达帕格列嗪
医学
肾脏疾病
肾功能
蛋白尿
危险系数
肌酐
安慰剂
急性肾损伤
泌尿科
内科学
不利影响
置信区间
随机对照试验
临床终点
糖尿病
2型糖尿病
内分泌学
病理
替代医学
作者
Hiddo J.L. Heerspink,David Z.I. Cherney,Douwe Postmus,Bergur V. Stefánsson,Glenn M. Chertow,Jamie P. Dwyer,Tom Greene,Mikhail Kosiborod,Anna Maria Langkilde,John J.V. McMurray,Ricardo Correa–Rotter,Peter Rossing,C. David Sjöström,Robert D. Toto,David C. Wheeler,Dapa-Ckd Trial Committees,Investigators
标识
DOI:10.1016/j.kint.2021.09.005
摘要
This pre-specified analysis of DAPA-CKD assessed the impact of sodium-glucose cotransporter 2 inhibition on abrupt declines in kidney function in high-risk patients based on having chronic kidney disease (CKD) and substantial albuminuria. DAPA-CKD was a randomized, double-blind, placebo-controlled trial that had a median follow-up of 2.4 years. Adults with CKD (urinary albumin-to-creatinine ratio 200-5000 mg/g and estimated glomerular filtration rate 25-75 mL/min/1.73m2) were randomized to dapagliflozin 10 mg/day matched to placebo (2152 individuals each). An abrupt decline in kidney function was defined as a pre-specified endpoint of doubling of serum creatinine between two subsequent study visits. We also assessed a post-hoc analysis of investigator-reported acute kidney injury-related serious adverse events. Doubling of serum creatinine between two subsequent visits (median time-interval 100 days) occurred in 63 (2.9%) and 91 (4.2%) participants in the dapagliflozin and placebo groups, respectively (hazard ratio 0.68 [95% confidence interval 0.49, 0.94]). Accounting for the competing risk of mortality did not alter our findings. There was no heterogeneity in the effect of dapagliflozin on abrupt declines in kidney function based on baseline subgroups. Acute kidney injury-related serious adverse events were not significantly different and occurred in 52 (2.5%) and 69 (3.2%) participants in the dapagliflozin and placebo groups, respectively (0.77 [0.54, 1.10]). Thus, in patients with CKD and substantial albuminuria, dapagliflozin reduced the risk of abrupt declines in kidney function.
科研通智能强力驱动
Strongly Powered by AbleSci AI