Homocyst(e)ine, oxidative stress, and endothelium function in uremic patients.
Kidney Int Suppl
; 78: S243-5, 2001 Feb.
Article
en En
| MEDLINE
| ID: mdl-11169019
ABSTRACT
Moderate hyperhomocyst(e)inemia and impaired endothelium-dependent vasodilatation are present in uremic patients. However, the precise mechanism(s) underlying the link between moderate hyperhomocyst(e)inemia and endothelium dysfunction in uremic patients remains to be determined. Experimental and clinical evidence have led to the suggestion that moderate hyperhomocyst(e)inemia may predispose to endothelium dysfunction through a mechanism that involves generation of reactive oxygen species and a decrease in nitric oxide bioavailability. Recent preliminary findings in uremic patients provide support for some aspects of this suggestion. These data must be confirmed in additional studies. Moreover, the relative importance of homocysteine-induced oxidant stress versus other potential mechanisms of endothelium dysfunction in these patients remains to be determined.
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Banco de datos:
MEDLINE
Asunto principal:
Uremia
/
Endotelio Vascular
/
Homocisteína
/
Homocistina
Tipo de estudio:
Etiology_studies
Límite:
Animals
/
Humans
Idioma:
En
Año:
2001
Tipo del documento:
Article