Renal artery thrombosis and embolism

　　First, Etiology

　　Renal artery occlusion can be caused by thrombosis or embolism. The causes of renal artery thrombosis include vascular and hematological factors. These two factors can exist singly or together and act on different stages of thrombosis. The causes of embolism are divided into two major categories: cardiac emboli and extracardiac emboli. Renal artery thrombosis often has varying degrees of pathological changes in the renal artery wall, while in renal artery embolism, there is often no organic lesion at the embolized site.

　　Second, Pathogenesis

　　Renal artery thrombosis can occur spontaneously or as a complication of blunt trauma or puncture wounds, or after vascular trauma or angiographic procedures. Trauma to the renal pedicle often leads to the tearing of the intima in the middle third of the renal artery, causing thrombosis. Less commonly, thrombosis can occur at the dilated aneurysmal areas of the renal artery or from thrombi originating from an aortic aneurysm. Vasculitis involving the main or branches of the renal artery can cause endothelial damage leading to thrombosis. Thrombosis caused by nodal polyarteritis, giant cell arteritis, vascular occlusive arteritis, and Kawasaki disease has been reported. Many other inflammatory diseases, including syphilitic vasculitis and tuberculosis, also affect the aorta and renal arteries. The hypercoagulable state in nephrotic syndrome can also lead to thromboembolic complications, including renal vein and renal artery thrombosis. Thrombosis of small branches of the renal artery can occur in thrombotic microangiopathy, including: hyperacute renal transplant rejection, hemolytic uremic syndrome, thrombotic thrombocytopenic purpura, postpartum renal vascular sclerosis, antiphospholipid syndrome, malignant hypertension, scleroderma, necrotizing vasculitis, and microthrombi associated with sickle cell anemia. In situ thrombosis of the renal artery is most common as a complication of extensive atherosclerosis of the aorta, where it can cause subacute narrowing of the vascular orifice or lumen, leading to progressive renal ischemia (ischemic nephropathy) and renal atrophy with or without renin-mediated hypertension.

　　1. Traumatic renal artery thrombosis:The causes of traumatic renal artery thrombosis include contusions, trauma secondary to angiography or nephrolithotomy, nephrostomy, renal biopsy, and surgical complications of percutaneous transluminal angioplasty (PTRA). The incidence of complications after PTRA is 3% to 10%, and complications leading to renal artery thromboembolism after PTRA include vascular rupture, intimal hernia, bleeding into the stenotic vascular embolism plaque, renal artery spasm, and embolism of external vessels.

　　Blunt trauma to the renal artery occurs in traffic accidents, fights, or sports injuries, leading to visceral injury, most commonly the liver or spleen, followed by the kidney. Gross hematuria is a sign of renal injury and vascular reconstruction should be performed within 4 to 6 hours after trauma.

　　2. Thrombosis in transplanted renal artery:The incidence of acute thrombosis in transplanted renal arteries is 0.5% to 4.4%, usually occurring within 1 to 2 months after transplantation. About 92% of transplant failures are related to delayed diagnosis and treatment intervention, leading to renal infarction and severe hypertension. The mortality rate reaches 11%, often with elevated plasma creatinine and malignant hypertension as the initial manifestations.

　　The most common cause of thrombosis in transplanted renal arteries is acute or superacute rejection, technical issues related to renal artery anastomosis, and the progression of renal artery stenosis. Transplanted renal arteries are usually anastomosed end-to-end with the internal iliac artery or side-to-side with the external iliac artery. End-to-end anastomosis is associated with a high incidence of stenosis, which is easy to damage the renal artery circulation. Cyclosporine is believed to increase the risk of thrombotic diseases, including glomerular capillaries, renal arteries, and systemic vessels. The possible mechanisms by which cyclosporine increases thrombosis include the inhibition of prostaglandin production in endothelial cells and the down-regulation of the protein C anticoagulant pathway. Cyclosporine reduces the activity of thrombomodulin in cultured endothelial cells in vitro. In addition, cyclosporine can reduce the production of PGI2 and E2 and increase ADP-induced platelet aggregation, TxA2 release, factor II activity, and fibrinogen levels. When other pathological conditions are present at the same time (such as rejection, hypertension, and further reduction in renal blood flow), these effects are more important for thrombosis.

　　3. Renal artery aneurysm and thrombosis:Renal artery aneurysms can lead to acute renal thromboembolic disease, with an incidence of about 1%, and the causes include atherosclerosis of the renal artery, congenital fibromuscular dysplasia, various arteritis, including polyarteritis nodosa, syphilis, tuberculosis, and trauma. Due to its potential for rupture, thrombosis, distant embolism, arteriovenous fistula, and renovascular hypertension, it is extremely important in clinical practice. The most common clinical symptom in 55% to 75% of patients is hypertension mediated by the renin-angiotensin system. About 30% of patients have hematuria, while back pain is less common. The risk of rupture is uncertain, but when the aneurysm is greater than 1.5 cm, the risk of rupture reaches 25%. A significant proportion of reported ruptured renal artery aneurysms occur in the last three months of pregnancy. Indications for selective surgical repair of renal artery aneurysms include the discovery of renal artery aneurysms in women of childbearing age, the presence of renovascular hypertension, patients with hypertension, and patients with hypertension and solitary kidney.

　　4. Renal Artery Embolism:Traube first reported renal circulation embolism in 1856. The incidence rate is 1.4% of the general population, but only 1% is diagnosed clinically. Although advances in imaging have shown an improvement in the ability to diagnose this disease, its clinical manifestations overlap with other diseases such as renal calculi, acute abdominal pain, pyelonephritis, and even myocardial infarction, leading to frequent delays in diagnosis. 25% of patients may have no pain. The most common clinical consequence of renal artery embolism is renal infarction. Isolated kidney or bilateral renal artery embolism occurs in about 1/3 of cases of renal artery embolism and is manifested by acute oliguric renal failure or hypertension. Extensive atherosclerotic embolic disease can also cause renal artery embolism.

　　5. Cardiac renal embolism:The heart is the most common source of renal artery embolism. Atrial fibrillation or diseases related to mitral valve repair are also common causes. The thromboembolic distribution study in patients with atrial fibrillation shows that the most common organs involved by thrombi are the brain (73%), mesenteric circulation (52%), and kidneys (40%). Other cardiac factors include mural emboli in myocardial infarction, cardiomyopathy, or other arrhythmias, infectious emboli in bacterial endocarditis, and left atrial myxoma, among others. If there is a history of heart disease, acute abdominal pain, lumbar pain, or chest pain, and renal insufficiency, hematuria, or proteinuria, one should highly suspect the possibility of renal artery thrombosis.

　　6. Renal embolism from non-cardiac sources

　　(1) Atherosclerotic Embolic Disease: The most common source of non-cardiac renal artery embolism is the rupture of aortic atherosclerotic plaques. The occurrence of cholesterol emboli is related to the rupture of large atherosclerotic plaques in the aorta, and it is more common during procedures within the aorta, such as angiography, aortic or cardiac surgery after surgery (involving the insertion or clamping of catheters in atherosclerotic aortic segments). Renal disease caused by atherosclerotic plaques can appear several days or months after an arterial procedure. Anticoagulation therapy with heparin, warfarin, and fibrinolytics can cause bleeding within atherosclerotic plaques, leading to the detachment of cholesterol crystals. This disease is seen in patients over 50 years old and is often accompanied by clinical manifestations and medical histories of diffuse vascular lesions (peripheral and cerebral vascular diseases).

　　(2) Abnormal Embolism: Abnormal systemic arterial embolism occurs in cases of venous thrombosis, pulmonary embolism, and those with right-to-left vascular shunts. The most common source of embolism is deep vein thrombosis in the lower extremities, but it also occurs in abnormal embolism from fat, tumor cells, marrow-derived cells, bacterial fragments, and venous catheters. Autopsy findings show that the most common anatomical site related to abnormal embolism pathways is the foramen ovale, seen in 35% of all autopsies. Other conditions include atrial septal defect, ventricular septal defect, pulmonary arteriovenous malformations, and other congenital heart diseases. When right atrial pressure acutely increases beyond left atrial pressure, it causes right-to-left blood shunting, and abnormal emboli pass through the gap into the left atrium.

　　反常栓塞可累及肾脏，大于40％病例可累及1个以上的动脉部位，包括脑循环。除非明确诊断后缺损得到修补。虽然与深静脉血栓形成或肺栓塞有关的动脉栓塞的诊断是较容易的，但反常栓塞常无明显的临床静脉血栓栓塞的表现。当寻找栓子的心源性来源未得到结果时，反常栓塞的诊断应予以接受。总之，任何肾动脉壁的病损导致肾动脉狭窄、内膜损伤、组织因子暴露，均可激活凝血机制，使动脉局部形成血栓导致肾动脉血栓形成。

　　7、血液高凝状态：先天性抗凝血物质缺乏或拮抗（如蛋白C、蛋白S、抗凝血酶Ⅲ因子缺乏等），或获得性的凝血功能异常（如肾病综合征，系统性红斑狼疮等），由于抗凝物质不足，易于形成血栓。近来由于这一类病因导致的血栓形成屡见报道。其中肾动脉、下肢动脉、肺动脉、肠系膜动脉等均有发现。

　　主要并发症是急性肾梗死、高血压及急性的快速恶化的肾功能衰竭。

　　肾功能不全：双侧肾脏同时发生梗死时，可因肾脏的缺血性坏死导致急性肾功能衰竭。最常见并发症是肾实质坏死，其次栓塞常常影响其他腹部器官（如胰腺，胃肠道）。为纤维斑块发生出血、坏死、溃疡、钙化季会壁血栓所形成。粥样斑块可因内膜表面破溃而形成所谓粥样溃疡；破溃后粥样物质进入血流成为栓子，破溃处可引起出血，溃疡表面粗糙易产生血栓，附壁血栓形成又加重管腔的狭窄甚至使之闭塞。

　　肾动脉血栓形成或栓塞的临床表现，取决于动脉堵塞的速度，程度和范围，小分支堵塞可能无任何症状或体征，而肾动脉主干及其大分支堵塞却常出现典型的临床表现。

　　1、急性肾梗死的表现：病人可突然出现剧烈的腰痛，腹痛，背痛，可类似于肾绞痛，向大腿放射，也可类似于急性胆囊炎，疼痛向肩背部放射，有些病例可类似于急性胰腺炎或急性心肌梗死，常有发热，呕吐，恶心，体查患侧肾叩击痛及压痛明显，血白细胞增加，核左移，可有血尿及蛋白尿，血清酶增高，谷草转氨酶常在梗死后立即升高，2周后恢复正常，碱性磷酸酶常于梗死后3～5天升至高峰，4周后恢复正常。

　　15. Hypertension:About 60% of patients may develop hypertension within a short period of time after renal artery occlusion due to renal ischemia and renin release, usually lasting 2 to 3 weeks, of which about 50% of patients have persistent hypertension, while the other half of the patients can recover normal blood pressure, and hypertension crisis may occur in occlusion of the main renal artery.

　　13. Acute renal failure:Chronic renal insufficiency may occur in thrombi that form slowly, acute occlusion of renal artery branches may lead to acute renal insufficiency, while renal artery embolism in both kidneys or solitary kidney may lead to acute rapid deterioration of renal function failure, often requiring immediate hemodialysis. If the occluded artery cannot be unblocked as soon as possible, the prognosis is poor. In addition, the clinical manifestations of renal cholesterol emboli are often different from those caused by renal embolic diseases due to other reasons. Renal infarction is rare, and the most common manifestation is acute, subacute, or chronic progressive renal insufficiency, and the diagnosis of renal cholesterol emboli is made accordingly. Atheromatous embolism fragments can reach small artery branches and affect the afferent arterioles, leading to a decrease in GFR. Due to ischemic renal segmental renin release in the embolized area, unstable hypertension may occur, and acute renal failure associated with atherosclerotic embolism disease often has a significant oliguria stage when there is obvious tubular injury, accompanied by increased sodium excretion fraction. However, renal insufficiency can also be non-oliguric and slowly progressive, due to repeated spontaneous plaque ulceration and rupture. Urinalysis may show moderate proteinuria, microscopic hematuria, or pyuria, the latter having no diagnostic significance.

　　9. 1. Actively prevent and treat the primary diseases that cause this disease, especially the middle-aged and elderly, who should pay more attention to early diagnosis and treatment of various common diseases that cause atherosclerosis.

　　8. Try to avoid trauma and traumatic examination and treatment methods.

　　7. Optimize lifestyle, including low-salt, low-fat diet, weight control, moderate exercise, no smoking and passive smoking, pay attention to rest, reduce mental stress, etc.

　　First, blood examination:Visible increase in blood leukocytes, left shift of nuclei; elevated serum lactate dehydrogenase (often more than 5 times the upper limit of normal) with mild elevation of plasma transaminase; aspartate aminotransferase often rises immediately after infarction, returns to normal after 2 weeks, alkaline phosphatase often reaches its peak 3 to 5 days after infarction, returns to normal after 4 weeks, renin-angiotensin in the blood increases, and when renal function failure occurs, renal function tests show significant abnormalities such as elevated plasma creatinine, elevated plasma enzymes, and increased excretion of lactate dehydrogenase in urine, one should highly suspect renal infarction.

　　Second, urine examination:Cholesterol embolism syndrome is commonly accompanied by increased eosinophils, with or without eosinophiluria, low complementemia, anemia, and thrombocytopenia, accelerated erythrocyte sedimentation rate, hyperamylasemia, elevated serum creatine kinase, elevated serum aspartate aminotransferase, urine examination may show hematuria and proteinuria, often moderate proteinuria, microscopic hematuria, and a few cases of pyuria.

　　Three, X-ray

　　1. Abdominal flat film:The renal shadow is mostly normal, and in a few cases, the renal shadow on the affected side is significantly reduced, and there are often reflexive intestinal distension symptoms.

　　2. Renal pelvis-ureterography:It shows that the affected kidney is non-functional, the renal pelvis is not visible, and retrograde renal pelvis-ureterography shows no abnormalities in the renal pelvis and calyces, which is a strong evidence for diagnosing acute renal artery embolism.

　　3. Renal arteriography:It is the first choice for diagnosing the disease. Renal arteriography can show the distribution area of the diseased blood vessels with filling defects, and the peripheral renal parenchyma or subcapsular area outside the defect can be visualized due to collateral circulation, forming what is called the 'renal shadow ring', but only the non-visualization of the affected renal segment can be seen when the small branches are occluded, and post-thrombotic extravasation bleeding can form a hematoma, causing the adjacent normal blood vessels to be pushed and displaced.

　　Four, Nuclear Medicine 99mTC-DTPA Renal Dynamic Imaging:After embolism formation, the renal blood perfusion curve on the affected side appears flat, without perfusion peaks, the renal shadow is faint and lower than the surrounding tissue, forming a 'black hole'; in the later stage, the formation of collateral circulation results in uneven imaging, and renal atrophy in cases where the renal artery is not reperfused in the late stage, leading to renal atrophy, which is difficult to differentiate from renal atrophy caused by other kidney diseases and renal insufficiency.

　　Five, Computed Tomography or Magnetic Resonance Imaging:It can show characteristic changes of renal parenchymal ischemic necrosis, which is a non-invasive examination method with high specificity.

　　Six, Echocardiography:It helps determine the etiology of cardiac renal embolism, the presence of wall emboli, valve calcification and dysfunction, vegetative valve emboli, and can monitor heart rhythm, which is helpful for diagnosing arrhythmias.

　　1.食疗 recipe for reflex sympathetic dystrophy

　　Maintain a balanced diet, eat more fruits and vegetables, high-fiber foods, more eggs, soybeans, and other high-protein foods. Pay attention to light food, and engage in moderate exercise.

　　2. What kind of food should be avoided for reflex sympathetic dystrophy

　　Avoid smoking, drinking, spicy, coffee, and other刺激性 food

　　(The above information is for reference only, please consult a doctor for details)

　　1. Treatment

　　The treatment of various acute and chronic renal thrombosis and embolic diseases aims to preserve renal function and prevent and treat renin-mediated hypertension. The key to the treatment of renal artery thrombosis and embolism is to quickly open the occluded vessels and restore renal blood flow. Previous medical treatments could only provide symptomatic treatment and reduce the occurrence of complications. However, surgical operations carry a high risk and trauma, and are also affected by the overall condition of the body. Since the 1980s, the development of vascular interventional treatment technology has turned a new page in the treatment of renal artery thrombosis and embolism. Percutaneous renal artery angioplasty can open the occluded renal artery early, restore renal blood flow, and achieve good therapeutic effects. The choice of treatment plan depends on the cause of renal artery thrombosis or embolism, the time from occlusion to the start of treatment, and the patient's age, as well as the original underlying disease and overall condition.

　　1. Surgical treatment:Performing surgery to remove thrombus or vascular reconstruction as soon as possible can minimize the area of ischemic necrosis in the diseased kidney, effectively save kidney function, but the surgery has a high degree of trauma. For patients with acute renal failure, refractory hypertension, even acute pulmonary edema, brain edema, and severe underlying diseases, the risk is very high. Therefore, whether to perform surgical treatment should consider the tolerance of the patient's overall condition. The main indications for surgery are:

　　(1) Traumatic renal artery occlusion.

　　(2) Bilateral renal artery trunk or large branch occlusion (or solitary renal artery occlusion).

　　(3) If the renal artery occlusion time is within 12 hours, the possibility of renal function recovery decreases for those who undergo surgery after 12 hours. The renal function recovery rate within 12 to 18 hours of surgery is only 50%, but for those with further delayed surgery, renal function recovery is not guaranteed.

　　2. Interventional therapy:Selective renal arteriography is a definitive diagnostic method for diagnosing renal infarction. On this basis, further renal artery thrombectomy, thrombolysis, and shaping surgery are performed, which is currently reported as a relatively effective and safe method in the literature. Although the early diagnosis rate of the disease is low, and there is a lack of summary of large-scale clinical treatment experience, interventional treatment is simple and easy to perform, has low trauma, can be repeated, and patients can still tolerate it when the condition is critical, which is worthy of development and application in hospitals with conditions. The method is to use about 4ml of 2% procaine for local anesthesia, puncture the femoral artery (usually the right side), and send a special renal arteriography catheter, thrombectomy catheter, or balloon catheter to the occlusion site of the renal artery, and perform intravascular thrombolysis, retrieval of thrombus, or balloon dilation as needed. Clinical diagnosis is acute thrombosis, thromboembolism, and the first choice is thrombolytic therapy. If diagnosed as cancer thrombus, valve赘生物栓塞, foreign body (such as vascular stent, atrial, ventricular septal patch, etc.) embolism, or old thrombus embolism that cannot be dissolved locally, it should be tried with thrombus retrieval surgery. If intravascular thrombolysis and thrombectomy are not successful, or if there is still significant renal artery stenosis after thrombolysis and thrombectomy (it is generally believed that stenosis ≥75% may cause pathological changes), balloon dilation should be performed to open the main trunk or large branch of the renal artery (after the thrombus is crushed by the balloon, it may block small artery branches, but the area of ischemic necrosis is significantly reduced), and to completely solve the anatomical cause of renal ischemia. The administration method of intravascular thrombolysis is to dilute 100,000U of urokinase or streptokinase with 20ml of normal saline, slowly inject it into the catheter, and it takes about half an hour to push it, which can be reused, and the local medication dose within 500,000U is generally considered to be relatively safe.

　　3. Medical treatment

　　(1) Intravenous thrombolytic therapy: Intravenous thrombolytic therapy is less effective than intravenous thrombolytic therapy, but because of its lower cost, it does not require expensive equipment and operation technology for interventional therapy, and can be performed in most hospitals. Therefore, it is worth promoting.

　　Indications: All patients with renal artery thrombosis or thromboembolism are applicable.

　　Contraindications: ① Elderly patients, it is generally considered that patients over 75 years of age are not suitable for intravenous thrombolytic therapy. ② Bleeding tendency. ③ History of deep tissue trauma or puncture within the past six months. ④ History of cerebrovascular accidents within the past six months. ⑤ Allergy to thrombolytic agents. ⑥ Uncontrolled hypertension.

　　Administration: Urokinase or streptokinase 200,000 to 400,000 units dissolved in 100 to 500 ml of liquid, intravenous infusion completed within 3 hours. Local arterial injection of streptokinase or urokinase is often more effective than intravenous thrombolytic therapy in low-risk patients with renal tissue still active. Once a day, for 3 to 7 days (some experts believe that daily dosage up to 500,000 to 1,000,000 units is still safe). The process of thrombolytic therapy should check coagulation and bleeding times and fibrinogen quantification every day.

　　(2) Anticoagulant therapy: Patients with a history of thrombosis or embolism, as well as those after surgical operations, interventional therapy, and intravenous thrombolytic therapy, should receive routine anticoagulant therapy to prevent recurrence of embolism. Hospitalized patients can be given heparin or low-molecular-weight heparin for intravenous infusion or subcutaneous administration. Long-term use can be given warfarin, cilostazol (Lipanor), or aspirin, and the dosage requirements should be individualized. The process of medication should be regularly monitored for coagulation and bleeding times, and the dosage should be adjusted in time to prevent bleeding complications.

　　(3) Symptomatic treatment:

　　① Treatment of hypertension: Hypertension often appears within 1 week of onset, and returns to normal within 2 to 3 weeks, with some patients experiencing lifelong symptoms. The pathogenesis is related to renal ischemia leading to increased renin secretion by juxtaglomerular cells, and increased activity of the renin-angiotensin system, hence angiotensin-converting enzyme inhibitors or angiotensin II receptor antagonists may be effective. However, since both types of drugs dilate both systemic arteries and efferent arterioles, when the perfusion pressure of the glomerular arterioles decreases due to renal artery thrombosis or embolism, it can further reduce glomerular blood flow, leading to deterioration of renal function, and therefore, careful consideration of medication should be given. Other antihypertensive drugs have poor efficacy, and hypertensive crises should be treated with sodium nitroprusside or phentolamine (Regitine) and other strong, fast-acting intravenous antihypertensive agents.

　　② Treatment of acute renal failure: For patients with acute renal failure, timely hemodialysis treatment can alleviate symptoms and can win time for further surgical or interventional treatment.

　　③ Correcting water, electrolyte, and acid-base balance disorders.

　　II. Prognosis

　　The prognosis of renal arterial embolism and thrombosis is related to the etiology, the extent of renal arterial occlusion, and the time of effective treatment initiation. In the case of traumatic renal arterial thrombosis, most cases have severe multi-organ damage, with a mortality rate of 44%, and many patients (about 25%) die of extrarenal complications (such as myocardial infarction, heart failure, cerebral infarction, etc.), while a small number of patients die of acute renal failure.

　　Patients with thrombosis occurring on the basis of atherosclerosis, due to long-term narrowing before renal arterial occlusion, repeated renal ischemia promotes the formation of collateral circulation, which reduces the pathological changes during the acute phase, and the recent prognosis may be better, but if there are simultaneous coronary artery or cerebral artery events, the prognosis may also be poor.

　　The short-term and long-term prognosis of thrombosis caused by congenital and acquired hypercoagulable states is related to the effectiveness of the treatment of the primary disease. For patients with congenital protein C deficiency, timely administration of protein C preparations can achieve significant efficacy. For diseases such as systemic lupus erythematosus and myelofibrosis, for which there are no definitive effective treatment methods, thrombolysis or thrombectomy is part of the symptomatic treatment, and the prognosis varies depending on the patient's response to the overall comprehensive treatment.

　　If renal arterial embolism can be treated with thrombolysis or thrombectomy in a timely manner, the prognosis during the acute phase is good, while the long-term prognosis is related to the source of the embolism, and the cause of death is often the progression of the underlying disease.