The role of uric acid in pediatric hypertension

Abstract

Over the past few years, increasing evidence has supported the possible role of uric acid as a mediator of high blood pressure. Both animal model data and tissue culture experiments suggest that uric acid might cause increased blood pressure through a 2-phase process. The first phase is dominated by a uric acid-mediated vasoconstriction followed by induction of renal afferent arteriolosclerosis and altered pressure natriuresis, leading to sodium-dependent hypertension. We have assessed children with newly diagnosed essential hypertension through cross-sectional studies and clinical trials. Elevated uric acid is closely associated with new-onset essential hypertension in children, and preliminary data suggest that lowering of uric acid can lower blood pressure in some patients. Future studies will be needed to determine whether the mechanisms shown in animal models can be extrapolated to children.

Figure 1

Correlation between systolic blood pressure and serum uric acid of 300 children consecutively evaluated in the Hypertension Clinic at Texas Children’s Hospital who did not have evident renal, cardiac or endocrine disease at the time of initial evaluation.