Renovascular hypertension is a type of secondary high blood pressure caused by the narrowing of the arteries that supply blood to the kidneys.
This narrowing of the renal artery reduces blood flow to the kidneys. In response, the kidney produces a protein called renin, which enters the bloodstream and acts as an enzyme, causing sodium retention and constriction of arterioles (small blood vessels), ultimately leading to high blood pressure.
Primary hypertension, the most common form of high blood pressure, occurs without a known cause and accounts for 90% of cases. In contrast, secondary hypertension is caused by a specific underlying condition. Renal hypertension is the most common cause of secondary hypertension, although it accounts for only about 1% of all cases of high blood pressure.
There are two main types of renovascular hypertension:
In addition, narrowing of the renal artery may result from other factors such as compression due to trauma, tumors, or blood clots (thrombosis or embolism).
The main risk factors that increase a person's chances of developing hypertension, including renovascular hypertension, are as follows:
Symptoms of renovascular hypertension are often absent or subtle and are similar to those of high blood pressure, which can sometimes be severe.
Kidney problems may also occur if glomerular filtration decreases. Kidney failure can be indicated by an abnormally high blood creatinine level or by a creatinine clearance test result that is lower than normal.
Renovascular hypertension should be suspected when hypertension suddenly develops in patients under 30 or over 55, or when hypertension abruptly worsens in any patient.
In many cases, increased levels of albumin in the urine (proteinuria) can be an early sign of renovascular hypertension. Sometimes, atherosclerosis in the renal arterioles causes protein loss in the urine even years before high blood pressure or kidney damage appears.
Narrowing of the renal arteries should also be suspected in individuals with other signs of atherosclerosis, such as coronary artery disease, aortic atherosclerosis, or peripheral artery disease.
Although there is no single test for diagnosing renovascular hypertension, about half of the patients with this condition may present a specific cardiovascular sound that can be detected by a doctor listening to the upper abdomen with a stethoscope.
There is a test called captopril enography with 99mTc-MAG3 that can be performed if renal artery damage is suspected before symptoms appear. A normal result from this test can provide high certainty that the renal arteries are healthy.
When symptoms are already present, imaging studies may be used to aid in diagnosis:
Today, efforts are made to avoid using intravenous urography, CT, and MRI with contrast due to the risk that the contrast medium used in these procedures may cause further kidney damage.
Renovascular hypertension can be managed with antihypertensive medications, although in many cases, the response to these treatments is limited.
For approximately 90% of patients with fibromuscular dysplasia, percutaneous transluminal angioplasty—a procedure that uses a catheter to widen the renal artery—can be effective. This procedure, however, is generally less effective in cases of atherosclerotic renovascular hypertension.
If there is significant kidney damage, surgery to create a bypass or repair a blockage in the renal artery may be effective.
In very severe cases, kidney removal (nephrectomy) may be necessary.
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