谷歌浏览器插件
订阅小程序
在清言上使用

#2635 A prospective cohort study of sodium-glucose cotransporter 2 inhibitor-treated glomerulonephritis in kidney transplant patients

Nephrology Dialysis Transplantation(2024)

引用 0|浏览0
暂无评分
摘要
Abstract Background and Aims Recurrent or de novo glomerulonephritis (GN) after kidney transplantation (KT) is one of the main causes of renal allograft failure without effective treatment. Recent randomized controlled trials have demonstrated the beneficial effects of sodium-glucose cotransporter 2 inhibitors (SGLT2i) in delaying the progression of chronic kidney disease of broad range, including GN. Method We conducted a single-center, prospective study on the treatment with SGLT2i in 24 patients with biopsy-proven GN of renal allograft. IgA nephropathy was the most frequent (n=16), followed by focal segmental glomerulosclerosis (n=2), membranous nephropathy (n=2) and others (n=4). Baseline mean eGFR was 58 ± 26 mL/min/1.73 m2. The primary outcome is the change in proteinuria from baseline to 6 and 12 months, and the change in eGFR slope before (−24 to 0 months) and after (3 to 15 months) the initiation of SGLT2i. The secondary outcome is the change in body weight (BW), systolic blood pressure (SBP) and doses of antihypertensives. Adverse reactions were closely observed. Results The post-SGLT2i follow-up period was 17.5 (median) ± 14.9 months. The eGFR slope improved from −4.762 ± 1.29 ml/min/1.73 m2/year(before SGLT2i) to −0.667 ± 4.07 (after SGLT2i). The urinary protein-creatinine ratio did not change significantly. BW decreased significantly at 3 months and maintained thereafter. SBP did not change significantly, but the number of antihypertensives decreased. There was no cases of acute pyelonephritis or AKI due to volume depletion. Conclusion SGLT2i slowed the eGFR decline of patients with GN of renal allograft and was well-tolerated. Our preliminary results warrant confirmation by further studies with a larger number of patients and prolonged follow-up.
更多
查看译文
AI 理解论文
溯源树
样例
生成溯源树,研究论文发展脉络
Chat Paper
正在生成论文摘要