Etiology and pathogenesis] Etiology Renovascular hypertension (RVH) is a narrowing lesion of the renal artery that causes ischemia in the affected kidney. Many causes can cause renal vascular >more’);”>hypertension. Europe and the United States reported that 60% to 70% are caused by atherosclerosis and fibromuscular abnormalities in development. In contrast, in our country >more’);”> polyarteritis major arteritis is the main cause of the disease, which is very different from the Western countries. 1, aortitis China and Southeast Asia >more’);”>polyarteritis is the main cause of RVH, can involve multiple sites of blood vessels, about 70% combined with renal artery stenosis. In 1989, we reported 315 cases of renal vascular >More’);”>hypertension, 68.6% of which were caused by aortitis. Aortitis occurs mostly in young women, and 67.7%-69% of the patients reported in China were women. The age of onset is 5 to 45 years old, and 89% are under 30 years old. The etiology of this disease is not clear, but it may be a specific inflammatory disease caused by autoimmune abnormalities after bacterial (Mycobacterium tuberculosis, Streptococcus or Rickettsia, etc.) infection. Symptoms such as fever, general malaise, lack of appetite, sweating, arthritis and >more’);”>nodular erythema may occur during the active phase of arteritis. Blood tests may reveal increased erythrocyte sedimentation rate, increased anti-streptococcal hemolysin “O” titer, positive C-reactive protein, decreased serum albumin, increased alpha and gamma globulin, increased immunoglobulins M and G, rheumatoid factor anti-aortic antibodies, and positive Coombs test. the appearance of RVH is already a clinical feature of aortitis. The presence of RVH is already a clinical feature of the chronic vascular obstruction phase. 2, atherosclerosis Atherosclerosis has become an epidemic common disease in Europe and the United States, causing RVH about 60% of all patients. In recent years, due to the improvement of people’s living standards, the development of health care and the growth of the average life expectancy of the population, atherosclerosis has increased year by year and has now jumped to be one of the main causes of death in the population. The disease is mostly seen in middle-aged and elderly people over 40 years old, and the lesion progresses faster after 50 years old. The lesions often involve the intima of large and medium arteries, the opening of the main trunk of the renal artery and the proximal 1/3, and are mostly bilateral. The prevalence factors are: ① hyperlipidemia; ② >more’);”> hypertension; ③ >more’);”> diabetes mellitus: >more’);”> the incidence of atherosclerosis in diabetic patients is twice as high as that in patients without >more’);”> diabetes mellitus; ④ smoking is also an important factor in the increased incidence. Multiple stenosing aortitis 3. Fibromuscular dysplasia In foreign countries, 1/4 to 1/3 of RVH is caused by fibromuscular dysplasia, which is common in female patients under 40 years old, but can also be seen in infants and elderly patients. Depending on the location of the abnormal arterial wall development, there are four types of abnormalities: intimal fibrodysplasia, fibromuscular hyperplasia, mesial fibromuscular hyperplasia, and epicardial (periarterial) fibrodysplasia. Mesangial fibromuscular hyperplasia is the most common, accounting for approximately 85% of cases. The etiology and pathogenesis of fibromuscular dysplasia are unclear and may be related to female endocrine effects. In patients with a family history of the disease, genetic factors play an important role in the pathogenesis. The incidence of this disease is significantly higher in Europe and the United States than in China. 4. Other With the widespread development of kidney transplantation, the stenosis of transplanted kidney vessels after kidney transplantation has become one of the causes of renal vascular >more’);”>hypertension. The incidence of >more’);”>hypertension is about 50% and the incidence of transplanted renal artery stenosis can be as high as 10%. It is generally believed that renal artery stenosis after renal transplantation is associated with rejection, atherosclerosis, poor surgical anastomosis technique, local injury, distortion, and fibrosis of the vessel. In addition, renal artery thrombosis or embolism, congenital renal aneurysm, extra-renal artery hematoma compression, >more’);”>retroperitoneal fibrosis, neuro >more’);”>fibromas, >more’);”>compression of renal artery by pheochromocytoma and nodular arteritis can cause RVH. Pathogenesis Due to the reduction of renal blood perfusion caused by renal vascular lesions, in the renal ischemia and hypoxia In the presence of renal ischemia and hypoxia, the kidneys can produce a variety of factors that increase >more’);”>hypertension to raise blood pressure. In addition, the lack of anti->more’);”>hypertensive factors is also an important factor in the increase of blood pressure. classical experiments by Goldblatt et al. in 1934 showed that clamping one renal artery of an animal or removing one kidney and clamping the renal artery of a preserved kidney produced >more’);”>hypertension. This established the theoretical basis for RVH. Currently, there are several mechanisms for the pathogenesis of renal vascular >more’);”>hypertension, as follows. 1, renin-angiotensin-aldosterone system (remin-angio-tensin-aldosterone, RAA) Renin in circulating blood is a protein hydrolase that is released by the glomerular paracellular apparatus. Renin breaks down α2 globulin produced in the liver, i.e. angiotensinogen (renin matrix, tetradecapeptide), converts to angiotensin I (angiotensin I, AⅠ, decapeptide), and under the action of converting enzymes produced in the lung, forms angiotensin II (AⅡ, octapeptide) into a substance with potent vasoconstrictive effect. aⅡ is hydrolyzed by the action of angiotensinase A into angiotensin III (AIII, heptapeptide), and the angiotensin system causes >more’);”>hypertension, called angiotensin-derived >more’);”>hypertension. The course of action of the angiotensin system was described by Vander in 1984. (1) Angiotensin stimulates increased synthesis and release of norepinephrine from the adrenal medulla. The vascular smooth muscle contracts, which raises blood pressure. (ii) Acting on the central and peripheral nervous system, it stimulates sympathetic nerves, causing fine blood vessels to constrict and increasing cardiac output, which raises arterial blood pressure. (iii) Stimulation of the adrenal cortical bulbous band, increasing secretion of aldosterone, causing sodium and water recycling: Na+ concentration increases, and the increase in osmotic pressure stimulates the pituitary gland to release antidiuretic hormone, prompting the renal tubules and collecting ducts to increase water recycling; angiotensin II causes the glomerular outflow artery to constrict and not the inlet artery, increasing renal artery pressure and causing sodium retention. Due to sodium and water retention, blood volume increases, causing volumetric >more’);”>hypertension. 2, kinin-releasing enzyme-kinin-prostaglandin system (kallidreinkininprostaglandin, KKP) The kinin-releasing enzyme produced by the renal cortex acts on the kininogen produced by the liver to form kinin. Goldblatt type >more’);”>hypertension (renal artery stenosis on one side and nephrectomy on the opposite side) is produced when kininogen hydrolysis is reduced in the urine, and kinin production is reduced, resulting in >more’);”>hypertension. The kidney also has the role of secreting kinin hydrolase, which can destroy kinins and cause an increase in blood pressure. Prostaglandins can stimulate the secretion of prostaglandins (i.e. PGE-2, PGA-2, PGF-2) from the renal medulla, which have hypotensive effects. Prostaglandins also have antagonistic effects on catecholamines. When kinin production is reduced, prostaglandin production is also affected, causing an increase in blood pressure. The role of kinin-releasing enzyme, kinin, and prostaglandin system in the development of renal vascular >more’);”>hypertension has also been emphasized. 3, cardiac natriuretic system (atrial natriurtic peptic, ANP) Cardiac natriuretic is antagonistic to the renin-angiotensin-aldosterone system and originates from the heart. However, it can be secondary to the brain, adrenal glands, pituitary and reproductive systems. Cardiac natriuretic hormone has an antagonistic effect on renin release, resulting in lower blood pressure. In 1987, Marris showed that cardiac natriuretic system inhibits sodium absorption by the renal tubules and glomerular filtration caused by angiotensin II. Therefore, the cardiac natriuretic system also plays an important role in the regulation of blood volume and blood pressure in the body.