Key result
Renal transplant is linked to elevated TAFI and thrombin markers, suggesting impaired fibrinolysis.
Why the study?
The reason for impaired fibrinolysis in renal transplant recipients is not fully understood despite observed suppression of fibrinolysis and accelerated atherosclerosis progression.
Are concentrations of TAFI and markers of thrombin generation and endothelial injury elevated in stable, non-diabetic renal transplant recipients compared to healthy volunteers?
Observational (n=47)
Are concentrations of TAFI and markers of thrombin generation and endothelial injury elevated in stable, non-diabetic renal transplant recipients compared to healthy volunteers?
Elevated TAFI antigen in renal transplant recipients may contribute to impaired fibrinolysis and accelerated atherosclerosis progression.
Elevated TAFI was associated with impaired fibrinolysis in renal transplant recipients; hypothesis-generating Level 5 data leave its causal role in atherosclerosis open.
BACKGROUND: Cardiovascular disease (CVD) is a major cause of death in renal transplant recipients (RTR). Suppression of fibrinolysis plays a role in the progression of atherosclerosis. Accelerated progression of atherosclerosis and fibrinolytic system suppression has been observed in RTR. Despite many years of intensive research, the reason for impaired fibrinolysis in this patient population is not fully understood. Thrombin-activatable fibrinolysis inhibitor (TAFI) is a recently discovered glycoprotein combining coagulation and fibrinolysis. This study was conducted to evaluate concentrations of TAFI, markers of thrombin generation, endothelial injury, and some standard laboratory parameters in RTR receiving triple immunosuppressive drug regimen. METHODS: The study was performed in 29 stable, non-diabetic kidney transplant recipients treated with cyclosporin A, azathioprine, and prednisone and in 18 age- and sex-matched healthy volunteers. Soluble thrombomodulin (sTM), prothrombin fragments F1+2 (F1+2), thrombin--antithrombin complexes (TAT), plasmin--antiplasmin complexes (PAP), and TAFI were measured with commercially available kits. RESULTS: The RTR group had significantly higher plasma levels of TAT, F1+2, sTM and TAFI than the healthy volunteers. There were no differences in PAP concentrations between the two groups. Plasma sTM correlated inversely with creatinine clearance, body mass index, haemoglobin, and albumin. Plasma TAT level was positively associated with total cholesterol. TAFI antigen influenced negatively PAP antigen concentration. CONCLUSIONS: On the basis of our research, we concluded that elevated circulating TAFI antigen might be a new link in the pathogenesis of impaired fibrinolysis in RTR, and thus atherosclerosis progression. In the patient group there is also evidence of endothelial injury, followed by secondary activation of the coagulation cascade. Hypercholesterolaemia in RTR is associated with enhanced thrombin activity.
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Hryszko et al. (2001) conducted an observational in Renal transplant recipients (n=47). Renal transplant recipient status vs. Healthy volunteers was evaluated on Concentrations of TAFI, markers of thrombin generation (F1+2, TAT), endothelial injury (sTM), and plasmin-antiplasmin complexes (PAP). Renal transplant recipients had significantly higher plasma levels of TAT, F1+2, sTM, and TAFI than healthy volunteers, suggesting elevated TAFI may contribute to impaired fibrinolysis.
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