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¿El ácido fólico disminuye la homocisteína plasmática y mejora la función endotelial en pacientes con insuficiencia

J Thambyrajah1, M J Landray, F J McGlynn

  • 1Division of Medical Sciences (Cardiology), University of Birmingham Birmingham, UK. J.Thambyrajah@bham.ac.uk

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|August 23, 2000
PubMed
Resumen
Este resumen es generado por máquina.

Las dosis altas de ácido fólico redujeron la hiperhomocisteinemia en pacientes con insuficiencia renal crónica, pero no mejoraron la función endotelial. Esto sugiere que el ácido fólico puede no reducir la carga de la enfermedad vascular en la uremia.

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Área de la Ciencia:

  • Nefrología Nefrología.
  • Medicina Cardiovascular La medicina cardiovascular es una especialidad de la salud.
  • Ciencias de la Nutrición Ciencias de la Nutrición

Sus antecedentes:

  • La hiperhomocisteinemia es un factor de riesgo vascular independiente relacionado con la aterosclerosis y la disfunción endotelial.
  • La insuficiencia renal crónica (IFC) se asocia tanto con la hiperhomocisteinemia como con la aterosclerosis.
  • El impacto del ácido fólico en los eventos vasculares en pacientes con FRC sigue sin estar claro.

Objetivo del estudio:

  • Para investigar el efecto del ácido fólico en la función endotelial en pacientes con insuficiencia renal crónica antes de la diálisis.
  • Para determinar si la suplementación con ácido fólico puede mejorar los marcadores de salud vascular en esta población de pacientes.

Principales métodos:

  • Un estudio prospectivo, doble ciego, controlado con placebo que involucró a 100 pacientes con FCR en prediálisis.
  • Los pacientes recibieron 5 mg de ácido fólico o un placebo al día durante 12 semanas.
  • La función endotelial se evaluó a través de la dilatación de la arteria braquial, los niveles séricos de nitrito / nitrato y la concentración plasmática del factor von Willebrand.

Principales resultados:

  • La suplementación con ácido fólico aumentó significativamente los niveles de folato y redujo la hiperhomocisteinemia en comparación con el placebo.
  • No se observaron diferencias significativas en la dilatación dependiente del endotelio, el nitrito / nitrato sérico o el factor von Willebrand en plasma entre los grupos de ácido fólico y placebo.
  • El tratamiento con ácido fólico redujo pero no normalizó los niveles de hiperhomocisteinemia.

Conclusiones:

  • Las dosis altas de ácido fólico reducen efectivamente, pero no normalizan, la hiperhomocisteinemia en pacientes con FCR en prediálisis.
  • La suplementación con ácido fólico no mejoró la función endotelial en esta cohorte.
  • Estos hallazgos sugieren que el tratamiento con ácido fólico puede no mitigar la carga de la enfermedad vascular asociada con la uremia.