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  • Title: [Hypofibrinolysis after venous occlusion in patients treated with long-term hemodialysis].
    Author: Opatrný K, Vít L, Opatrná S, Sulková S, Bodláková B.
    Journal: Cas Lek Cesk; 1994 May 30; 133(11):346-9. PubMed ID: 8004664.
    Abstract:
    BACKGROUND: Haemodialysis patients with chronic renal failure suffer not only from thromboses of the vascular access but frequently also from atherosclerosis with thrombotic complications. Knowledge of the etiopathogenesis of thrombotic complications in haemodialysis patients are incomplete. The aim of the present study was to evaluate fibrinolysis at the level of plasminogen activation under conditions of a dynamic test, using methods which reflect sensitively and specifically the activity of the tissue-type plasminogen activator (t-PA) and the activity of the inhibitor of the tissue-type plasminogen activator (PAI-1). METHODS AND RESULTS: The group of examined subjects was formed by 16 patients (9 men and 7 women, mean age 42 years, range 26-63) who suffered from chronic renal failure (causes: 9x chronic glomerulonephritis, 6x interstitial nephritis, 1x polycystic kidneys) treated by long-term haemodialysis on average for 52 (20-110) months; the control group of 11 healthy volunteers was very close as regards age distribution. t-PA and PAI-1 were examined after stimulation by venous occlusion (VO). In healthy subjects VO significantly raises the t-PA activity (first value before, second after VO: t-PA 0.81-2.19 IU/ml, p < 0.01), specific t-PA activity (0.19-0.31 IU/ng, p < 0.05) and t-PA/PAI (0.06-0.24 IU/U, p < 0.01, decreases PAI activity (11.80-10.98 U/ml, p < 0.05) and specific PAI activity (0.52-0.40 U/ng, p < 0.01). In the group of haemodialysis patients VO did not change significantly the t-PA activity (p = NS), the specific t-PA activity (p = NS), nor the ratio of t-PA/PAI (p = NS); the PAI declined significantly (13.78-10.65 U/ml, p < 0.05), similarly as the specific PAI activity (0.97-0.65 U/ng, p < 0.01). From comparison of the results of fibrinolysis from healthy and dialysis subjects ensues that the response to VO in dialysis patients differs from that in healthy subjects. CONCLUSIONS: Dialysis patients have impaired fibrinolysis manifested by a lacking rise of activity of the plasminogen tissue activator after stimulation by venous occlusion. The small rise of t-PA activity after venous occlusion can contribute to the development of thrombotic complications in haemodialyzed patients.
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