PLASMA XANTHINE OXIDASE ACTIVITY IS ASSOCIATED WITH LOW ESTIMATED GLOMERULAR FILTRATION RATE IN NEWLY DIAGNOSED HYPERTENSIVES

Abstract Objective: Elevated circulating uric acid level has emerged as an independent predictor of adverse outcomes in hypertension. Increased reactive oxygen species that could be caused by increased activity of xanthine oxidase (XO) during the production of uric acid has been attributed to hypertension. However, the predictive value of XO on impaired glomerular filtration rate in hypertension is unknown. The present study aims at evaluating the correlations between plasma uric acid concentration and XO activity, and estimated glomerular filtration rate (eGFR) in newly diagnosed non-diabetic hypertensive subjects. Design and method: Cross-sectional analyses were performed in treatment-naïve hypertensives with blood pressure equals to or more than 140/90 mmHg (n = 46) and normotensive with blood pressure equals to or less than 120/80 mmHg (n = 17), who were without history of diabetes mellitus, hyperlipidemia, smoking, thyroid disease and insulin or steroid use. Both groups were matched for age, sex and BMI. Using the modification of diet in renal disease equation, individuals with < median value of 91 ml/min/1.73 m2 were considered to have impaired eGFR. Results: Our results showed that hypertensives had higher uric acid level than the normotensives. Activity of XO was comparable in both the hypertensives and normotensives. Interestingly, hypertensives or normotensives with impaired eGFR had higher (p < 0.0001) XO activity than those with normal eGFR. Using multivariate regression analysis, results showed that XO activity (beta = 0.277; p < 0.0001) was an independent determinant of impaired eGFR in hypertensives only. The receiver operating characteristic curve analysis also showed that plasma XO activity (0.699) was a better predictor of impaired eGFR in hypertensives than plasma uric acid. Conclusions: These results demonstrate that plasma XO activity is significantly associated with low eGFR in hypertensives, independently of plasma uric acid level. The findings could imply that elevated plasma activity of XO may be a stronger risk factor that would promote the development of hypertension-related renal dysfunction.