Effects of xanthine oxidase inhibitors on renal function and blood pressure in hypertensive patients with hyperuricemia

Abstract

Hyperuricemia may promote the progression of hypertension and renal dysfunction. However, the effects of hyperuricemia treatment on blood pressure and renal function in adult hypertensive patients with hyperuricemia remain unclear. A total of 137 hypertensive patients with hyperuricemia (96 men and 41 women; mean age of 67 years) who recently started taking xanthine oxidase inhibitors (allopurinol or febuxostat) as outpatients were recruited. Serum uric acid level, estimated glomerular filtration rate (eGFR, ml min(-1) per 1.73 m(2)) and blood pressure (mm Hg) were retrospectively compared immediately before and shortly after starting treatment with xanthine oxidase inhibitors. The mean blood pressure and the eGFR immediately before starting treatment were 128/71 mm Hg and 44.6 ml min(-1) per 1.73 m(2), respectively. Although the eGFR decreased from 46.6 to 44.6 ml min(-1) per 1.73 m(2) before starting treatment with xanthine oxidase inhibitors, it increased to 46.2 ml min(-1) per 1.73 m(2) (P=0.001, compared with immediately before treatment) without any significant changes in blood pressure after the administration of xanthine oxidase inhibitors. Multiple regression analysis revealed that the increase in eGFR after starting xanthine oxidase inhibitor treatment positively correlated with the changes in systolic blood pressure and negatively correlated with the changes in uric acid levels and the use of renin-angiotensin system inhibitors. These results suggest that xanthine oxidase inhibitors may delay the progression of renal dysfunction in adult hypertensive patients with hyperuricemia.

Is Serum Uric Acid Independently Associated With Left Ventricular Mass Index, Ejection Fraction, and B-Type Natriuretic Peptide Among Female and Male Cardiac Patients?

“…Although previous studies failed to show that SUA lowering or xanthine oxidase inhibition slows the progression of renal dysfunction 36) or reduces cardiovascular risk, 37) further investigations are required before we can make any definitive conclusions concerning the use of different classes of SUA-lowering drugs, such as new non-purine xanthine oxidase inhibitors, and the measurement of multiple outcomes, some of which are ongoing. [38][39][40][41][42] In summary, SUA was found to be associated positively with LVMI and BNP, and negatively with LVEF in both genders. However, after taking diuretic use into consideration in the statistical model, association between SUA and LVEF among male patients and that between SUA and LVEF or BNP among female patients lost statistical significance.…”

Oxidative stress in chronic kidney disease

“…If there is a role for XO and/or hyperuricemia on CKD progression remains contradictory. One recent study by Kohagura et al, in 137 patients with hypertension and hyperuricemia who started treatment with XO inhibitors, showed a, albeit modest, protective effect on renal function in hypertensive patients [74].…”

Uric acid in the pathogenesis of metabolic, renal, and cardiovascular diseases: A review

“…In a retrospective cohort study of 803 CKD patients, propensity score analysis using three different methods showed a consistent impact of high UA on progression to end-stage renal disease (ESRD) [118]. XO inhibitors possibly delay the progression of CKD in adult hyperuricemic and hypertensive patients [119]. The target SUA should be <6.5 mg/dL to delay progression [77], [118].…”