Infection, nephrotic syndrome in patients with decreased resistance to the most important reason is due to: ① urine loss of a large number of IgG. ② lack of B factor (complement pathway alternative ingredients) lead to the role of bacterial immune conditioning defects; ③ malnutrition, the body non-specific immune response ability weakened, resulting in impaired immune function. ④ transferrin and zinc are lost from the urine. Transferrin is necessary to maintain normal lymphocyte function, zinc ion concentration and thymosin synthesis. ⑤ local factors. Pleural effusion, ascites, skin edema caused by high skin rupture and severe edema to dilute the local body fluid factor, defensive function weakened, are susceptible factors in patients with nephrotic syndrome. Before the advent of antibiotics, bacterial infection was one of the major causes of death in patients with nephrotic syndrome, severe infections occur mainly in children and the elderly, adults are rare. Common clinical infections are: primary peritonitis, cellulitis, respiratory infections and urinary tract infections. Once the infection diagnosis is established, should be treated immediately.
Hypercoagulable state and venous thrombosis, nephrotic syndrome, hypercoagulable state, mainly due to changes in blood clotting factor. Including Ⅸ, Ⅺ factor decreased, V, Ⅷ, X factor, fibrinogen, β-thromboglobulin and platelet levels increased. Platelet adhesion and increased cohesion. Antithrombin Ⅲ and antiplasmin activity decreased. Therefore, the accumulation of coagulation and procoagulant factors, anti-agglutination and anticoagulant factor decline and fibrinolysis mechanism damage, nephrotic syndrome is hypercoagulable state. Antibiotics, hormones and diuretics for the application of venous thrombosis factors, hormones play a role in coagulation protein, and diuretics to make the blood concentration, blood viscosity increased.
In the case of nephrotic syndrome, when plasma albumin is less than 2.0 g / d1, the risk of renal vein thrombosis increases. Most of the thrombosis first in the formation of small veins, and then extended, and ultimately involving the renal vein. Renal vein thrombosis, in patients with membranous nephropathy can be as high as 50%, in other pathological types, the incidence of 5% to 16%. Renal venous thrombosis in acute patients can be expressed as sudden onset of low back pain, hematuria, white blood cell urine, increased protein and renal dysfunction. Chronic patients without any symptoms, but after thrombosis of renal stasis often increase proteinuria, or poor response to treatment. Due to thrombosis, renal embolism symptoms common, can occur pulmonary embolism. Can also be associated with renal tubular dysfunction, such as diabetes, amino acid urine and renal tubular acidosis. A clear diagnosis of renal vein angiography. Doppler ultrasound, CT, IMR and other non-invasive examination also help to diagnose. Elevated plasma beta thromboplastin suggests a potential thrombosis, and the increase in blood alpha2-antipathrin is also considered a sign of renal vein thrombosis. Peripheral deep vein thrombosis rate of about 6%, common in the deep vein of the calf, only 12% of clinical symptoms, 25% can be found by Doppler ultrasound. The incidence of pulmonary embolism was 7%, and 12% had no clinical symptoms. Other venous involvement is rare. Arterial thrombosis is rare, but in children, although the incidence of thrombosis is very low, but the arteries and veins involved as common.
Acute renal failure, acute renal failure for nephrotic syndrome, the most serious complications, often need dialysis treatment. Common causes are: hemodynamic changes: nephrotic syndrome often hypoproteinemia and vascular disease, especially in elderly patients with multiple renal arteriosclerosis, blood volume and blood pressure is very sensitive, so when the acute blood loss, vomiting, Diarrhea caused by loss of body fluids, surgical damage, ascites, a large number of diuretic and the use of antihypertensive drugs, can make a further decline in blood pressure, resulting in a substantial reduction in renal perfusion, and thus reduce the glomerular filtration rate, and after acute ischemia Tubular epithelial cell swelling, degeneration and necrosis, leading to acute renal failure.