Renal artery stenosis (RAS) refers to unilateral or bilateral narrowing of the main trunk or branches of the renal artery caused by various reasons, 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 the last decade or so, atherosclerosis has replaced atherosclerosis as the primary cause of RAS at present. Renal artery stenosis can occur in the main trunk or branches of the renal artery. As a result of renal artery stenosis, there is a significant difference in blood pressure before and after the stenosis, leading to renal ischemia, which stimulates increased renin secretion in the body and activates the renin-angiotensin-aldosterone system, which in turn causes hypertension. Atherosclerosis occurs mostly in elderly patients. Fibromuscular dysplasia is common in young people and is also common in Western countries. Aortitis is more common in young women. Other rare causes include congenital renal artery dysplasia, renal aneurysm, renal artery embolism, renal arteriovenous fistula, and trauma or surgical injury to the renal arteries. 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 major cause of secondary hypertension. It is characterized by stubborn hypertension, which is difficult to control by ordinary antihypertensive drugs. 2. Renal atrophy: Renal atrophy is a direct consequence of renal artery stenosis. Patients who develop renal atrophy mostly show progressive renal insufficiency. 3, end-stage renal disease (ESRD): A study analyzed a total of 683 patients who eventually received dialysis treatment for ESRD in the last 20 years, of which 83 cases (12%) were diagnosed as caused by RAS. However, the effect of RAS on ESRD cannot be fully defined based on current data. 4. Recurrent pulmonary edema: Patients with renal artery stenosis may have sudden or “recurrent” pulmonary edema. Patients with severe bilateral or unilateral RAS may present with volume overload. Patients with unilateral RAS may also experience pulmonary edema due to angiotensin-mediated vasoconstriction, which can cause an increase in left ventricular afterload. 5. Cardiovascular events: Patients with RAS have a higher risk of cardiovascular events, which may be due to more severe systemic atherosclerosis. Patients with severe RAS have higher levels of angiotensin II in the body, leading to peripheral arterial vasoconstriction, which can induce coronary ischemia. 6. Asymptomatic renal artery stenosis, patients with renal artery stenosis may also present without any clinical symptoms but are found to have renal artery stenosis lesions during the course of 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? This system protects the kidneys. When the blood pressure drops, the blood flow to the kidneys decreases, and this system sends a signal to raise the blood pressure and maintain the blood flow to the kidneys. 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? 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 with ischemic kidney disease, gradually leading to glomerulosclerosis, tubular atrophy and interstitial fibrosis. The clinical manifestations are progressive decrease of renal function (early onset of tubular concentration damage, patients with nocturia, decreased urine specific gravity and osmolality; later on, impaired glomerular function, patients with 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 of kidney size (the size of the two kidneys is often asymmetric).