Vázquez-Ávila JA, Zetina-Martínez M, Duarte-Mote J

Idioma: Español
Referencias bibliográficas: 33
Paginas: 278-287
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RESUMEN

El ácido úrico es producto final del metabolismo de las purinas, transformadas finalmente a ácido úrico. No existe definición universal de hiperuricemia, en la práctica, el punto de corte es a partir de 6.8 mg/dL en plasma. Estudios experimentales han demostrado una correlación positiva lineal entre la presión arterial y las concentraciones de ácido úrico, así como disminución de las cifras tensionales al administrar tratamiento hipouricemiante con alopurinol. Se han identificado numerosos mecanismos a través de los cuales la hiperuricemia puede causar hipertensión: reducción de las concentraciones de óxido nítrico endotelial, estimulación de estrés oxidativo, expresión en las células de músculo liso del endotelio vascular de receptor URAT-1, activación del eje renina angiotensina, estimulación de la proliferación de músculo liso vascular, además, favorece la enfermedad microvascular renal. La evidencia reciente ha aportado nuevo conocimiento acerca de los múltiples mecanismos a través de los cuales el ácido úrico tendría un papel preponderante en la hipertensión arterial sistémica y en múltiples alteraciones metabólicas; sin embargo, hace falta desarrollar estudios clínicos a gran escala, bien diseñados, que comprueben de manera más contundente estas teorías, antes de considerar tratamientos enfocados en el manejo de la hiperuricemia asintomática en la práctica clínica diaria

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