Renovascular hypertension is a specific type of high blood pressure caused by the narrowing of one or both of the main arteries that supply blood to the kidneys. This condition is classified as secondary hypertension, meaning it has an identifiable underlying cause, unlike primary hypertension which develops without a known reason. Because the root cause is structural, this form of high blood pressure is potentially correctable through targeted intervention.
The Mechanism of Renovascular Hypertension
The narrowing of the renal artery reduces blood flow to the kidney, creating a state of perceived dehydration or low blood pressure within the organ. The kidney interprets this reduction in flow as a body-wide emergency, triggering a complex hormonal cascade known as the Renin-Angiotensin-Aldosterone (RAA) system. Specialized cells in the kidney respond to the low pressure by releasing an enzyme called renin into the bloodstream.
Renin acts on a protein produced by the liver, converting it into Angiotensin I, which is then transformed into Angiotensin II by an enzyme found predominantly in the lungs. Angiotensin II has two powerful effects on the circulatory system. First, it causes the muscular walls of small arteries throughout the body to constrict, which dramatically increases systemic blood pressure.
Second, Angiotensin II stimulates the adrenal glands to release the hormone aldosterone. Aldosterone signals the kidney tubules to retain salt (sodium) and water, increasing the volume of fluid circulating in the bloodstream. This dual action of constricting blood vessels and increasing blood volume raises the body’s overall blood pressure, resulting in sustained hypertension throughout the body.
Primary Causes of Renal Artery Narrowing
Renal artery stenosis is overwhelmingly caused by one of two distinct diseases. The most common cause is atherosclerosis, which involves the hardening and plaque buildup within the artery wall. This typically affects older patients, particularly those with existing risk factors such as high cholesterol, diabetes, and smoking. The blockage usually forms near the opening where the renal artery branches off the aorta.
The second major cause is Fibromuscular Dysplasia (FMD), an abnormal growth of cells within the walls of the artery unrelated to plaque buildup. FMD most often affects younger individuals, particularly women between the ages of 25 and 50. Unlike atherosclerosis, FMD often creates multiple constrictions and bulges along the middle and end segments of the artery, giving it a characteristic “string-of-beads” appearance on imaging.
Identifying and Confirming Renovascular Hypertension
Clinical suspicion for renovascular hypertension often arises when a patient presents with specific, atypical features of high blood pressure. These clues include a sudden onset of severe hypertension, blood pressure resistant to standard medications, or a rapid worsening of previously controlled hypertension. Another finding that raises suspicion is an abdominal bruit, a whooshing sound caused by turbulent blood flow through the narrowed artery.
To move from suspicion to confirmed diagnosis, non-invasive imaging techniques are used to visualize the renal arteries and assess blood flow. Renal Duplex ultrasound is a common initial test that uses sound waves to measure the speed of blood flow, which accelerates significantly through a narrowed segment. More detailed anatomical confirmation is often achieved with Computed Tomography Angiography (CTA) or Magnetic Resonance Angiography (MRA).
Both CTA and MRA provide high-resolution images of the renal arteries, clearly showing the location and extent of the narrowing. While these non-invasive methods are highly effective for screening, the most definitive test remains catheter-based renal angiography. This more invasive procedure involves threading a small tube through the blood vessels to inject a contrast dye directly into the renal artery, providing the clearest possible image of the blockage.
Management and Treatment Options
Treatment for renovascular hypertension focuses on two concurrent goals: controlling the patient’s high blood pressure and restoring proper blood flow to the affected kidney. Medical management involves the use of anti-hypertensive medications to lower blood pressure and protect organs from damage. However, caution is necessary with certain drug classes, such as ACE inhibitors and Angiotensin Receptor Blockers (ARBs), which block the RAA system. These medications can be highly effective when only one kidney artery is narrowed, but they can cause a sudden, severe decline in kidney function if the stenosis is present in both renal arteries.
For patients with significant or progressive narrowing, interventional procedures are often considered to physically open the blocked vessel. The primary minimally invasive treatment is percutaneous transluminal renal angioplasty. During this procedure, a balloon-tipped catheter is guided to the stenosis and inflated to compress the plaque or abnormal tissue against the artery wall.
For cases of atherosclerotic disease, a small mesh tube called a stent is frequently placed after the balloon expansion to keep the artery open and prevent it from narrowing again. In rare and complex cases, such as those involving extensive disease or failed angioplasty, surgical revascularization, which involves a bypass graft to reroute blood flow around the blockage, may be necessary.