Renal artery stenosis (narrowing) is a decrease in the diameter of the renal arteries. The resulting restriction of blood flow to the kidneys may lead to impaired kidney function (renal failure) and high blood pressure (hypertension), referred to as renovascular hypertension, or RVHT (“reno” for kidney and “vascular” for blood vessel).
Renovascular hypertension is as likely to occur with bilateral stenosis (when arteries to both kidneys are narrowed) as with unilateral stenosis (when the artery to one kidney is narrowed).
The decreased blood flow to the kidneys impairs renal function. Renal artery stenosis may cause renal failure in some patients. There is no predictable relationship between renal failure and renal artery stenosis.
Some patients have very severe bilateral stenosis and normal renal function. Most cases of renal failure are related to diabetes, hypertension, glomerular sclerosis, contrast nephropathy, drug toxicity and other causes.
What are the causes of renal artery stenosis?
The majority of renal artery stenosis is caused by atherosclerosis (hardening and narrowing of blood vessel wall from the inside) similar to the process that occurs in blood vessels in the heart and other parts of the body.
Risk factors for atherosclerosis include:
- high cholesterol levels
- high blood pressure
- cigarette smoking
Less common causes of renal artery stenosis are fibromuscular dysplasia of the vessels (narrowing of the vessel due to internal thickening of the blood vessel wall), arteritis (inflammation of the blood vessel), or dissection (tearing and division of the blood vessel wall).
How common is renal artery stenosis?
Narrowing of the kidney arteries is more common in individuals 50 years of age and older. It is estimated that some degree of narrowing (greater than 50%) is found in about 18% of adults between 65-75 years of age and 42% of those older than 75 years of age.
This may be due to the fact that atherosclerosis is more common in this age group.
In younger patients, the narrowing of the renal artery usually is due to the thickening of the artery (fibromuscular dysplasia) and it is more common in women than men.
It is estimated that renal artery stenosis accounts for approximately 1% of mild to moderate cases of high blood pressure.
It may be responsible for more than 10% of cases of severely elevated or difficult to treat high blood pressure (hypertension).
Symptoms and Signs
Manifestations depend on rapidity of onset, extent, whether unilateral or bilateral, and duration of renal hypoperfusion.
Stenosis of one renal artery is often asymptomatic for a considerable time.
Acute complete occlusion of one or both renal arteries causes steady and aching flank pain, abdominal pain, fever, nausea, and vomiting.
Gross hematuria, oliguria, or anuria may occur; hypertension is rare. After 24 h, symptoms and signs of acute kidney injury may develop (see Symptoms and Signs).
If the cause was thromboembolic, features of thromboembolism at other sites (eg, blue toes, livedo reticularis, retinal lesions on funduscopic examination) also may be present.
Chronic progressive stenosis causes hypertension, which may begin at an atypical age (eg, < 30 yr or after age 50 yr) and which may be refractory to control despite use of multiple antihypertensives.
Physical examination may detect an abdominal bruit or signs of atherosclerosis. Symptoms and signs of chronic kidney disease (see Symptoms and Signs) develop slowly.
Diagnosis Clinical suspicion Imaging Diagnosis is suspected in patients with renal failure and who have Symptoms of acute renal artery occlusion Symptoms or signs of thromboembolism Hypertension that begins before age 30 or is refractory to treatment with > 3 antihypertensive drugs
Blood and urine tests are done to confirm renal failure. Diagnosis is confirmed by imaging tests.
Which tests are done depends on the patient’s renal function and other characteristics and on test availability.
Some tests (CT angiography, arteriography, digital subtraction angiography) require an IV ionic radiocontrast agent, which may be nephrotoxic; this risk is lower with the nonionic hypo-osmolar or iso-osmolar contrast agents that are now in widespread use (see Radiographic Contrast Agents and Contrast Reactions).
Magnetic resonance angiography (MRA) requires the use of gadolinium contrast; in patients with severe chronic kidney disease, gadolinium contrast carries the risk of nephrogenic systemic fibrosis, a condition that closely resembles systemic sclerosis and that has no satisfactory method of treatment.
When results of other tests are inconclusive or negative but clinical suspicion is strong, arteriography is necessary for definitive diagnosis. Arteriography may also be needed before invasive interventions.
When a thromboembolic disorder is suspected, ECG (to detect atrial fibrillation) and hypercoagulability studies may be needed to identify treatable embolic sources.
Transesophageal echocardiography is done to detect atheromatous lesions in the ascending and thoracic aorta and cardiac sources of thrombi or valvular vegetations.
Blood and urine tests are nondiagnostic but are done to confirm renal failure, indicated by elevated creatinine and BUN and by hyperkalemia. Leukocytosis, gross or microscopic hematuria, and proteinuria may also be present.
Restoration of vascular patency in acute occlusions and, if patients have refractory hypertension or potential for renal failure, in chronic stenosis
Treatment depends on the cause.
Acute renal artery occlusion: A renal thromboembolic disorder may be treated with a combination of anticoagulation, fibrinolytics, and surgical or catheter-based embolectomy.
Treatment within 3 h of symptom onset is likely to improve renal function. However, complete recovery is unusual, and early and late mortality rates are high because of extrarenal embolization or underlying atherosclerotic heart disease.
Patients presenting within 3 h may benefit from fibrinolytic (thrombolytic) therapy (eg, streptokinase, alteplase) given IV or by local intra-arterial infusion (see Fibrinolytics). However, such rapid diagnosis and treatment are rare.
All patients with a thromboembolic disorder require anticoagulation with IV heparin, unless contraindicated.
Long-term anticoagulation with oral warfarin can be initiated simultaneously with heparin if no invasive intervention is planned.
Anticoagulation should be continued for at least 6 to 12 mo—indefinitely for patients with a recurrent thromboembolic disorder or a hypercoagulability disorder.
Surgery to restore vascular patency has a higher mortality rate than fibrinolytic therapy and has no advantage in recovery of renal function.
However, surgery, particularly if done within the first few hours, is preferred for patients with traumatic renal artery thrombosis.
If patients with nontraumatic, severe renal failure do not recover function after 4 to 6 wk of drug therapy, surgical revascularization (embolectomy) can be considered, but it helps only a few.