Association of different glucose traits with kidney function decline risk in a Chinese community-based population without chronic kidney disease
Received 4 March 2018
Accepted for publication 21 June 2018
Published 17 September 2018 Volume 2018:14 Pages 1725—1734
Checked for plagiarism Yes
Review by Single-blind
Peer reviewer comments 2
Editor who approved publication: Professor Deyun Wang
Xingang Wang,1 Fangfang Fan,1 Jia Jia,1 Xin Xu,2 Xianhui Qin,2 Bo Zheng,1 Haixia Li,3 Liguang Dong,4 Shuyu Wang,5 Jianping Li,1 Yong Huo,1 Jingtao Dou,6 Yan Zhang1
1Department of Cardiology, Peking University First Hospital, Beijing, China; 2National Clinical Research Center for Kidney Disease, State Key Laboratory for Organ Failure Research, Renal Division, Nanfang Hospital, Southern Medical University, Guangzhou, China; 3Clinical Laboratory, Peking University First Hospital, Beijing, China; 4Peking University Shougang Hospital, Beijing, China; 5Beijing Hypertension League Institute, Beijing, China; 6Department of Endocrinology, Chinese PLA General Hospital, Beijing, China
Background: Chronic kidney disease (CKD) has become a major issue worldwide and hyperglycemia is known as an important risk factor responsible for CKD progression. Few studies have investigated whether fasting plasma glucose (FPG) could predict kidney function decline (KFD) risk better than postprandial plasma glucose, and vice versa. In this study, we investigated the roles of FPG and 2-hour plasma glucose (2 h-PG) in predicting KFD risk in a Chinese community-based population without baseline deterioration of kidney functions.
Methods: Subjects with normal kidney function from an atherosclerosis cohort in Beijing, China were followed up for 2.3 years. The outcome was KFD (a drop in glomerular filtration rate category accompanied by 25% or greater decline of estimated glomerular filtration rate from the baseline or a sustained decline of more than 5 mL/min/1.73 m2/year rate).
Results: A total of 3,738 subjects were included of which, 7.7% of the subjects suffered from KFD. After covariates adjustments, both FPG (OR =1.23, P<0.001) and 2 h-PG (OR =1.07, P<0.001) were associated with KFD. Furthermore, FPG was independent of 2 h-PG to predict KFD (OR =1.26, P<0.001). Subgroup analyses and interaction tests including diabetes mellitus, after adjusting all covariates, revealed no significant heterogeneity among analyzed subgroups. We also found subjects with FPG level of 6.1–7.0 mmol/L and >7.0 mmol/L had 1.83 times and 2.51 times KFD risk respectively, compared to subjects with FPG level <5.6 mmol/L.
Conclusion: FPG was superior to 2 h-PG in predicting KFD in a Chinese community-based population without CKD. FPG screening may be an important measure for CKD primary prevention even in subjects with impaired fasting glucose.
Keywords: fasting plasma glucose, postprandial plasma glucose, kidney function decline, chronic kidney disease
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