Hypercoagulability in the Nephrotic syndrome.

摘要: The risk of thromboembolic complications in patients with the nephrotic syndrome (NS) is higher than any other condition encountered internal medicine. Such comprise venous thromboses (calf, thigh, renal vein) or without pulmonary embolism and arterial (coronary thromboses, cerebral artery peripheral thromboses). Several defects plasmatic coagulation system, fibrinolysis platelet function had been recognized syndrome. Increased hepatic synthesis causes a rise factors, I, II, VII, VIII, X increased loss lowering plasma concentration antithrombin III concentration. There little evidence for DIC. Plasminogen diminished, whereas total antiplasmin activity increased. Low alpha-1-antitrypsin secondary to outweighed by concentrations inhibitors especially alpha-2-macroglobulin alpha-2-antiplasmin. common presence material urine reacting as fibrin degradation products passive hemagglutination techniques appears be proteolytically degraded fibrinogen excreted result non-selective glomerular proteinuria. Platelet counts are normal slightly elevated survival time slightly, decreased. Definite abnormalities spontaneous aggregation ADP- collagen-induced demonstrable. Furthermore, arachidonic acid induced malondialdehyde formation platelets NS Addition albumin normalises aggregation. This finding points some acquired defect function.