Effect of Glomerular Filtration Rate on Uric Acid Metabolism in a Retrospective Cohort of Type-2 Diabetes Mellitus Patients on SGLT-2 Inhibitor Therapy

回顾性队列研究:肾小球滤过率对接受SGLT-2抑制剂治疗的2型糖尿病患者尿酸代谢的影响

阅读:1

Abstract

OBJECTIVE: This study aimed to investigate the effects of different glomerular filtration rates (GFRs) on serum uric acid (SUA) levels in patients with type 2 diabetes mellitus receiving sodium-glucose transporter 2 (SGLT-2) inhibitor therapy. MATERIALS AND METHODS: A total of 3,004 patients with type 2 diabetes mellitus treated with SGLT-2 inhibitors between January 2017 and September 2022 were analyzed. Patients who did not attend follow-up visits, had missing data, discontinued SGLT-2 inhibitors, were taking medications that affect SUA levels, or were being treated for gout were excluded. The final study group consisted of 410 patients. Biochemical parameters were retrospectively compared before treatment and at the 3(rd) and 12(th) months of drug therapy. To evaluate the effect of GFR on uric acid levels during SGLT-2 inhibitor treatment, patients were analyzed with and without grouping based on GFR levels. RESULTS: The study showed that glycated hemoglobin, fasting plasma glucose, creatinine, low-density lipoprotein, triglycerides, and SUA levels decreased with SGLT-2 inhibitor treatment, while high-density lipoprotein and urine glucose levels increased. The efficacy of SGLT-2 inhibitors in reducing SUA levels was found to correlate closely with changes in GFR, with a notable reduction observed at GFR levels below 60 mL/min/1.73 m(2). Moreover, the effect was independent of the specific active substance used. CONCLUSION: SGLT-2 inhibitors not only regulate blood glucose levels and lipid profiles but also have a significant impact on uric acid levels. However, this study found that this effect is considerably diminished in patients with extremely low GFR.

特别声明

1、本页面内容包含部分的内容是基于公开信息的合理引用;引用内容仅为补充信息,不代表本站立场。

2、若认为本页面引用内容涉及侵权,请及时与本站联系,我们将第一时间处理。

3、其他媒体/个人如需使用本页面原创内容,需注明“来源:[生知库]”并获得授权;使用引用内容的,需自行联系原作者获得许可。

4、投稿及合作请联系:info@biocloudy.com。