高凝状态和血栓、栓塞并发症（Hypercoagulable state and complications of thrombosis and embolism）

高凝状态和血栓、栓塞并发症（Hypercoagulable state and complications of thrombosis and embolism） 高凝状态和血栓、栓塞并发症(Hypercoagulable state and complications of thrombosis and embolism) Hypercoagulable state and complications of thrombosis and embolism Nephrotic syndrome with hypercoagulable state, prone to thrombosis and embolism complications, including renal vein thrombosis (the most common occurrence rate is as high as 10%~50%, which 3/4 cases with chronic form, no clinical symptoms); in addition, pulmonary vascular thrombosis, embolism, lower extremity vein, inferior vena cava, cerebral vascular thrombosis and coronary artery vascular thrombosis is not uncommon, and portal vein thrombosis in foreign literature reports. Thrombosis and embolism complications are the important factors that directly affect the treatment effect and prognosis of nephrotic syndrome. Etiology and pathogenesis 1. blood concentration nephrotic syndrome patients due to plasma protein (especially albumin) concentration decreased, plasma extravasation, resulting in intravascular dehydration, effective blood volume reduction, blood concentration. 2. hyperlipidemia and hyperlipidemia make the blood viscosity increase, and promote the occurrence of thrombosis and embolism complications. 3. blood coagulation, anticoagulation and fibrinolysis abnormalities in nephrotic syndrome due to certain proteins (especially molecular weight smaller "lost in the urine and liver protein synthesis increase, caused by coagulation, anticoagulation and fibrinolysis system disequilibrium. These exceptions mainly include the following points. (1) the coagulation and anticoagulation system: nephrotic syndrome decreased clotting factor, factor XII in blood, which is due to coagulation factor XII, small molecular weight, easy from urine loss, if the amount is not enough to replace lost synthesis from the urine volume decreased, IX molecule V factor XII; and eighth, X factor, fibrinogen, beta thromboglobulin due to high molecular weight (above 200 thousand Dalton), not through the glomerular filtration barrier, so the level in the blood increased significantly. Domestic experiments have shown that the lower the albumin, the higher the fibrinogen; small molecules of anticoagulant factors such as antithrombin 1, protein C and S are often reduced. I is the most important anticoagulant thrombin in plasma, antithrombin I and its cofactor of heparin plasma anticoagulant activity all accounted for about 50%, which can inhibit the activation of factor XII, Xi, XIII, VII and thrombin, prevent thrombosis. The reduction of antithrombin III levels does not adequately inhibit coagulation factors, and is also one of the causes of thrombosis. Domestic studies have shown that serum antithrombin I levels in patients with renal syndrome have decreased significantly, while urinary levels have increased, in addition to the loss of urine output, but also with hypercoagulability and consumption of thrombosis related: (2) fibrinolytic system: plasminogen is often reduced in small and medium-sized molecules of the blood, while plasminogen activator, competitive inhibitor, lipoprotein and plasmin inhibitor alpha 2 globulin are often increased, resulting in decreased fibrinolysis. 4. platelet hyperfunction Nephrotic syndrome, platelet adhesion and aggregation function were significantly increased, and sometimes the number increased, the change and hypoalbuminemia and hyperlipidemia are closely related, the hypercholesterolemia induced TXA2 generation increased and hypoproteinemia caused by anticoagulant increased platelet aggregation is increased. In addition, because of the immune injury, platelets release various bioactive substances, adhesion to the glomerular capillary wall is damaged, the release of platelet aggregation, platelet embolism formation in the local, prompted in the surrounding fibrin deposition; release of platelet factor, leading to activation of coagulation factor XIII, promote thrombin generation, thereby accelerating blood coagulation. 5. use of diuretics In nephrotic syndrome, the use of diuretics leads to insufficient blood volume, blood concentration, and increased blood viscosity. 6. application of glucocorticoids The use of glucocorticoids in nephrotic syndrome aggravates the hypercoagulable state of the blood. Steroid hormone can inhibit monocyte macrophage system function, weaken to some activated coagulation factors phagocytosis; glucocorticoid can increase factor VIII activity, increased lipid content and promote blood coagulation function and hypercoagulability. 7., vascular endothelial damage There are reports of nephrotic syndrome due to immune function of vascular endothelial damage, collagen fiber is exposed, the activation of coagulation factors in plasma, and the activation of endogenous and exogenous coagulation system, promoting hypercoagulability and thrombosis. Two 、 clinical manifestation Thromboembolic complications are common in the vein and can also occur in the arteries. The common venous thrombosis is renal vein thrombosis, inferior vena cava thrombosis and limb vein thrombosis. The clinical manifestations vary with the location of the thrombus, the location of the embolism, the rate of formation, and the degree of occlusion of the vessel. 1. renal vein thrombosis, renal vein thrombosis is one of the most serious complications of nephrotic syndrome, which is caused by thrombosis or thrombosis of the main and main branches of the renal vein. In nephrotic syndrome, the risk of renal vein thrombosis increases when plasma albumin is less than 20g/L. The incidence rate was 20%~40%. Primary nephrotic syndrome of all pathological types can occur, but membranous nephropathy and mesangial proliferative glomerulonephritis are more common. According to reports, renal vein thrombosis in patients with membranous nephropathy can be as high as 50%, in other pathological types, the incidence rate of 5%~16%, especially in small lesions and mesangial proliferative glomerulonephritis less. Renal vein thrombosis most occult, renal vein thrombosis in the short term patients presented with sudden onset of upper abdomen, costovertebral angle or lateral abdominal pain is often severe, may be associated with renal pain; patients may have pleuritic chest pain; microscopic or gross hematuria, a sudden increase in urinary protein, kidney function loss were found in renal disease; the increase in size, can also have a fever, nausea, vomiting, hypertension etc.. Small branch of chronic renal vein thrombosis, especially in patients with collateral circulation, is often asymptomatic and does not require renal venography. According to the report, this kind of clinical asymptomatic about 3/4. However, the renal congestion after thrombosis often aggravates proteinuria, or has a poor response to treatment. It can cause progressive impairment of renal function and is accompanied by tubular dysfunction, which can easily be misdiagnosed as chronic renal failure. As a result of thrombus shedding, the symptoms of renal embolism are common, and pulmonary embolism can occur. 2. the incidence of cerebral infarction caused by nephrotic syndrome is low. The complication rate was reported to be 2%. Its characteristic is the age of onset is mild, the average age is only 37.8 years old, obviously lower than the general ischemic cerebrovascular disease (average age 56 years old). This may be due to nephrotic syndrome occurring in children and young adults, while hypertension and atherosclerosis are common in middle-aged and elderly people: Nephrotic syndrome complicated with cerebral infarction time had no obvious rule, can occur at any stage of nephrotic syndrome, nephrotic syndrome disease did not improve as long as it is possible to form and infarction associated with proteinuria, hypoproteinemia, abnormal degree. But some scholars believe that nephrotic syndrome is prone to thrombosis and embolic complications in the first few months. The location of infarction is mostly distributed in the large and middle arteries. It can occur in the basal ganglia, thalamus, temporal parietal lobe, pontine infarction and so on. The infarct size ranged from lacunar infarction to large infarct. The extent of infarction was below 2.3cmx5.5cm, and the maximum was 6cmx4cm. Other venous thrombosis, peripheral deep vein thrombosis rate is about, common in the deep vein of the leg, only clinical symptoms, 25% by Doppler ultrasound findings. The incidence of pulmonary embolism was 7%. Changsha Puji hospital to remind other venous involvement rare nephropathy. Arterial thrombosis can be formed in the pulmonary, cerebral and limb arteries. The first two can be fatal, and the latter often causes gangrene. Three, auxiliary examination 1. the diagnosis of venous branch thrombosis in renal venography often relies on selective renal venography. 2. Doppler ultrasonography, CT, MRI and ECT are of great value in the diagnosis of renal vein thrombosis. 3.. Plasma daily thrombosis, egg alpha 2, plasmin, and increased plasma beta thrombus suggest potential thrombosis, increased alpha 2 plasmin in blood, and is also considered a marker of renal vein thrombosis. Four Renal function test showed a progressive deterioration of renal function in patients with renal vein thrombosis in the short term, and showed a progressive increase in serum creatinine and blood urea nitrogen. 5. routine urine urine visible red blood cell tube, urine protein increased significantly. 6. renal biopsy pathological examination of renal interstitial edema, glomerular capillary loop, peritubular capillary wall cellulose deposition. Four. Diagnosis 1. in line with the diagnosis of nephrotic syndrome in patients with proteinuria (> 3.5g/24h), hypoproteinemia (less than 30g/L), accompanied by severe edema and hyperlipidemia. 2., there are clinical manifestations of thrombosis and embolism, such as sudden low back pain, neurological positioning, signs and so on. The definitive diagnosis requires renal venography, and noninvasive examinations such as Doppler ultrasonography, CT, and MRI are also helpful. Increased levels of plasma beta thrombus suggest potential thrombosis, an increase of alpha 2 plasmin in blood, and is also considered a marker of renal vein thrombosis.