Tranexamic acid inhibits fibrinolysis, shortens the bleeding time and improves platelet function in patients with chronic renal failure

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dc.contributor.authorMezzano, D
dc.contributor.authorPanes, O
dc.contributor.authorMunoz, B
dc.contributor.authorPais, E
dc.contributor.authorTagle, R
dc.contributor.authorGonzalez, F
dc.contributor.authorMezzano, S
dc.contributor.authorBarriga, F
dc.contributor.authorPereira, J
dc.date.accessioned2024-01-10T13:44:01Z
dc.date.available2024-01-10T13:44:01Z
dc.date.issued1999
dc.description.abstractBackground: 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.
dc.format.extent5 páginas
dc.fuente.origenWOS
dc.identifier.doi10.1055/s-0037-1614370
dc.identifier.issn0340-6245
dc.identifier.pubmedidMEDLINE:10544908
dc.identifier.uri10.1055/s-0037-1614370
dc.identifier.wosidWOS:000083145000010
dc.information.autorucMedicina;Mezzano D;S/I;99455
dc.information.autorucMedicina;Pereira J;S/I;99371
dc.issue.numero4
dc.language.isoen
dc.nota.accesocontenido parcial
dc.pagina.final1254
dc.pagina.inicio1250
dc.publisherF K SCHATTAUER VERLAG GMBH
dc.revistaTHROMBOSIS AND HAEMOSTASIS
dc.rightsacceso restringido
dc.subjectGLYCOPROTEIN-IIB-IIIA
dc.subjectUREMIA
dc.subjectDEFECT
dc.subjectPLASMINOGEN
dc.subjectVASOPRESSIN
dc.subjectACTIVATION
dc.subjectESTROGENS
dc.subjectBINDING
dc.subjectDISEASE
dc.subjectRISK
dc.subject.ods03 Good Health and Well-being
dc.subject.odspa03 Salud y bienestar
dc.titleTranexamic acid inhibits fibrinolysis, shortens the bleeding time and improves platelet function in patients with chronic renal failure
dc.typeartículo
dc.volumen82
sipa.codpersvinculados99455
sipa.codpersvinculados99371
sipa.indexWOS
sipa.indexScopus
sipa.trazabilidadCarga SIPA;09-01-2024
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