We studied the prevalence of high blood ASP1517 pressure in a longitudinal cohort study of children with NAFLD from pediatric centers across the United States. Children with NAFLD had a high rate of high blood pressure both at baseline and again at 48 weeks. The odds of having high blood pressure at baseline and high blood pressure that persisted at 48 weeks were associated with BMI, LDL-cholesterol and uric acid. Hepatic steatosis was associated with high blood pressure at baseline. The rates of high blood pressure in children with NAFLD exceeded what would be expected based upon the contribution of obesity alone. Population-based cohort studies estimate the prevalence of high blood pressure in obese, Although most children with NAFLD are overweight or obese, our finding that more than one of every three children with NAFLD had high blood pressure at baseline indicates that children with NAFLD are at particularly increased risk for high blood pressure. A previous single center study in overweight and obese children with biopsy-confirmed NAFLD demonstrated that mean systolic and diastolic blood pressure were significantly higher compared to overweight and obese controls without evidence of NAFLD. Similarly, studies in children have shown that hepatic steatosis, independent of degree of obesity, is associated with cardiac dysfunction., Notably, in our cohort, children with NAFLD who had high blood pressure at baseline had higher degrees of hepatic steatosis. Data are extremely limited on the persistence of high blood pressure in children. In our study, the prevalence of 21.4% for persistent high blood pressure over 48 weeks in children with NAFLD was much higher than reported for other groups of children with longitudinal data available. For example, in the National Heart, Lung, and Blood Institute Growth and Health Study, the rate of persistent high blood pressure over 18 months in girls was 0.6% overall and 3% in obese girls. NAFLD and high blood pressure share pathophysiologic factors such as systemic oxidative stress and vascular and adipose tissue inflammation, which can produce vascular endothelial dysfunction. In the setting of hepatic steatosis, liver endothelial dysfunction can occur even prior to development of hepatic inflammation and fibrosis. While it is not yet clear whether hypertension is a cause or consequence of endothelial dysfunction, exogenous infusion of endothelium-derived nitric oxide synthase inhibitors can produce hypertension in humans. Our finding that elevated serum levels of LDL-cholesterol and uric acid were associated with increased odds for both baseline and persistent high blood pressure in this cohort also supports a possible role for underlying endothelial dysfunction. High levels of LDL cholesterol have been shown to alter the activity of endothelial-derived nitric oxide synthase. Oxidized LDL is also associated with endothelial dysfunction and activation of the renin-angiotensin system., Likewise, elevated uric acid has been functionally linked to decreased endothelial nitric oxide synthase activity and nitric oxide production and in turn endothelial dysfunction.