非布司他对非透析3/4期慢性肾病患者高尿酸血症和肾小球滤过率的疗效及心功能评估:一项为期12个月的介入研究

Frontiers in nephrology Pub Date : 2025-03-26 eCollection Date: 2025-01-01 DOI:10.3389/fneph.2025.1526182
Yousuf Abdulkarim Waheed, Fan Yang, Jie Liu, Shifaa Almayahe, Karthick Kumaran Munisamy Selvam, Disheng Wang, Dong Sun
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引用次数: 0

摘要

目的:非布司他是一种用于治疗高尿酸血症(HUA)的口服药物,是一种非嘌呤黄嘌呤氧化酶抑制剂,可调节慢性肾病(CKD)患者的血清尿酸(SUA)代谢。然而,该药在改善非透析3/4期CKD患者肾功能方面的有效性尚不清楚。我们的目的是研究非布司他对肾功能的影响。此外,还将评估心功能。方法:我们进行了一项单中心、介入性、随机、对照、开放标签的研究。共有316例非透析期3/4期CKD患者,女性SUA≥6mg/dL,男性SUA≥7mg/dL,被分配到非布司他组(n=156)或对照组(n=160)。主要终点是评估肾脏生物标志物从基线到治疗12个月的变化,心脏生物标志物和超声心动图的任何变化是次要终点。结果:主要终点是两组从基线到治疗12个月的比较。非布司他40mg治疗的患者SUA显著降低(基线时为6.85±0.41mg/dL,治疗12个月时为5.27±0.70mg/dL, P),这与eGFR升高(基线时为34.48±8.42ml/min,治疗12个月时为38.46±8.87ml/min)相关。非布司他组高敏感性肌钙蛋白T(基线值19.50±7.24ng/L,治疗12个月时16.98±7.32ng/L)和n -末端前脑利钠肽(基线值941.35±374.30pg/ml,治疗12个月时762.22±303.32 pg/ml) P均显著降低。这些变化也与非布司他组左心室射血分数升高有关(基线时为50.47±3.95%,研究结束时为51.12±3.96%,P)。结论:在介入组中,非布司他耐受性良好,SUA的降低与eGFR的增加相关。这减缓了非透析3/4期CKD患者肾脏疾病的进展,并改善了心功能。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Efficacy of febuxostat on hyperuricemia and estimated glomerular filtration rate in patients with non-dialysis stage 3/4 chronic kidney disease and assessment of cardiac function: a 12-month interventional study.

Objectives: Febuxostat, an oral medication for treating hyperuricemia (HUA), is a non-purine xanthine oxidase inhibitor that regulates serum uric acid (SUA) metabolism in patients with chronic kidney disease (CKD). However, the drug's effectiveness in improving renal function in patients with non-dialysis stage 3/4 CKD remains unclear. Our aim is to investigate the efficacy of febuxostat on kidney function. In addition, the cardiac function will be assessed.

Method: We conducted a single-center, interventional, randomized, controlled, open-label study. A total of 316 patients with non-dialysis stage 3/4 CKD, with SUA ≥6mg/dL in women and ≥7mg/dL in men, were assigned to either the febuxostat group (n=156) or the control group (n=160). The primary endpoint was the evaluation of changes in kidney biomarkers from baseline to 12 months of treatment, and any changes in cardiac biomarkers and echocardiographs were the secondary endpoint.

Results: The primary endpoint was a comparison between the two groups from baseline to 12 months of treatment. SUA was significantly decreased in patients treated with febuxostat 40 mg (6.85 ± 0.41mg/dL at baseline and 5.27 ± 0.70mg/dL at 12 months of treatment, P<0.001) and this was associated with increased eGFR (34.48 ± 8.42ml/min at baseline and 38.46 ± 8.87ml/min at 12 months of treatment, P<0.001). There were significant decreases in high-sensitivity troponin T (19.50 ± 7.24ng/L at baseline and 16.98 ± 7.32ng/L at 12 months of treatment, P<0.001) and N-terminal-pro brain natriuretic peptide (941.35 ± 374.30pg/ml at baseline and 762.22 ± 303.32 pg/ml at 12 months of treatment, P<0.001) in the febuxostat group. These changes were also associated with increased left ventricular ejection fraction in the febuxostat group (50.47 ± 3.95% at baseline and 51.12 ± 3.96% at the end of the study, P<0.001).

Conclusion: In the interventional group, febuxostat was well-tolerated and demonstrated a reduction in SUA associated with an increase in eGFR. This slowed down the progression of renal disease in patients with non-dialysis stage 3/4 CKD and improved cardiac function.

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