Increased fibrin formation and impaired fibrinolytic capacity in severe chronic kidney disease. Issue 4 (June 2016)

• Record Type: Journal Article
• Authors: Mörtberg, Josefin; Blombäck, Margareta; Wallén, Håkan; He, Shu; Jacobson, Stefan H.; Spaak, Jonas
• Is Part Of: Blood coagulation and fibrinolysis. Volume 27:Issue 4(2016)
• Page Start: 401
• Page End: 407
• Publication Date: 2016-06
• Subjects: coagulation -- fibrin network -- fibrinolysis -- haemodialysis -- haemostasis; Blood -- Coagulation -- Periodicals; Fibrinolysis -- Periodicals; Hemostasis -- Periodicals; Thrombosis -- Periodicals; Blood Coagulation -- Periodicals; Fibrinolysis -- Periodicals; Hemostasis -- Periodicals; Thrombosis -- Periodicals; 612.115
• DOI: 10.1097/MBC.0000000000000462
• Languages: English
• ISSNs: 0957-5235

Abstract

Abstract : Chronic kidney disease (CKD) is associated with a concurrent increased risk of thrombosis and bleeding. We aimed to investigate whether CKD is associated with increased fibrin formation, impaired fibrin degradation, or both. Twenty-one patients with CKD stage 4 (CKD 4), 15 haemodialysis patients, and 13 controls (C) without kidney disease were studied. We used a global assay to determine fibrin formation and degradation in plasma. Fibrin turbidity was measured over time to obtain a value of the coagulation activation profile ( C p ) and the fibrinolysis activation profile ( F p ), and the amount of fibrin formed, termed fibrin optical density sum (fibrin OD-sum). We used scanning electron microscopy (SEM) to visualize the fibrin network. Plasminogen activator inhibitor type-1 antigen, thrombin-activatable fibrinolysis inhibitor activity, fibrinogen, von Willebrand factor, antithrombin, albumin, and C-reactive protein were measured in plasma. Fibrin OD-sum was significantly elevated in haemodialysis patients [312 a.u.; 278–435 (median; interquartile range); P < 0.0013] and in CKD 4 (293 a.u.; 169–434; P = 0.0119) compared with controls (115 a.u.; 82–234). SEM showed a tight fibrin network in haemodialysis and CKD 4 patients. F p was lower in the haemodialysis group than in controls ( P = 0.030). Plasminogen activator inhibitor type-1 was lower in haemodialysis patients ( P = 0.034). Thrombin-activatable fibrinolysis inhibitor activity, C p, antithrombin, and C-reactive protein did not differ between groups. Fibrinogen was significantly elevated and albumin decreased in both haemodialysis and CKD 4 patients compared with controls. Von Willebrand factor was elevated in haemodialysis patients compared with controls ( P = 0.010). The prothrombotic state in severe CKD is characterized by impaired fibrinolysis in association with increased fibrin formation despite normal levels of endogenous fibrinolysis inhibitors.