High levels of serum C-peptide are associated with a decreased risk for incident renal progression in patients with type 2 diabetes: a retrospective cohort study

一项回顾性队列研究表明,血清C肽水平升高与2型糖尿病患者肾脏疾病进展风险降低相关。

阅读:1

Abstract

INTRODUCTION: C-peptide has been reported to provide renoprotective effects. This study aims to explore the relationship between C-peptide and progression of renal function in patients with type 2 diabetes mellitus (T2DM). RESEARCH DESIGN AND METHODS: We retrospectively collected clinical data from 854 T2DM patients over a median follow-up of 5 years. Renal events included an annual decline in estimated glomerular filtration rate (eGFR), a rapid kidney function decline and a renal composite endpoint. A linear mixed-effects model and Cox regression analysis were used to investigate the effect of C-peptide on renal events, and a subgroup analysis was performed after stratification by risk factors. RESULTS: The highest-level C-peptide group had a smaller annual eGFR decline compared with those in the group with the lowest level (p<0.05). Higher levels of 2 h postprandial C-peptide (2hPCP) (adjusted HR 0.53; 95% CI 0.31 to 0.92), difference between 2 h postprandial and fasting C-peptide (ΔCP) (adjusted HR 0.39; 95% CI 0.22 to 0.69), and 2 h postprandial C-peptide-to-glucose ratio (PCGR) (adjusted HR 0.44; 95% CI 0.24 to 0.82) were independently related to a decreased risk for the renal composite endpoint. 2hPCP <2.92 ng/mL, ΔCP <1.86 ng/mL, and PCGR <1.11 significantly increased the risk of progression in kidney function (adjusted HRs <0.50, p<0.05) among T2DM patients with male sex, an age of <65 years old, a disease course of <10 years, an glycosylated hemoglobin value of ≥7%, or a history of hypertension. CONCLUSIONS: Higher levels of 2hPCP, ΔCP and PCGR could protect T2DM patients from renal progression, especially in the aforementioned population with diabetes.

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。