Diabetes and chronic kidney disease in Chinese adults: a population-based cohort study.

INTRODUCTION: Cohort evidence of the association of diabetes mellitus (DM) with chronic kidney disease (CKD) is limited. Previous studies often describe patients with kidney disease and diabetes as diabetic kidney disease (DKD) or CKD, ignoring other subtypes. The present study aimed to assess the prospective association of diabetes status (no diabetes, pre-diabetes, screened diabetes, previously diagnosed controlled/uncontrolled diabetes with/without antidiabetic treatment) and random plasma glucose (RPG) with CKD risk (including CKD subtypes) among Chinese adults. RESEARCH DESIGN AND METHODS: The present study included 472 545 participants from the China Kadoorie Biobank, using baseline information on diabetes and RPG. The incident CKD and its subtypes were collected through linkage with the national health insurance system during follow-up. Cox regression models were used to calculate the HR and 95% CI. RESULTS: During 11.8 years of mean follow-up, 5417 adults developed CKD. Screened plus previously diagnosed diabetes was positively associated with CKD (HR=4.52, 95% CI 4.23 to 4.83), DKD (HR=33.85, 95% CI 29.56 to 38.76), and glomerulonephritis (HR=1.66, 95% CI 1.40 to 1.97). In those with previously diagnosed diabetes, participants with uncontrolled diabetes represented higher risks of CKD, DKD, and glomerulonephritis compared with those with controlled RPG. The risk of DKD was found to rise in participants with pre-diabetes and increased with the elevated RPG level, even in those without diabetes. CONCLUSIONS: Among Chinese adults, diabetes was positively associated with CKD, DKD, and glomerulonephritis. Screen-detected and uncontrolled DM had a high risk of CKD, and pre-diabetes was associated with a greater risk of DKD, highlighting the significance of lifelong glycemic management.

Life-course adiposity and severe liver disease: a Mendelian randomization analysis.

OBJECTIVE: There is little evidence on the genetic associations between life-course adiposity (including birth weight, childhood BMI, and adulthood BMI) and severe liver disease (SLD; including cirrhosis and liver cancer). The current study aimed to examine and contrast these associations. METHODS: Genetic variants were obtained from genome-wide association studies. Two-sample Mendelian randomization (MR) analyses were performed to assess the genetic associations of life-course adiposity with SLD and liver biomarkers. Cox regression was used to estimate adjusted hazard ratios for SLD associated with genetic risk scores of life-course adiposity and adulthood weight change in the China Kadoorie Biobank. RESULTS: In observational analyses, genetic predispositions to childhood adiposity and adulthood adiposity were each associated with SLD. There was a U-shaped association between adulthood weight change and risk of SLD. In meta-analyses of MR results, genetically predicted 1-standard deviation increase in birth weight was inversely associated with SLD at a marginal significance (odds ratio: 0.81 [95% CI: 0.65-1.00]), whereas genetically predicted 1-standard deviation higher childhood BMI and adulthood BMI were positively associated with SLD (odds ratio: 1.27 [95% CI: 1.05-1.55] and 1.79 [95% CI: 1.59-2.01], respectively). The results of liver biomarkers mirrored those of SLD. CONCLUSIONS: The current study provided genetic evidence on the associations between life-course adiposity and SLD.