Inflammation, not hyperhomocysteinemia, is related to oxidative stress and hemostatic and endothelial dysfunction in uremia

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dc.contributor.authorMezzano, D
dc.contributor.authorPais, EO
dc.contributor.authorAranda, E
dc.contributor.authorPanes, O
dc.contributor.authorDowney, P
dc.contributor.authorOrtiz, M
dc.contributor.authorTagle, R
dc.contributor.authorGonzalez, F
dc.contributor.authorQuiroga, T
dc.contributor.authorCaceres, MS
dc.contributor.authorLeighton, F
dc.contributor.authorPereira, J
dc.date.accessioned2024-01-10T12:39:45Z
dc.date.available2024-01-10T12:39:45Z
dc.date.issued2001
dc.description.abstractBackground. 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.
dc.description.abstractMethods. The relationships of inflammatory proteins and tHcy with plasma markers of these processes were studied in 64 patients with CRF (serum creatinine 526 +/- 319 mu mol/L) on conservative treatment, comparing the results with healthy controls (N=15 to 40, depending on the measured variable) of similar sex and age.
dc.description.abstractResults. Patients had significant increases in inflammatory cytokines (TNF-alpha and IL-8) and acute-phase proteins (C-reactive protein, fibrinogen and al-antitrypsin). tHcy was increased in 87.5% of patients (mean=27.1 mu mol/L, range 6.5 to 118). Patients had significant increases in (1) indices of oxidative stress: TBARS (thiobarbituric acid-reactive species), a marker of lipid peroxidation and AOPP (advanced oxidation protein products), a marker of protein oxidation; (2) endothelial cell markers such as von Willebrand factor (vWF:Ag), soluble ICAM-1 and soluble thrombomodulin (sTM); (3) markers of intravascular thrombin generation: thrombin-antithrombin complexes (TAT) and prothrombin fragment F1+2 (PF1+2); and (4) indices of activation of fibrinolysis: plasmin-antiplasmin complexes (PAP), fibrin degradation products (FnDP) and fibrinogen degradation products (FgDP). tHcy was significantly correlated with plasma creatinine (r=0.29, P<0.018) and with serum folate (r=-0.38, P<0.002). However, no significant correlations were observed between tHcy and TBARS, AOPP, vWF:Ag, sICAM-1, sTM, TAT, F1+2, sTF, PAP, FnDP, and FgDP. Conversely, acute-phase proteins showed significant, positive correlations with most markers of oxidative stress, endothelial dysfunction and hemostatic activation.
dc.description.abstractConclusions. Systemic inflammation, which is closely associated with augmented oxidative stress, endothelial cell dysfunction and hemostatic activation, emerges as a major cardiovascular risk factor in CRF. tHcy is unrelated to these events. Thus, alternative mechanisms through which hyperhomocysteinemia could predispose to vascular lesion and thrombotic events in CRF needs to be investigated.
dc.fechaingreso.objetodigital2024-05-02
dc.format.extent7 páginas
dc.fuente.origenWOS
dc.identifier.doi10.1046/j.1523-1755.2001.00998.x
dc.identifier.issn0085-2538
dc.identifier.pubmedidMEDLINE:11703602
dc.identifier.urihttps://doi.org/10.1046/j.1523-1755.2001.00998.x
dc.identifier.urihttps://repositorio.uc.cl/handle/11534/77231
dc.identifier.wosidWOS:000171764300023
dc.information.autorucMedicina;Aranda E;S/I;102381
dc.information.autorucMedicina;Downey P;S/I;68164
dc.information.autorucCiencias Biológicas;Leighton F;S/I;98261
dc.information.autorucMedicina;Mezzano D;S/I;99455
dc.information.autorucActividades Universitarias;Pereira J;S/I;99371
dc.information.autorucMedicina;Quiroga S;S/I;52601
dc.issue.numero5
dc.language.isoen
dc.nota.accesocontenido parcial
dc.pagina.final1850
dc.pagina.inicio1844
dc.publisherBLACKWELL SCIENCE INC
dc.revistaKIDNEY INTERNATIONAL
dc.rightsacceso restringido
dc.subjecthyperhomocysteinemia
dc.subjectcardiovascular disease
dc.subjectthrombosis
dc.subjectvascular lesion
dc.subjectplasma homocysteine
dc.subjecturemia
dc.subjectischemia
dc.subjectCHRONIC-RENAL-FAILURE
dc.subjectCARDIOVASCULAR RISK-FACTORS
dc.subjectEPIDEMIOLOGIC EVIDENCE
dc.subjectHEMODIALYSIS-PATIENTS
dc.subjectPLASMA HOMOCYSTEINE
dc.subjectPROTEIN PRODUCTS
dc.subjectBLEEDING-TIME
dc.subjectTISSUE FACTOR
dc.subjectDISEASE
dc.subjectFIBRINOLYSIS
dc.subject.ods03 Good Health and Well-being
dc.subject.odspa03 Salud y bienestar
dc.titleInflammation, not hyperhomocysteinemia, is related to oxidative stress and hemostatic and endothelial dysfunction in uremia
dc.typeartículo
dc.volumen60
sipa.codpersvinculados102381
sipa.codpersvinculados68164
sipa.codpersvinculados98261
sipa.codpersvinculados99455
sipa.codpersvinculados99371
sipa.codpersvinculados52601
sipa.indexWOS
sipa.indexScopus
sipa.trazabilidadCarga SIPA;09-01-2024
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