Browsing by Author "Downey, P"

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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.