Renal vein thrombosis

Introduction to renal vein thrombosis Renal vein thrombosis (RVT) refers to the formation of thrombus in the trunk and/or branch of the renal vein, resulting in partial or complete blockage of the renal vein causing a series of pathological changes and clinical manifestations. Some patients with nephrotic syndrome may have increased or normal platelet counts, and some patients may have increased platelet aggregation. This effect may also be related to decreased plasma protein content and elevated blood lipids. The specific mechanism is not clear, clinically diuretic, blood viscosity Increase, increase hypercoagulable state; long-term large amount of cortisol treatment, stimulate platelet production, increase the content of certain coagulation factors, make hypercoagulable state worse, patients with nephrotic syndrome due to interstitial and intracellular edema, impaired vascular endothelial function The balance between prostacgclin (PGI2) and thromboxane A2 (TXA2) in endothelial cells is disrupted, which is conducive to the formation of thrombus. basic knowledge The proportion of patients: 0.01%-0.03% (the incidence of this disease in patients with kidney disease is about 0.01%-0.03%) Susceptible people: no special people Mode of infection: non-infectious Complications: pulmonary embolism, hypertensive crisis

Cause of renal vein thrombosis

Hypercoagulable state of blood (30%):

Common diseases causing hypercoagulability of the blood are nephrotic syndrome; severe dehydration in infants; pregnancy or oral contraceptives; congenital thrombosis such as congenital antithrombin III deficiency, congenital protein C deficiency, systemic lupus erythematosus , myelofibrosis, etc.

High coagulation factor (25%):

Some patients with nephrotic syndrome may have increased or normal platelet counts, and some patients may have increased platelet aggregation. This effect may also be related to decreased plasma protein content and elevated blood lipids. The specific mechanism is not clear, clinically diuretic, blood viscosity Increase, increase hypercoagulable state; long-term large amount of cortisol treatment, stimulate platelet production, increase the content of certain coagulation factors, make hypercoagulable state worse, patients with nephrotic syndrome due to interstitial and intracellular edema, impaired vascular endothelial function The balance between prostacgclin (PGI2) and thromboxane A2 (TXA2) in endothelial cells is disrupted, which is conducive to the formation of thrombus.

Damage to the vein wall (20%):

Common diseases causing damage to the vein wall are renal cell carcinoma invading the renal vein; renal trauma; adjacent organ tissue lesions compress the renal vein, such as enlarged lymph nodes, abdominal aortic aneurysm.

Pathogenesis

The mechanism of renal vein thrombosis mainly includes excessive synthesis and inactivation of coagulation factors, decreased activity of fibrinolytic system, increased platelet count, enhanced activity, and abnormal function of vascular endothelial cells. These factors often coexist and affect each other. For causality, in an extremely complex dynamic change, the mechanism of renal vein thrombosis is discussed below with nephrotic syndrome as an example.

1. Coagulation and anticoagulant system A large amount of protein is lost with urine excretion during nephrotic syndrome, especially the molecular weight of anticoagulant substances such as small molecular weight protein, antithrombin III, anticoagulant protein C, protein S, antitrypsin, etc. Both are small (54,000 ~ 69,000 Da), easy to be lost with the discharge of urine, resulting in decreased anticoagulant activity, while coagulation factors V, VII, VIII and coagulation factor I are large molecular weight proteins (200,000 to 800,000) Da), which is not easily excreted by the kidneys, but can increase with the compensatory increase in liver synthesis, and enhances blood coagulation activity.

2. The normal activity of the fibrinolytic system of the fiber dissolution system is the dynamic balance of the blood flow state with the coagulation system, preventing the occurrence of bleeding or thrombosis, and the excessive loss of plasminogen in the patients with nephrotic syndrome (molecular weight). The plasmin inhibitor (such as 2-macroglobulin) is difficult to be excreted from the urine due to its large molecular weight, and the plasma concentration is increased, which in turn increases the inactivation of plasmin. Therefore, the fibrinolytic activity is negligible in nephrotic syndrome, and it is easy. Form a thrombus.

3. The contradiction imbalance between coagulation and fibrinolysis will make the body easy to form thrombus, whether it is nephrotic syndrome or other causes of renal vein thrombosis, more or less related to the above-mentioned pathogenesis, understand the kidney The mechanism of venous thrombosis is conducive to our understanding of the occurrence of clinical manifestations and further guidance of treatment.

Renal venous thrombosis prevention

1. Promote blood circulation to encourage patients to increase activities, if necessary, assist patients to turn over regularly, pay attention to active or passive exercise of the limbs, such as limbs' extension and flexion, or massage the leg muscles, 4 times / d, each 10 minutes to promote veins Reflux.

2. Avoid blood stasis for high-risk patients, including elderly people with reduced activity, obese people, post-operative or brave patients, after the surgery, put elastic bandages on the lower limbs or wear elastic stockings to promote blood return; avoid under the knee pad Hard pillow, excessive hip flexion, so as not to affect venous return.

3. Protect the venous blood vessels and avoid damage to the blood vessel wall. Especially for patients who have long-term infusion after surgery, try to protect their veins, especially the lower extremity veins, and avoid repeated puncture in the same vein. When stimulating drugs, try to avoid drug osmosis. Out of the blood vessels.

4. Inhibition of platelet aggregation Oral administration of small doses of enteric-coated aspirin, compound Danshen tablets, etc. to reduce platelet accumulation.

Renal venous thrombosis Complications, pulmonary embolism, hypertensive crisis

Mainly complicated by acute renal failure and pulmonary embolism, individual patients may have complications such as hypertensive crisis.

Symptoms of renal vein thrombosis Common symptoms Upper vena cava obstruction Hypertension Proteinuria Chronic venous insufficiency Venous hypercoagulable state Rib pain Nursing lower extremity edema Kidney area tenderness

The clinical manifestations of this disease have great individual differences, depending on the severity and severity of RVT, acute complete thrombosis of the renal vein, more common in children, due to insufficient collateral circulation, clinical manifestations of chills, fever Severe lumbar pain and abdominal pain, obvious tenderness of the rib angle, pain in the kidney area, elevated white blood cells, loss of function of hematuria and kidney, imaging can be found in renal enlargement, such as thrombosis in both renal veins Or, if one side of the kidney has no function, and the other side of the renal vein thrombosis, oliguria and acute renal failure may occur, in patients with nephrotic syndrome, pregnancy, oral contraceptives, etc., usually patients are younger, often Unexplained acute or rapid deterioration of renal function, accompanied by progressive exacerbation of proteinuria and hematuria, and RVT caused by suspicion and further examination. In older people, if the thrombosis is slower, the collateral circulation has been Fully established, impaired renal function is not large, clinical can only be manifested as multiple embolism or embolism in other parts of the body, some patients can develop hypertension, lower extremity edema, all RVT disease If the inferior vena cava is involved, the inferior vena cava obstruction syndrome may occur, and the lower extremity edema and the collateral circulation of the abdominal wall may occur. The most serious complication in renal vein thrombosis is pulmonary embolism, and about half of the chronic kidneys. Venous thrombosis has pulmonary embolism and is often the first symptom.

Patients with nephrotic syndrome may develop thrombosis due to hypercoagulable state of the blood, and their clinical manifestations are also highly individual. RVT may have no special clinical manifestations, and may have certain clinical symptoms such as fever (17%). Acute low back pain (10% to 64%) and tenderness and tenderness in the kidney area, sudden onset of hematuria (74%), elevated serum creatinine, and B-ultrasound examination revealed an enlarged kidney (43%). These were found in patients with nephrotic syndrome. Symptoms should pay attention to the possibility of RVT, but most (75%) RVT has no typical clinical manifestations (chronic or subclinical), and there is no obvious relationship with the fluctuation of nephrotic syndrome, so for these RVT It is difficult to make a diagnosis.

Renal venous thrombosis

1. Blood examination increased white blood cells; plasma lactate dehydrogenase increased; antithrombin III and plasminogen levels decreased, which is the cause of renal vein thrombosis, and the body's compensatory coagulation-fibrinolytic activity after thrombus formation As a result, the fibrinogen and plasma plasmin inhibitor 2-macroglobulin levels are increased, and may be low or normal due to consumption in the acute phase.

2. Urine examination showed a significant increase in hematuria and urinary protein; a sharp decrease in renal function showed a significant increase in urea nitrogen and creatinine.

3. Imaging examination Non-invasive imaging examinations such as B-ultrasound, CT, magnetic resonance and renal nucleus scanning are only useful for the diagnosis of renal vein thrombosis. Typical signs are low-density thrombus in enlarged renal vein. The surrounding vein of the diseased kidney presents a reptile collateral circulation, which is of little value in the diagnosis of renal vein branch thrombosis.

4. The diagnosis of renal vein thrombosis by venous puncture selective renal venography has a definite diagnosis. It can clearly show the location of the thrombus obstruction, the scope, whether there is collateral circulation, etc., but due to the large renal blood flow, the contrast agent is retrogradely filled. It is difficult, even false positive results can be obtained. It is important to master the depth of intubation, the speed and total amount of contrast agent injected. Some clinicians take renal artery cannulation and inject 10g of adrenaline to reduce renal blood flow before renal venography. Or use renal venous balloon to temporarily block renal blood flow during angiography to ensure that the contrast agent is fully retrograde to each renal vein branch, and the development effect is improved. Renal venography may cause serious complications and should be prevented as much as possible. During the operation, the thrombus may be touched, and the embolism may cause the embolism of the lung; secondly, the patient often has a hypercoagulable state of the blood, and the blood vessel wall (such as the puncture mouth) may form a thrombus during the contrast process, causing blockage of the renal vein or the lower extremity vein; Third, the contrast agent on the kidney damage, the first two can be avoided by correct, careful operation, the latter can be through a lot of drinking water or infusion Light concentration of the contrast agent, non-ionic iodinated contrast media used in recent years, compared with the original common ionic contrast agents reduce a lot of damage to the kidneys, but the price is more expensive.

5. Histopathological examination of renal vein thrombosis when the pathological changes of the affected side to the dirty volume, can be a pathological change of hemorrhagic infarction, in patients with nephrotic syndrome, acute renal biopsy can show the tissue type of nephrotic syndrome In addition, renal interstitial edema can also be seen, glomerular capillary vasospasm dilatation and congestion, there may be microthrombus formation, sometimes visible in the capillary wall with polymorphonuclear cell adhesion, long-term unresolved renal vein thrombosis, can lead to tubular atrophy , renal interstitial fibrosis changes.

Diagnosis and differential diagnosis of renal vein thrombosis

Diagnostic criteria

The clinical diagnosis of renal vein thrombosis has certain difficulties. The rate of missed diagnosis is high. The doctor must be vigilant. Patients with pathogenic factors of renal vein thrombosis should be further assisted in the examination to confirm the diagnosis.

1. Sudden onset of severe low back pain.

2. It is difficult to explain the increase in hematuria.

3. Unexplained increase in urine protein.

4. Difficult to explain the sharp decline in renal function.

5. Asymmetrical lower extremity edema.

6. Patients with nephrotic syndrome have refractory hormone resistance.

7. Patients with nephrotic syndrome have pulmonary embolism or embolization at other sites.

Add laboratory tests and imaging examinations to meet the characteristics of this disease, can make a diagnosis of renal vein thrombosis.

Differential diagnosis

Identification of kidney diseases such as renal artery thrombosis and embolism and other causes should be identified with other embolic diseases.

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