The kidneys filter waste, maintain fluid balance, and regulate blood pressure. Blood reaches these organs through the renal arteries, direct branches off the aorta. Renal artery stenosis (RAS) occurs when one or both arteries become narrowed, limiting blood supply to the kidneys. This restriction affects the circulatory system, potentially leading to chronic high blood pressure and a decline in kidney function.
Defining Renal Artery Stenosis
The term “stenosis” refers to the abnormal narrowing of a bodily passage, describing the restriction of the renal arteries that supply blood to the kidneys. When the kidney detects decreased blood flow, it misinterprets this signal as low overall body blood pressure (renal ischemia). In response, the kidney activates the Renin-Angiotensin-Aldosterone System (RAAS) to restore its perceived blood flow.
The kidney releases the enzyme renin, which ultimately produces the hormone angiotensin II. Angiotensin II is a potent vasoconstrictor, narrowing blood vessels and causing blood pressure to rise. It also prompts the release of aldosterone, a hormone that causes the body to retain salt and water, further increasing blood volume and pressure. The resulting systemic hypertension can damage blood vessels and heart tissue over time.
Primary Causes and Risk Factors
Most RAS cases (approximately 90%) are caused by atherosclerosis. This involves the gradual buildup of plaque—composed of cholesterol, fat, and other substances—on the inner walls of the renal arteries. This narrowing typically affects the opening or the first two centimeters of the main renal artery. Risk factors for RAS mirror those for other cardiovascular diseases, including advanced age, smoking, high cholesterol, diabetes, and pre-existing high blood pressure.
A less common cause, particularly in younger individuals, is Fibromuscular Dysplasia (FMD), accounting for 10% to 20% of cases. FMD is a non-inflammatory, non-atherosclerotic condition where cells in the artery walls grow abnormally, causing sections of the artery to constrict and dilate, often giving the vessel a characteristic “string of beads” appearance on imaging. FMD is more frequently seen in women under the age of 50 and often involves the middle or outer portions of the renal artery. FMD is a systemic disorder that can also affect other vessels, such as the carotid arteries.
Recognizable Signs and Symptoms
RAS often remains asymptomatic, becoming apparent only when narrowing significantly impairs blood flow. The most common presentation is resistant or secondary hypertension—high blood pressure difficult to control despite treatment with three or more different classes of anti-hypertensive medications. This secondary hypertension can appear suddenly, especially in patients younger than 30 or older than 55.
Another warning sign is an unexplained worsening of kidney function, often detected through elevated creatinine levels. This decline may be noticeable after a patient begins taking certain blood pressure medications, such as Angiotensin-Converting Enzyme (ACE) inhibitors or Angiotensin II Receptor Blockers (ARBs). These medications interfere with the RAAS and can reduce the pressure needed to filter blood through the narrowed artery. In severe cases, patients may experience flash pulmonary edema, a sudden buildup of fluid in the lungs resulting from the heart’s inability to manage fluid and pressure overload.
Methods of Diagnosis and Assessment
Diagnosis begins with a physician’s suspicion based on symptoms like resistant hypertension or a sudden decline in kidney function. A physical examination might reveal an abdominal bruit, a whooshing sound caused by turbulent blood flow through the narrowed artery, heard over the abdomen. Non-invasive imaging techniques are then used to visualize the arteries and confirm the diagnosis.
The most common initial test is Duplex Ultrasound, which uses sound waves to measure blood flow in the renal arteries, indicating the severity of narrowing. Other non-invasive methods include Computed Tomography Angiography (CTA) and Magnetic Resonance Angiography (MRA). Both provide detailed cross-sectional images of the blood vessels, often using a contrast agent to highlight the degree of stenosis. While effective for screening, definitive confirmation often requires a more invasive procedure, such as Renal Angiography, which involves threading a catheter through the arteries to visualize the blockage and measure pressure differences.
Treatment Approaches
Management focuses on controlling blood pressure, preserving kidney function, and minimizing cardiovascular complications. The primary treatment is medical management, which includes anti-hypertensive medications to counteract the effects of the overactive RAAS. While ACE inhibitors and ARBs are commonly used, they must be used cautiously in patients with severe bilateral disease or a single functioning kidney, as they can sometimes worsen kidney function. Diuretics, beta-blockers, and calcium channel blockers are also prescribed to help manage blood volume and reduce the heart’s workload.
Lifestyle modifications are a fundamental part of the treatment plan, particularly for those with atherosclerotic disease. Patients are advised to adopt a diet low in sodium and fat, engage in regular physical activity, and cease smoking, as tobacco use accelerates arterial damage. These changes help manage the underlying risk factors for plaque buildup and cardiovascular health.
Revascularization procedures may be considered when high blood pressure remains uncontrolled or when kidney function is rapidly declining. The most common procedure is percutaneous transluminal renal angioplasty, often combined with stent placement. This involves inflating a balloon to widen the narrowed artery and leaving a small mesh tube in place to keep the vessel open. Stenting is typically preferred for atherosclerotic RAS, while balloon angioplasty alone is often sufficient for FMD-related stenosis. Although revascularization can improve blood flow, studies suggest that for many patients with atherosclerotic disease, it may not be superior to aggressive medical therapy in preventing long-term cardiovascular events.