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El suero y los solutos urémicos aumentan el riesgo trombótico intervencionista post-vascular a través de la
Vipul C Chitalia1, Sowmya Shivanna, Jordi Martorell
1Harvard-MIT Division of Science and Technology, Bldg E25-449, Massachusetts Institute of Technology, 77 Mass Ave, Cambridge, MA 02139, USA. vichital@mit.edu
Circulation
|December 28, 2012
Resumen
El riesgo de trombosis de stent (ST) es elevado en pacientes con insuficiencia renal crónica debido a la uremia que aumenta la estabilidad del factor tisular (TF). Este estudio revela que los solutos urémicos prolongan la vida media de TF, lo que sugiere nuevas estrategias de prevención para ST.
Área de la Ciencia:
- Biología Cardiovascular Biología Cardiovascular
- Nefrología Nefrología.
- Investigación de la trombosis.
Sus antecedentes:
- La trombosis de stent (ST) es una complicación peligrosa con una alta mortalidad.
- La insuficiencia renal crónica y la enfermedad renal en etapa terminal (ESRD) son factores de riesgo significativos para ST.
- Todavía no están claros los mecanismos subyacentes que vinculan la ESRD a la ST.
Objetivo del estudio:
- Para investigar el papel de la uremia en el factor de modulación del tejido (TF) en las células del músculo liso vascular (vSMC).
- Para determinar si la uremia contribuye a la trombosis posintervencionista en pacientes con ESRD.
- Identificar factores y mecanismos urémicos específicos involucrados en el aumento de la trombogenicidad.
Principales métodos:
- Los vSMC humanos primarios fueron expuestos a un flujo sanguíneo similar al coronario después del pretratamiento con suero urémico o solutos urémicos aislados.
- Se analizaron la expresión, la actividad, la estabilidad y la modificación post-traduccional (ubiquitinación) de TF.
- La formación de coágulos se evaluó en un modelo de bucle de flujo.
Principales resultados:
- El suero urémico aumentó significativamente la formación de coágulos, la expresión de TF vSMC y la actividad de TF.
- Los solutos urémicos aislados (ácido indole-3-acético, sulfato de indoxilo, ácido úrico) replicaron estos efectos protrombóticos.
- El suero urémico y los solutos específicos prolongaron la vida media de TF inhibiendo su ubiquitinación.
Conclusiones:
- El entorno urémico promueve la trombosis al aumentar la estabilidad del TF vSMC a través de una ubiquitinación reducida.
- La regulación postraslacional de TF en la uremia es un factor potencial causante de un mayor riesgo de ST en pacientes con ESRD.
- Dirigirse al TF vSMC o considerar los solutos urémicos como nuevos factores de riesgo puede ayudar en la prevención de ST.
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