A study of fibrinogen and fibrinolysis in 10 adults with nephrotic syndrome.
In 10 patients with nephrotic syndrome (NS), the coagulation inhibitors, the fibrinolytic system and several functions of the fibrinogen-fibrin molecule were studied. Among the coagulation inhibitors, only antithrombin III (AT III) was found decreased and correlated with serum-albumin levels. Venous occlusion test provoked a normal tissue plasminogen activator (tPA) release in all patients. The plasminogen activator inhibitor (PAI) had an increased activity in 5 out of the 10 patients. Thrombin and reptilase times were found abnormal in most patients. The thrombin time (TT) prolongation correlated with serum albumin levels and was corrected by adding purified albumin. The fibrinogen was purified from each of the 10 patients' plasma. Only 2 of them showed abnormal polymerization in purified system, suggesting dysfibrinogenaemia. Other functions (thrombin binding, tPA stimulating activity, lysis by purified plasmin) were found normal except in one of the 2 patients with dysfibrinogenaemia whose fibrinogen lysis by plasmin was delayed. It is concluded that an abnormal fibrinogen molecule is not the most frequent explanation for thrombin time prolongation in NS.
D000328:Adult; D005340:Fibrinogen / Q000032:analysis / Q000302:isolation & purification*; D005342:Fibrinolysis; D006023:Glycoproteins / Q000097:blood; D006801:Humans; D009404:Nephrotic Syndrome / Q000097:blood*; D010960:Plasminogen Activators / Q000037:antagonists & inhibitors; D015849:Plasminogen Inactivators; D013918:Thrombin Time; D010959:Tissue Plasminogen Activator / Q000097:blood
D006023:Glycoproteins; D015849:Plasminogen Inactivators; D005340:Fibrinogen; D010960:Plasminogen Activators; D010959:Tissue Plasminogen Activator