What is renal artery stenosis and what is its etiology?
Renal artery stenosis (RAS) refers to unilateral or bilateral narrowing of the main trunk or branches of the renal artery due to various causes, and it is one of the most common causes of secondary hypertension. The causes of renal artery stenosis are complex and can be congenital or caused by aortitis, atherosclerosis, or abnormal arterial wall development. In recent decades, atherosclerosis has replaced atherosclerosis as the leading cause of RAS.
Usually, childhood patients are more likely to have congenital anomalies, young adults are more likely to have renal arteritis or fibromuscular hyperplasia, and the elderly are more likely to have atherosclerotic renal arteries.
What are the consequences of untreated renal artery stenosis?
(1) Renal vascular hypertension
Hypertension is the main clinical manifestation of renal artery stenosis, and renal vascular hypertension is the second leading cause of secondary hypertension. It is characterized by stubborn hypertension, which is difficult to be controlled by ordinary antihypertensive drugs.
(2) Renal atrophy
Renal atrophy is a direct consequence of renal artery stenosis. Patients who develop renal atrophy mostly present with progressive renal insufficiency.
(3) End-stage renal disease (ESRD)
One study analyzed a total of 683 patients who ended up on dialysis for ESRD in the last 20 years, and 83 of them (12%) were diagnosed as being caused by RAS. However, the effect of RAS on ESRD cannot be fully defined based on current data.
(4) Recurrent episodes of pulmonary edema
Patients with renal artery stenosis may have sudden onset or “recurrent” pulmonary edema. Patients with severe bilateral or unilateral RAS may present with volume overload. Patients with unilateral RAS may also develop pulmonary edema due to angiotensin-mediated vasoconstriction that can cause an increase in left ventricular afterload.
(5) Cardiovascular events
Patients with RAS are at higher risk for cardiovascular events, probably due to more severe systemic atherosclerosis. Patients with severe RAS have higher levels of angiotensin II in the body, which leads to peripheral arterial vasoconstriction and can induce coronary ischemia.
(6) Asymptomatic renal artery stenosis
Patients with renal artery stenosis may also present without any clinical symptoms, but rather the presence of renal artery stenosis lesions are detected during coronary angiography and peripheral angiography. Patients with asymptomatic renal artery stenosis have a poorer prognosis compared to those without renal artery stenosis, and their prognosis is related to the degree of stenosis. One study found that the 4-year survival rate for asymptomatic, severe RAS (≥75%) found incidentally during cardiac catheterization was 57% compared with 89% for patients with non-severe RAS.
Why does renal artery stenosis cause hypertension?
Because there is a “signal” system in our kidney to regulate blood pressure – “renin-angiotensin-aldosterone system”, this system is to protect the kidney, when the body’s blood pressure drops, the blood flow to the kidney decreases, this system will send a signal to raise the blood pressure to maintain the blood flow to the kidney. Angiotensin constricts micro-arteries throughout the body and increases the resistance of peripheral blood vessels, which raises blood pressure, while increased aldosterone leads to increased blood volume, which also raises blood pressure. And when renal artery stenosis occurs, blood flow to the kidney is reduced, and this regulatory system, also thought to be caused by a drop in blood pressure, is similarly activated to raise blood pressure, leading to hypertension in patients with renal artery stenosis. This hypertension is intractable and difficult to control with medication. This type of hypertension caused by renal ischemia due to renal artery stenosis is clinically known as renal vascular hypertension. While in the later stages of the disease plasma renin levels are reduced and the mechanism of hypertension is dominated by impaired glomerular filtration rate and water and sodium retention in both kidneys.
Why are there patients with renal artery stenosis who have not previously been found to have significant hypertension?
As we said before, some patients with renal artery stenosis may have no specific clinical manifestations, and some patients with renal artery stenosis due to renal artery atherosclerosis may not develop hypertension, but present ischemic kidney disease, which gradually leads to glomerulosclerosis, tubular atrophy and interstitial fibrosis. The clinical manifestations are progressive renal decompensation (early onset of tubular concentration damage, high nocturia, decreased urine specific gravity and osmolality; later on, impaired glomerular function, decreased endogenous creatinine clearance and increased serum creatinine), mild urinary abnormalities (mild proteinuria, small amount of red blood cells and tubular pattern) and progressive reduction in kidney size (the size of the two kidneys is often asymmetric).
How to diagnose renal artery stenosis early? What are the conditions that indicate the possibility of renal artery stenosis?
The onset of renal artery stenosis is usually insidious and has a tendency to get progressively worse, and once symptoms appear, they are often advanced. Since there is no difference in clinical symptoms between hypertension caused by renal artery stenosis and primary hypertension, the diagnosis relies on a high degree of vigilance. Therefore, the presence of this disease should be thought of promptly when some clinical clues are found, and the presence of the following conditions may indicate the presence of RAS
(1) The following types of hypertensive manifestations.
(i) Hypertension before the age of 30 years or severe hypertension after the age of 55 years.
(ii) Acute hypertension (sudden and persistent deterioration of previously controllable hypertension).
(iii) Persistent hypertension (difficulty in achieving target blood pressure when a combination of three antihypertensive drugs, including diuretics, is applied in sufficient doses).
(iv) Malignant hypertension (hypertension combined with acute target organ damage, such as acute renal failure, acute heart failure or new onset of optic nerve or other cerebral neuropathy and III-IV retinopathy).
(2) When new-onset azotemia or worsening renal function (elevated blood creatinine greater than 50%) occurs with the application of angiotensin-converting enzyme inhibitors (ACEI) or angiotensin receptor antagonist class (ARB) drugs, or when there is unexplained renal hypofunction in the elderly.
(3) Presence of unexplained renal atrophy.
(4) Sudden onset of pulmonary edema.
(5) Vascular murmurs can be heard in the abdomen.
(6) Significant asymmetry in the size of both kidneys on ultrasound and other examinations.
(7) Concomitant other vascular diseases, such as coronary artery disease, carotid artery stenosis or lower limb artery stenosis.
What are the clinical manifestations of renal artery stenosis?
1. Renal vascular hypertension
Most patients with renal artery stenosis do not have a family history of hypertension, which is characterized by rapid progression of hypertension and blood pressure that is not easily controlled. Diastolic blood pressure increases significantly (often more than 110-120 mmHg) and may manifest as malignant hypertension (rapid increase in blood pressure, diastolic blood pressure persistently greater than 130 mmHg, with headache, blurred vision, fundus bleeding, exudation and papilledema, even sudden blindness, grand mal seizures, persistent proteinuria, hematuria with tubuluria).
2. Abdominal and lumbar murmurs
Systolic murmurs can be heard in about 50% of patients at 2-7 cm above the umbilicus and 2.5 cm to the left and right.
3. Primary disease manifestation
Those caused by atherosclerosis or aortitis often have primary manifestations. The former occurs mostly in the elderly and can present with stroke, coronary artery disease, peripheral arteriosclerosis and fundus changes; the latter is mostly in young women and can present with fever, arthralgia, pulselessness and other manifestations.
4. Other: some patients have hyperaldosteronism (leading to hypokalemia), mild urinary abnormalities, and impaired renal function (ischemic kidney disease).
What tests are needed in patients with suspected renal artery stenosis?
Patients with renal artery stenosis often require the following tests.
1. Routine tests include blood routine, urine routine, stool routine and blood biochemical tests. Anemia is often a sign of renal insufficiency, and the possibility of renal artery stenosis should be considered. Blood creatinine and endogenous creatinine clearance are the most commonly used indicators to determine renal function. Hypokalemia is a manifestation of secondary aldosteronism.
2.Imaging examination
(1) Ultrasound of both renal arteries: Ultrasound finds that the difference in the length of the two kidneys is greater than 1.5cm, which often indicates the possibility of renal artery stenosis on one side of the small kidney. Color Doppler ultrasound can observe the renal artery trunk and intrarenal blood flow changes. Compared with imaging, its sensitivity is 84% to 98% and specificity 92% to 99%. It can also be used to measure the renal artery resistance index, and an increase in the index indicates small renal artery sclerosis or glomerulosclerosis. It can also determine the effect of renal artery after recanalization.
(2)Renogram
(3) Plasma renin-angiotensin system tests and renin excitation tests: are not necessary to diagnose renal artery stenosis, but some endocrine tests are sometimes very useful in certain cases.
(4) CT and/or MRI of the renal arteries: CT and MRI of the renal arteries may reveal the site and extent of stenosis.
(5) Renal arteriogram: the most diagnostic value (golden indicator). It can clarify the lesion site, scope, severity, and formation of collateral circulation, and the treatment can be performed at the same time of imaging. Atherosclerotic lesions are mostly in the beginning of the renal artery and the abdominal aorta. Atherosclerotic lesions are more often found in the descending aorta and the proximal 1/3 of the renal artery. Fibromuscular dysplasia lesions are most often found in the distal 1/3 segment of the renal artery and its primary branches.
What does the treatment of renal artery stenosis involve?
The goal of treatment for renal artery stenosis is to lower blood pressure and, more importantly, to preserve renal function. It includes.
1. Internal medication: It cannot improve the ischemia of the affected kidney and can only help control hypertension. However, lowering the blood pressure can prevent complications caused by hypertension, such as cerebral hemorrhage, hypertensive encephalopathy, acute renal failure, aortic coarctation, etc. It is very important to lower the blood pressure quickly in such cases. The usual treatment of hypertension should not be neglected. ACEI drugs and calcium antagonists can effectively control hypertension in patients with RAS and delay the progression of renal disease. ACE inhibitors and ARB can effectively treat hypertension caused by unilateral RAS. beta blockers are effective drugs for the treatment of hypertension due to RAS. Diuretics can also bring down the blood pressure of RAS patients to the target level.
2. Hemodynamic reconstruction therapy: Surgical treatment for renal artery stenosis can be divided into two main categories, namely, transabdominal renal artery reconstruction surgery and percutaneous transluminal renal arterioplasty. Regardless of the treatment, the aim is to make the narrowed renal artery smooth, so that the blood flow in the kidney can be restored to normal levels and the blood pressure regulation system in the kidney can no longer release the “signal” that raises blood pressure, thus lowering the patient’s blood pressure.
(1) Percutaneous transluminal renal arterioplasty. This is performed by puncturing the femoral artery at the root of the thigh, inserting a catheter with a balloon into the narrowed renal artery, and then expanding the balloon with a contrast agent to dilate the narrowed renal artery to a normal caliber from the inside out, especially in patients with fibromuscular dysplasia. Since patients with atherosclerosis and aortitis are prone to restenosis and treatment failure after dilatation, these patients can be placed with a stent after dilatation to prevent postoperative stenosis. This procedure, invented by a Swedish physician in 1978, has the advantages of minimal trauma, safety, and rapid postoperative recovery, and is now widely used worldwide as the treatment of choice for renal artery stenosis.
Indications for endoluminal therapy
Intraluminal therapy is indicated for: (1) patients with significant hemodynamic abnormalities and a combination of the following conditions: acute hypertension, intractable hypertension, malignant hypertension, hypertension with unexplained unilateral renal shrinkage, and hypertension intolerant to medication; (2) patients with bilateral RAS or RAS with isolated kidney in combination with progressive chronic renal disease; (3) patients with RAS with significant hemodynamic significance and patients with unexplained, recurrent congestive heart failure or unexplained sudden pulmonary edema in combination with RAS; ④ patients with RAS of hemodynamic significance in combination with unstable angina.
There are some insurmountable disadvantages of percutaneous transluminal renal arterioplasty, such as low success rate, high recurrence rate of stenosis, etc. Some patients are unable to undergo the procedure due to contrast allergy or twisting of the iliac artery, and then they have to resort to traditional transabdominal renal artery reconstruction surgery, including: abdominal aorta-renal artery bypass, renal artery endarterectomy, renal artery stenosis segment resection with end-to-end anastomosis If the above treatment is not possible, resection of the diseased kidney may be considered. Abdominal aorta-renal artery bypass surgery, also known as renal artery “bypass” surgery, is a surgical procedure in which a section of the saphenous vein is taken from the patient’s thigh, one end is anastomosed to the patient’s abdominal aorta, and the other end is anastomosed to the patient’s renal artery by bypassing the stenotic segment of the renal artery, so that the blood flow from the abdominal aorta is bypassed to the kidney to solve the patient’s renal ischemia. The disadvantage of this surgical approach is that it is more invasive, but the treatment results are very reliable and can also be used to treat patients who are not suitable for percutaneous transluminal renal arterioplasty.