to 40 and rarely affects African Americans or Asians.

Risk Factors
Risk factors associated with the development of atherosclerotic RAS include the following:

• Carotid artery disease
• Coronary artery disease
• Diabetes mellitus
• Hypertension (high blood pressure)
• Obesity
• Age
• Peripheral vascular disease (vascular disease in the extremities, e.g., the legs)
• Smoking

There is often a familial history of FMD RAS.

Causes

Most RAS is caused by atherosclerosis or "hardening of the arteries." Atherosclerosis is the build up of cholesterol deposits, or plaque, in the lining of the arteries.

Signs and Symptoms

Conditions that may indicate atherosclerotic RAS include the following:

• Asymmetrical (differently sized and shaped) kidneys seen on ultrasound
• History of calf pain when walking—indicates impaired circulation to the legs
• Intolerance of specific antihypertensive medications—angiotensin-I (ACE-I) inhibitors or angiotensin receptor blockers (ARBs)—with a sudden worsening of renal function
• More than three antihypertensive medications needed for blood pressure control
• New onset of hypertension in a patient over 55
• Presence of a bruit (sound or murmur heard with a stethoscope) in the abdomen (e.g., groin), neck, or other area
• Sudden worsening of high blood pressure in a patient whose blood pressure had been well controlled, especially if the patient is over 60

Diagnosis

The diagnostic method used for renal artery stenosis (RAS) is similar to that used for ischemic nephropathy. The physician may also measure and compare the level of renin, (blood pressure-regulating hormone released by the kidneys), within the right to the left renal veins. If the amount of renin that is released by one-side is markedly higher than the other, this identifies a high renin-releasing kidney consistent with RAS.

Treatment

Medication (e.g., antihypertensive drugs) may be used to control hypertension (high blood pressure).

Diuretics, ACE inhibitors, beta blockers, calcium channel blockers, and angiotensin receptor blockers (ARBs) may be effective. A selective aldosterone inhibitor (e.g., eplerenone [Inspra®]) may be used to treat mild RAS.

These medications are discontinued if they cause a decrease in renal function. In some cases, patients with RAS are resistant to medication for control of blood pressure.

Angioplasty and stenting may be used to improve blood flow. The goal is to improve the circulation of blood flow to the kidney and prevent the release of excess renin, which can help to decrease blood pressure. This helps to prevent atrophy of the kidney. In general, patients with AS-RAS should have stenting done because plasty by itself has a very high incidence of re-stenosis.

Surgery to bypass the narrowing may be performed. If the kidney with RAS has atrophied, a nephrectomy, surgical removal of the kidney, may be advised.

Prognosis
Patients with fibromuscular dysplasia (FMD) RAS often have good, long-term results with angioplasty, but those with atherosclerotic RAS frequently experience a recurrence. Even after partial or complete repair of the narrowed blood vessel, most patients still have hypertension, but require less medication to control it.

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