Browsing by Author "Tagle, R"

Now showing 1 - 4 of 4
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    Hemostatic disorder of uremia: The platelet defect, main determinant of the prolonged bleeding time, is correlated with indices of activation of coagulation and fibrinolysis
    (GEORG THIEME VERLAG KG, 1996) Mezzano, D; Tagle, R; Panes, O; Perez, M; Downey, P; Munoz, B; Aranda, E; Barja, P; Thambo, S; Gonzalez, F; Mezzano, S; Pereira, J
    Several parameters of primary hemostasis and markers of activation of coagulation and fibrinolysis were measured in 38 patients with severe (creatinine clearance <20 ml/min) chronic renal failure (CRF) without dialysis and diseases or drugs affecting hemostasis. Bleeding time (BT) was prolonged in 25/48 patients, and was correlated with age of patients, severity of renal failure, hematocrit, impairment in platelet aggregation-secretion and decrease in platelet ATP content. Defects in von Willebrand factor played no role in the prolongation of the BT. Multivariate analysis showed that only platelet dysfunction and severity of renal disease were independent predictors of the BT in uremia. The platelet functional disorder was significantly correlated with a reduction in platelet ATP and ADP.
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    Inflammation, not hyperhomocysteinemia, is related to oxidative stress and hemostatic and endothelial dysfunction in uremia
    (BLACKWELL SCIENCE INC, 2001) Mezzano, D; Pais, EO; Aranda, E; Panes, O; Downey, P; Ortiz, M; Tagle, R; Gonzalez, F; Quiroga, T; Caceres, MS; Leighton, F; Pereira, J
    Background. Several cardiovascular risk factors are present in patients with chronic renal failure (CRF), among which are systemic inflammation and hyperhomocysteinemia. Increased oxidative stress, endothelial activation/dysfunction, and coagulation activation are considered integral components of the inflammatory response, but have also been proposed as mediators of plasma homocysteine (tHcy)-induced cell damage. Using correlation analysis, we assessed the relative contributions of inflammation and hyperhomocysteinemia in the abnormal oxidative stress, endothelial activation/dysfunction, and hemostasis activation in patients with CRF.
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    Pharmacokinetics of vancomycin in patients with severely impaired renal function
    (DUSTRI-VERLAG DR KARL FEISTLE, 1996) GonzalezMartin, G; Acuna, V; Perez, C; Labarca, J; Guevara, A; Tagle, R
    The pharmacokinetics of 1 g dose of intravenous vancomycin was studied in 8 patients with severe renal failure. Serum vancomycin levels were determined by fluorescence polarization immunoassay. After single dose of vancomycin peak concentrations ranged from 37.8 mu g.ml(-1) to 109.3 mu g. ml(-1) (mean 64.9 +/- 21.7 mu g.ml(-1)). Vancomycin trough concentration 168h after administration of the antibiotic ranged from 2.23 mu g.ml(-1) to 11.42 mu g.ml(-1) (mean 6.55 +/- 2.8 mu g.ml(-1)). The data were analyzed using a PCNONLINE computer program, and in all patients a triexponential model described how concentrations decreased in time. Three-compartment parameters obtained from the 8 patients were t(1/2) alpha = 0.312 +/- 0.242 h, t(1/2) beta 6.012 +/- 5.36 h, and t(1/2) gamma = 131.0 +/- 46.7 h. Vd = 0.158 +/- 0.121 1.kg(-1), Vdss = 0.920 +/- 0.248 1.kg(-1) and total Cl = 0.10 +/- 0.049 1.h(-1) per kg of weight. Between 1.5% and 21.2% of the administered vancomycin dose was eliminated during hemodialysis. The dialysis clearance of vancomycin ranged from 50.6 ml.min(-1) to 76.8 ml.min(-1) (average: 62.4 +/- 10.4 ml.min(-1)). However, after dialysis plasma concentrations returned to pre-dialysis values. In accordance to our kinetic study 1 g of vancomycin given every 7 days is adequate treatment for methicillin-resistant Staphylococcus aureus infections in patients with severe renal failure whose creatinine clearance is lower than 10 ml.min(-1).
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    Tranexamic acid inhibits fibrinolysis, shortens the bleeding time and improves platelet function in patients with chronic renal failure
    (F K SCHATTAUER VERLAG GMBH, 1999) Mezzano, D; Panes, O; Munoz, B; Pais, E; Tagle, R; Gonzalez, F; Mezzano, S; Barriga, F; Pereira, J
    Background: A defect in platelet function is the main determinant of the prolonged bleeding time in chronic renal failure (CRF). We previously reported a significant correlation between platelet abnormalities and elevated plasma markers of plasmin and thrombin generation. Our aim was to explore thr effect of inhibiting both plasmin action with tranexamic acid (TA) and thrombin production with low molecular weight heparin (LMWH), on the bleeding time (BT) and platelet function in patients with CRF. Methods: 37 patients with CRF (mean creatinine 8.6 +/- 4.4 mg/dl) under conservative treatment, with prolonged BT, entered this study and received TA during 6 days, with (n = 24) and without LMWH (n = 13). BT, platelet aggregation/secretion, platelet granule contents, von Willebrand factor and parameters of coagulation and fibrinolysis were recorded before and at the end of treatment. Results: The BT was shortened in 26/37 (67%) patients. This effect was associated with significant improvement of platelet aggregation and secretion, with decrease to a normal range of fibrin/fibrinogen degradation products, mild increase in plasmin-antiplasmin complexes and pronounced reduction of circulating plasminogen. No differences were seen among patients with or without LMWH. No serious side effects or complications were observed. Interpretation: These findings indicate that the activation of fibrinolysis plays a significant role in the defect of primary hemostasis in patients with CRF. inhibition of plasmin activity with TA shortens the BT and improves platelet function in the majority of patients with severe disease.