Renal artery thrombosis and embolism

Introduction to renal artery thrombosis and embolism Renal artery thrombosis and embolism refers to the complete occlusion of the renal artery lumen due to vascular wall factors or blood factors, causing renal dysfunction, transient hypertension, renal pain and renal tissue deficiency. Blood necrosis, the main manifestations of patients are fever, changes in urine routine, increased cell enzymology and other clinical syndromes. basic knowledge Sickness ratio: 0.0004%-0.0008% Susceptible people: no special people Mode of infection: non-infectious Complications: high blood pressure

Renal artery thrombosis and embolism etiology

Causes:

Renal artery occlusion can be caused by thrombosis or embolism. The causes of renal artery thrombosis are blood vessel and blood. These two factors can exist alone or coexist, and interact with each other at different stages of thrombosis. There are two types of cardiac emboli and extracardiac emboli. Renal artery thrombosis often has different degrees of renal artery wall lesions, and there are many organic lesions in the embolization site during renal artery embolization.

Pathogenesis:

Renal artery thrombosis can occur spontaneously or as a blunt injury, a complication after a stab wound, or a vascular trauma. After an angiographic procedure, the renal pedicle trauma often causes a tear in the 1/3 intima of the renal artery. Less common is the thrombosis of the aneurysm dilatation of the renal artery or caused by aortic aneurysm clot. Vasculitis involving the trunk or branch of the renal artery can cause endothelial damage leading to thrombosis, nodular polyarteritis, giant cell arteritis , vascular occlusive vasculitis and Kawasaki disease caused by thrombosis have been reported, many other inflammatory diseases, including syphilitic vasculitis and tuberculosis also affect the aorta and renal artery, hypercoagulable state of nephrotic syndrome can also cause thromboembolism Complications, including renal vein and renal artery thrombosis, thrombosis of small branches of the renal arteries 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 sickle cell anemia Suppository, renal artery in situ thrombosis is most common in a wide range of aortic atherosclerotic complications, in which case subacute stenosis of the vascular orifice or lumen can result, leading to progressive renal ischemia (ischemic nephropathy) And renal atrophy with or without renin-mediated hypertension.

1. Traumatic renal artery thrombosis: Causes of traumatic renal artery thrombosis include blunt trauma, trauma or renal stone resection secondary to angiography, nephrostomy, renal biopsy and percutaneous transluminal angioplasty Surgical complications of (PTRA), the incidence of complications of PTRA is 3% to 10%. In the complications of renal artery thromboembolism after PTRA, there are vascular ruptures, endothelial wall tumors, and hemorrhage into stenotic plaques. Embolization of renal artery spasm and external blood vessels.

The blunt trauma of the renal artery occurs in a car accident, fighting or sports trauma, leading to visceral injury, the most common is the liver or spleen, followed by the kidney, gross hematuria is a sign of kidney damage, requiring revascularization within 4 to 6 hours after trauma Surgery.

2. Transplantation of renal artery thrombosis: The incidence of acute graft renal artery thrombosis is 0.5% to 4.4%, usually occurring within 1 to 2 months after transplantation, and about 92% of graft failures are related to delays in diagnosis and treatment intervention. It leads to renal infarction and severe hypertension, with a mortality rate of 11%. It is often preceded by elevated plasma creatinine and malignant hypertension.

The most common causes of renal artery thrombosis are acute or hyperacute rejection, technical problems associated with renal artery anastomosis, and progression of renal artery stenosis, which is usually end-to-end or lateral to the internal iliac artery. End-to-side anastomosis, end-to-end anastomosis is associated with a high incidence of stenosis and is prone to damage to the renal arterial circulation. Cyclosporine is thought to increase the risk of renal artery thrombotic disease, including glomerular capillaries and renal arteries. As well as systemic blood vessels, possible mechanisms by which cyclosporine increases thrombosis include inhibition of prostaglandin production by endothelial cells and down-regulation of protein C anticoagulant pathway. Cyclosporine reduces thrombomodulin in cultured endothelial cells in vitro. Activity, 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 exist (such as rejection, hypertension and Further reduction of renal blood flow) These effects are more important for thrombosis.

3. Renal aneurysms and thrombosis: Renal aneurysms can cause acute renal thromboembolic disease, the incidence rate is about 1%, including renal atherosclerosis, congenital fibromuscular dysplasia, various arteritis, including knots Segmental polyarteritis, syphilis, tuberculosis and trauma, due to its rupture, thrombosis, long-distance embolism, arteriovenous fistula, renal vascular hypertension, it is extremely important clinically, 55% to 75% of patients, most Common clinical symptoms are RAS-mediated hypertension, 30% of patients have hematuria, low back pain is rare, and the risk of rupture is not certain, but when the aneurysm is larger than 1.5cm, the risk of rupture is 25%. A large proportion of ruptured renal aneurysms occur in the third trimester of pregnancy. Indications for selective surgical repair of renal aneurysms include renal aneurysms in women of childbearing age, renovascular hypertension, hypertension, and hypertension With isolated kidney patients.

4. Renal artery embolism: Traube first reported renal circulatory embolism in 1856, accounting for 1.4% of the overall population, but only 1% of them were clinically diagnosed, although imaging advances have shown improved ability to diagnose the disease, but due to Its clinical manifestations overlap with other diseases such as kidney stones, acute abdomen, pyelonephritis, and even myocardial infarction, so it is often delayed in diagnosis. 25% of patients may have no pain. The most common clinical consequence of renal artery embolization is renal infarction, isolated kidney or Bilateral renal artery embolization occurs in about one-third of cases of renal artery embolism, and is marked by acute oliguric renal failure or hypertension. Extensive atherosclerotic 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 associated with mitral valve repair are also common causes. The study of thromboembolism in patients with atrial fibrillation shows that common thrombosis Organ midbrain 73%, mesenteric circulation 52%, kidney 40%, other cardiogenic factors including myocardial infarction, cardiomyopathy of cardiomyopathy or other arrhythmias, infectious emboli of bacterial endocarditis and left Atrial mucinous tumor, etc., if there is a history of heart disease, acute abdomen, low back pain or chest pain and renal insufficiency, hematuria or proteinuria, the possibility of renal artery thrombosis should be highly suspected.

6. Non-cardiac source of renal embolism:

(1) Atherosclerotic embolism: The most common source of non-cardiac renal artery embolism is rupture of aortic atherosclerotic plaque. The occurrence of cholesterol emboli is related to the rupture of large aortic atherosclerotic plaque in patients. More common are operations occurring in the aorta, such as angiography, aortic or cardiac surgery (intubation or clamping involving atherosclerotic aortic segments), renal disease caused by atherosclerotic plaque It can occur several days or months after arterial operation. Anticoagulant therapy with heparin, warfarin and fibrin can cause hemorrhage in atherosclerotic plaque, causing cholesterol crystals to fall off. This disease is seen in patients older than 50 years old. And patients often have clinical manifestations and medical history of diffuse vascular disease (peripheral blood vessels and cerebrovascular).

(2) paradoxical embolism: abnormal systemic arterial embolism occurs in venous thrombosis, pulmonary embolism, and cases of right-to-left vascular shunt, the most common source of embolism is deep vein thrombosis from the lower extremities, but also Found in fat, tumor cells, bone marrow-derived cells, bacterial debris and abnormal embolization of venous catheters, the most common anesthesia associated with abnormal embolization pathways is the foramen ovale, found in all autopsy 35 %, other conditions found in atrial septal defect, ventricular septal defect, pulmonary arteriovenous malformation and other congenital heart disease, when the right atrial pressure increased acutely beyond the left atrial pressure, causing a right to left blood shunt, abnormal emboli through the gap Enter the left room.

Abnormal embolism can affect the kidneys, more than 40% of cases can involve more than one artery, including the cerebral circulation, unless the defect is repaired after a clear diagnosis, although the diagnosis of arterial embolism associated with deep vein thrombosis or pulmonary embolism is easier. However, abnormal embolism often has no obvious clinical venous thromboembolism. When the cardiac origin of the embolus is not obtained, the diagnosis of abnormal embolism should be accepted. In short, any renal artery wall lesion leads to renal artery stenosis. Intimal injury, tissue factor exposure, can activate the coagulation mechanism, causing local thrombosis of the arteries leading to renal artery thrombosis.

7. Hypercoagulable state: Congenital anticoagulant deficiency or antagonism (such as protein C, protein S, antithrombin III factor deficiency, etc.), or acquired coagulation abnormalities (such as nephrotic syndrome, systemic erythema) Lupus, etc., due to insufficient anticoagulant substances, is prone to thrombosis. Recently, thrombosis due to this type of cause has been reported frequently, including renal artery, lower extremity artery, pulmonary artery, and mesenteric artery.

Renal artery thrombosis and embolization prevention

1. Active prevention and treatment of the primary diseases causing the disease, especially in the elderly, should pay attention to the early diagnosis and treatment of various common diseases causing arteriosclerosis.

2. Try to avoid trauma and traumatic examination and treatment.

Renal artery thrombosis and embolization complications Complications

The main complications are acute renal infarction, hypertension, and acute, rapidly worsening renal failure.

Renal artery thrombosis and embolism symptoms Common symptoms Low complement hypertensive aorta blood supply disorders Abdominal pain Low fever Proteinuria Hypertension Back pain Nausea oliguria

The clinical manifestations of renal artery thrombosis or embolization depend on the rate, extent and extent of arterial occlusion. Small branches may be devoid of any symptoms or signs, and the renal artery trunk and its large branches are often blocked for typical clinical manifestations.

1. The performance of acute renal infarction: The patient may suddenly have severe low back pain, abdominal pain, back pain, similar to renal colic, radiation to the thigh, but also similar to acute cholecystitis, pain to the shoulder and back, some cases can be similar In acute pancreatitis or acute myocardial infarction, often have fever, vomiting, nausea, physical examination of the affected side of the renal pelvis pain and tenderness, increased white blood cells, nuclear left shift, may have hematuria and proteinuria, serum enzyme increased, aspartate aminotransferase It usually rises immediately after infarction, and returns to normal after 2 weeks. Alkaline phosphatase usually rises to the peak 3 to 5 days after infarction and returns to normal after 4 weeks.

2. Hypertension: About 60% of patients have high blood pressure in the short term due to renal ischemia and renin release after renal artery occlusion, generally lasting 2 to 3 weeks, of which about 50% of patients have persistent hypertension. While the other half of the patient's blood pressure can return to normal, renal artery occlusion can occur hypertensive crisis.

3. Acute renal failure: Chronic renal insufficiency may occur in slowly forming thrombus, acute renal insufficiency may occur in the blockage of renal occlusion of acute occlusion, and acute rapid deterioration of renal artery embolism in double renal artery or isolated kidney Renal failure often requires immediate hemodialysis. If the occlusion artery cannot be opened as soon as possible, the prognosis is poor. In addition, the clinical manifestations of renal cholesterol emboli are often different from renal embolism caused by other causes. Renal infarction is rare, the most common The clinical manifestations are acute, subacute or chronic progressive renal insufficiency, and thus the diagnosis of renal cholesterol emboli, atherosclerotic debris can be applied to the branch of the small arteries and affect the balllet arteries, resulting in decreased GFR due to embolism The release of regional ischemic renal segment renin can cause unstable hypertension, acute renal failure associated with atheromatous embolism, often with significant oliguria, with sodium excretion The score is increased, but renal insufficiency may also be non-oliguric and progress slowly due to spontaneous plaque ulcer and rupture. , Urine can be found in moderate proteinuria, microscopic hematuria or pyuria, which does not have diagnostic significance.

Renal artery thrombosis and embolization

1. Blood examination: visible increase of white blood cells, nuclear left shift; serum lactate dehydrogenase increased (usually more than 5 times the upper limit of normal) with a slight increase in plasma transaminase; aspartate aminotransferase often increased immediately after infarction, 2 After returning to normal after week, alkaline phosphatase often rose to the peak 3 to 5 days after infarction, returned to normal after 4 weeks, elevated renin-angiotensin in the blood, and abnormal renal function tests such as plasma creatinine in renal failure. Increased plasma enzyme levels and increased lactate dehydrogenase excretion in the urine should be highly suspected of renal infarction.

2. Urine examination: Cholesterol embolism syndrome common eosinophilia with or without eosinophilic urine, hypocomplementemia, anemia and thrombocytopenia, ESR, hyperamylasemia, serum creatine kinase Elevated, serum aspartate aminotransferase increased, urine test may have hematuria and proteinuria, often moderate proteinuria, microscopic hematuria and a small amount of pyuria.

3.X line:

(1) Abdominal plain film: The renal shadow is more normal. In a few cases, the renal shadow of the affected side is obviously reduced, and there is often a manifestation of reflex flatulence.

(2) intravenous pyelography: visible kidney function, renal pelvis is not developed, and retrograde angiography showed no abnormality of renal pelvis and renal pelvis, is a strong evidence for the diagnosis of acute renal artery embolism.

(3) renal angiography: the first choice for the diagnosis of this disease, renal angiography can be seen in the lesion area of the lesion appears filling defects, and the defect of the peripheral renal parenchyma or subcapsular can be developed due to collateral circulation, forming the so-called "kidney Shadow ring", but the small branch occlusion can only be seen when the affected part of the renal parenchyma is not developed, leakage of bleeding after infarction can form a hematoma caused by the displacement of adjacent normal blood vessels.

4. Nuclear medicine 99mTC-DTPA renal dynamic imaging: After embolization, the renal blood perfusion curve of the affected side is low, no perfusion peak, the kidney is lightly developed and lower than the surrounding tissue, forming a "black hole"; In the case of formation, uneven imaging occurs, and if the renal artery is not recanalized, renal atrophy occurs, and renal atrophy caused by other kidney diseases is difficult to distinguish.

5. Computerized tomography or magnetic resonance imaging: It can show characteristic changes of ischemic necrosis of renal parenchyma and is a non-invasive method with high specificity.

6. Echocardiography: Helps to determine cardiogenic renal embolism, presence of luminal emboli, valvular calcification and insufficiency, biologic valve emboli, and monitoring of heart rhythm, which can help diagnose arrhythmias.

Diagnosis of renal artery thrombosis and embolization

diagnosis

Acute occlusion of the larger branch or trunk of the renal artery may have obvious clinical manifestations, but the occlusion of the small renal artery branch is more likely to be missed and misdiagnosed. Because the disease does not have specific symptoms or signs of definite diagnosis, therefore, each clinical Specialists should be vigilant, and the following conditions should be suspected and the possibility of the disease:

1. There are pathogenic factors of renal infarction.

2. Persistent low back pain with nausea and vomiting, fever, sputum pain and tenderness in the kidney area.

3. Sudden appearance of hematuria.

4. Unexplained progressive exacerbation of azotemia and refractory hypertension.

5. Unexplained increase in serum enzymology.

Once the above performance occurs, relevant imaging examinations should be performed to assist in the diagnosis, and renal angiography should be performed for the diagnosis.

At present, there are many imaging diagnostic methods commonly used in clinical practice, and the above-mentioned auxiliary examinations are of high value for the diagnosis of acute renal artery occlusion.

The diagnosis of cholesterol embolism syndrome only stays in the clinic. In patients with diffuse vascular disease or recent intra-arterial surgery, renal failure occurs. It is necessary to suspect the disease. The embolus from the aorta often goes to other organs. Demonstrated as transient or local neuropathy, muscle or kidney pain, gangrene at the end of the limb, muscle necrosis, gastrointestinal bleeding, pancreatitis or reticular bluish, kidney is the most common organ involved (74% of cases), in patients There is often hypothermia in the first visit, and serological abnormalities associated with atherosclerosis include: leukocytosis, eosinophilia with or without eosinophilic urine, hypocomplementemia, anemia and thrombocytopenia, erythrocyte sedimentation rate, high Amylaseemia, elevated serum creatine kinase, elevated serum aspartate aminotransferase.

Differential diagnosis

1. The disease must be differentiated from acute cholecystitis, pancreatitis and other acute abdomen: patients with acute cholecystitis have fever, abdominal pain, jaundice and other "Xiaco" triad, physical examination of Moh's sign positive, abdominal B-ultrasound can be seen in gallbladder inflammation Or the presence of gallstones; acute pancreatitis abdominal pain can be "belly-like", blood, urine amylase increase and dynamic curve has a diagnostic significance.

2. Identification with other kidney diseases: Kidney stones with urinary tract infections may have symptoms and signs similar to renal infarction, but also transient hematuria, but mild or normal renal function impairment, no hypertension and increased serum enzymes.

3. Identification of arterial embolism with other sites: The early manifestation of intestinal ischemic necrosis caused by mesenteric artery occlusion is similar to that of renal infarction, but abdominal pain is heavy without fixed tenderness and rebound tenderness. The former is characterized by bloody stool or hematemesis. Typical acute myocardial infarction, symptoms can also be confused with acute renal infarction, dynamic observation of myocardial enzymes and ECG is very important, radionuclide myocardial thermal imaging, such as the discovery of segmental myocardial abnormal concentration can assist diagnosis; selective angiography It is the "gold standard" for diagnosis and an important basis for determining further treatment methods.

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