Patients with RAS may be asymptomatic in many individuals, especially in those with unilateral occlusion. When symptoms are present, they will manifest in accordance with the length of onset, the severity, duration of renal vascular insufficiency, and whether the blockage is unilateral or bilateral.

In acute cases of complete obstruction, the clinical picture includes fever, nausea, emesis, abdominal pain, flank pain, hematuria, and oliguria/anuria. Furthermore, evidence of acute kidney injury develops after 24 hours. Patients will also exhibit signs of the underlying etiology such as thromboembolism.

Chronic stenosis results in hypertension that is resistant to antihypertensives. Hypertension will initially present at an atypical age, prior to the age of 35 or after 55. Moreover, previously well-controlled hypertension that suddenly worsens is another profile for longstanding RAS. Patients with chronic RAS slowly develop features of chronic renal disease.

Physical exam

Remarkable findings on the physical exam include abdominal bruit, especially on the flank. Additionally, patients with congestive heart failure (CHF) will exhibit signs such as peripheral edema among others.

Any patient with a clinical picture that is suggestive of RAS, such as presenting with hypertension at an atypical age or becoming suddenly refractory to antihypertensives, warrants a clinical evaluation. The workup consists of a thorough history including pre-existing risk factors, a complete physical examination, and pertinent studies.

Laboratory tests

Renal function is assessed by the serum creatinine level, which is also a variable used in predicting the GFR in the Modification of Diet in Renal Disease (MDRD) formula [14]. Further studies include a 24-hour urine collection and the protein-creatinine ratio of a urine sample, which would determine the degree of proteinuria. A urinalysis should be performed to exclude causes such as glomerulonephritis, which is typified by the presence of red blood cells and casts. Finally, serologic tests such as antinuclear antibodies and complements can evaluate for the presence of vasculitis and systemic lupus erythematosus (SLE).

Imaging

There are numerous studies that can be utilized in the evaluation of patients suspected to have RAS as described below.

The preferred method for confirmation of renal artery occlusion in patients with intermediate renal disease is arteriography. While conventional aortography yields superior images of the renal artery, the procedure is associated with serious risks since it entails arterial puncture and requires contrast. The complication rate is as much as 10% and encompasses sequelae such as cholesterol thromboembolism and contrast-induced acute tubular necrosis (ATN).

The noninvasive magnetic resonance angiography (MRA) technique reveals the anatomy of the renal vasculature and provides detailed information regarding the physiological renal function such as the GFR, blood flow rate, and perfusion rate. It also depicts the size of the kidneys. The shortcomings of this test are that it is expensive and is contraindicated in individuals with metallic clips, devices, and pacemakers.

Another useful tool is the spiral computed tomography (CT) angiography, which produces imaging of the renal artery and its anatomy. It does not involve catheterization.

Ultrasonography of the kidneys is a commonly performed study in those with renal impairment. Asymmetrical kidney size is suggestive of RAS.

A helpful noninvasive test is the Duplex ultrasonographic scanning, which ascertains the flow velocity by incorporating B-mode imaging with a pulse Doppler. This test demonstrates both 98% sensitivity and specificity. While it can be used in patients with any degree of dysfunction, it is not widely available since it requires specialized technicians.

Patients suspected to have fibromuscular disease with normal kidney function should undergo radionuclide scanning preceded by a dose of captopril.

Limitations of imaging tests

Contrast dyes place the patients at risk for nephrotoxicity in up to 40% of patients with chronic renal failure. They exhibit a brief elevation in creatinine 3 to 6 days following exposure. Fortunately, the majority recover as less than 10% requires permanent dialysis.

The treatment of RAS depends on its etiology, the degree of renal insufficiency, and how well the blood pressure is controlled.

Revascularization

The therapeutic approach for patients with significant obstruction in both renal arteries or in a sole functioning one is the same regardless of the functional renal status. With regards to those with normal function, revascularization is recommended for prevention of kidney failure in patients with 1) stenosis greater than 80% to 85% and 2) stenosis ranging from 50% to 80% with infrarenal occlusion demonstrated on captopril-enhanced scintigraphy.

Additionally, revascularization is performed to improve renal function and to prevent further deterioration of renal impairment. The criteria for this group of patients include 1) serum creatinine concentration below 4 mg/dL or 2) serum creatinine concentration above 4 mg/dL accompanied by a probable acute thrombosis of the renal artery.

Some studies have reported that greater than 50% of patients showed improvement in renal function after surgery [7].

Angioplasty

Patients with chronic RAS warrant percutaneous transluminal angioplasty (PTA) with stenting if they have refractory hypertension despite treatment with at least three drugs, worsening renal function, recurrent episodes of flash pulmonary edema, or rapid deterioration of renal impairment of unknown cause. Revascularization and surgical resection of the infarcted kidney are other options for longstanding stenosis.

The treatment of acute RAS secondary to renal thromboembolism may consist of anticoagulation, fibrinolytics, and/or surgical intervention. The latter is associated with a higher mortality although it is favored in cases of traumatic etiology.

Other indications for angioplasty are renovascular hypertension (due to atheromas) and fibromuscular dysplasia of the renal artery.

Renal hypertension

Treatment of renal hypertension is effective when vascular patency is established. Pharmacologic therapy such as angiotensin-converting enzyme (ACE) inhibitors, angiotensin II receptor blockers, or renin inhibitors is beneficial in unilateral stenosis. They may be used in bilateral occlusion if the GFR is measured periodically.

Other

Patients should adhere to a healthy diet with salt restriction, physical exercise, smoking cessation, and control of hypertension and diabetes.

In patients receiving medical therapy, studies have demonstrated that progressive occlusion was observed in up to 53% of those with RAS secondary to atherosclerosis, especially in those with a high degree of obstruction [13].

Since atherosclerosis is responsible for a large percentage of RAS cases, the prognosis is poor. Renovascular disease encompasses the medical syndromes involving cardiac complications, ischemic nephropathy, and hypertension.

There are numerous risk factors associated with the development of RAS such as hypertension, older age especially in those over 60, renal impairment, atherosclerosis, diabetes mellitus, and smoking.

Acute cases are attributed to thromboembolism. The emboli mostly emerge from the heart or the aorta although fat and tumor may be the causative factors. Clots form either spontaneously or as a consequence of events such as dissection, trauma, surgery, or cardiovascular procedures such as angiography or angioplasty. Acute conditions have unilateral involvement.

The etiology of chronic renal artery stenosis is atherosclerosis in 90% of patients. The second most common cause is fibromuscular dysplasia (FMD), which occurs in young women [1]. The obstruction is bilateral in the former while typically unilateral in the latter.

The patient demographics for RAS demonstrates a strong predilection for men, who have twice the prevalence of women. With regards to race, white and African Americans are affected equally [2].

Structural changes

Chronic ischemia in RAS results in structural changes at the tubular level of the kidneys, which include atrophy of tubular cells, fibrosis, inflammation, tubulosclerosis, and thickening of the medial layer of the renal artery and Bowman capsule.

Physiologic changes

To compensate for the decreased perfusion, the kidneys employ adaptive physiologic mechanisms. The autoregulatory system maintains the glomerular filtration rate (GFR) during systemic blood pressure fluctuations ranging from 80 to 180mmHg. In the case of RAS, key modulators such as angiotensin II play a role in the autoregulation between afferent and efferent arteries. When the renal perfusion pressure is reduced to less than 70 to 85mm Hg, the autoregulatory mechanisms struggle to restore GFR. Significant compromise of this system occurs when the stenosis is above 50%.

Complications

RAS is the second most common cause of hypertension [3]. and leads to end-stage kidney disease in 10% receiving renal dialysis [4] [5].

Nearly 25% of elderly patients with renal impairment have undiagnosed underlying RAS [6] [7]. The latter is likely to manifest in patients with atherosclerosis in the cerebral, coronary, or peripheral vasculature [8].

Additionally, RAS is present in 30% to 40% of cases with abdominal aortic aneurysm or peripheral artery disease [9] [10]. and in as much as a third of individuals undergoing cardiac catheterization for heart disease [11] [12].

Strategies for the prevention of atherosclerosis is the same for RAS. Patients are advised to address key lifestyle modifications such as eating a healthy diet, engaging in physical activity, smoking cessation, limiting alcohol intake, control of hypertension and diabetes, and weight maintenance. All individuals are encouraged to follow-up regularly with their physician.

Renal artery stenosis (RAS) is defined as the unilateral or bilateral occlusion of renal arteries. This condition has varying etiologies depending on its onset. For example, acute RAS is attributed to thromboembolism originating from the heart or other sites while the majority of patients with chronic progressive stenosis is the result of atherosclerosis. There are also risk factors associated with RAS that include hypertension, atherosclerosis, advanced age, renal dysfunction, hypertension, diabetes mellitus, and smoking.

The symptoms in acute occlusion are fever, flank pain, hematuria, and other related symptoms. Furthermore, hypertension in patients with chronic blockage develops at an atypical age and is unresponsive to antihypertensives.

Patients suspected to have RAS should be evaluated in terms of their overall clinical picture, history and risk factors, and diagnostic studies. There are important laboratory measurements and imaging techniques employed to determine the presence of obstruction and the function of the kidney.

Treatment is selected based on but not limited to the onset of RAS, degree of narrowing, renal dysfunction, and the number of renal arteries affected. Surgical revascularization, angioplasty, and medical drugs may be options depending on the overall clinical presentation of the patient.

Prevention of RAS is based on prevention of atherosclerosis. Therefore, patients are advised to address the modifiable risk factors.

What is renal artery stenosis?

The renal arteries carry blood to the kidneys. Stenosis means blockage. Hence, this condition refers to the disease in which there is a blockage in one or both arteries the supply the kidney(s).

What are its causes?

When the stenosis is acute (rapid onset), the condition is due to a blood clot in the renal artery. When the stenosis is chronic (long-term), the majority of cases is due to atherosclerosis while a few cases are due to fibromuscular dysplasia (in young women).

There are risk factors for developing renal artery stenosis:

• Hypertension
• Older age especially in those over 60
• Kidney impairment
• Atherosclerosis
• Diabetes mellitus
• Smoking

What are the signs and symptoms of this disease?

In acute cases due to blood clots, the symptoms are:

• Fever
• Nausea
• Vomiting
• Achy flank pain
• Blood in the urine
• Low volume or no volume of urine
• Acute kidney failure

In chronic cases, the clinical presentation includes:

• Hypertension that presents for the first time prior to the age of 35 or after 55
• Previously well-controlled hypertension that suddenly worsens
• Hypertension does not successfully respond to medications

How is it diagnosed?

The doctor will assess the patient's overall clinical picture, history, and risk factors. Also, the doctor will perform a physical exam and obtain important studies such as:

Labs

• Serum creatinine level
• 24-hour urine collection
• Urinalysis
• Serologic tests such as antinuclear antibodies and complements

Imaging tests

• Spiral computed tomography (CT) angiography
• Magnetic resonance angiography
• Arteriography
• Ultrasonography

How is it treated?

In patients with acute renal artery blockage, the treatment consists of anticoagulation medications, fibrinolytics, and/or surgical procedures.

In patients with chronic blockage, the treatment includes surgical bypass, angioplasty with stent placement, and resection of the affected kidney.

How can it be prevented?

Patients are advised to adhere to lifestyle changes such as the following:

• Eating a healthy diet
• Exercising
• Quitting smoking
• Limiting alcohol intake
• Controlling hypertension
• Controlling diabetes
• Weight loss

All individuals are encouraged to follow-up regularly with their physician.

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