Diabetes Control and the Risks of ESRD and Mortality in Patients With CKD

糖尿病控制与慢性肾脏病患者终末期肾病和死亡风险的关系

阅读:1

Abstract

BACKGROUND: Diabetes is the leading cause of end-stage renal disease (ESRD) and a significant contributor to mortality in the general population. We examined the associations of hemoglobin A(1c) (HbA(1c)) levels with ESRD and death in a population with diabetes and chronic kidney disease (CKD). STUDY DESIGN: Cohort study. SETTING & PARTICIPANTS: 6,165 patients with diabetes (treated with oral hypoglycemic agents and/or insulin) and CKD stages 1 to 5 at a large health care system. PREDICTOR: HbA(1c) level (examined as a categorical and continuous measure). OUTCOMES: All-cause and cause-specific mortality ascertained from the Ohio Department of Health mortality files and ESRD ascertained from the US Renal Data System. RESULTS: During a median 2.3 years of follow-up, 957 patients died (887 pre-ESRD deaths) and 205 patients reached ESRD. In a Cox proportional hazards model, after multivariable adjustment including for kidney function, HbA(1c) level < 6% was associated with higher risk for death when compared with HbA(1c) levels of 6% to 6.9% (HR, 1.23; 95% CI, 1.01-1.50). Similarly, HbA(1c) level ≥ 9% was associated with higher risk for all-cause death (HR, 1.34; 95% CI, 1.06-1.69). In competing-risk models, baseline HbA(1c) level was not associated with ESRD. For cause-specific mortality, diabetes accounted for >12% of deaths overall and >19% of deaths among those with HbA(1c) levels > 9%. LIMITATIONS: Small proportion of participants with advanced kidney disease; single-center population. CONCLUSIONS: In this cohort of patients with CKD with diabetes, HbA(1c) levels < 6% and ≥9% were associated with higher risk for death. HbA(1c) levels were not associated with ESRD in this specific CKD population. Diabetes-related deaths increased with higher HbA(1c) levels.

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。