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. Author manuscript; available in PMC: 2023 May 30.
Published in final edited form as: Clin Chem. 2022 Mar 4;68(3):461–472. doi: 10.1093/clinchem/hvab249

Figure 3. Total causal effects of obesity on eGFR decline and UACR in the European population.

Figure 3

Estimates (β coefficients and 95% confidence intervals [CIs]) are from the inverse variance weighted random-effects Mendelian randomization analysis, and expressed in log units per standard deviation increase in the relevant exposure.

Obesity exposures from the GIANT Consortium were BMI (body mass index, N=795,624), WHR (waist-to-hip ratio, N=697,702), and WHRadjBMI (WHR adjusted for BMI, N=694,469). For each obesity exposure, the number of single nucleotide polymorphisms (SNPs) included in the analysis is shown in parenthesis.

BMI, T2D and BMI, adverse (obesity) refer to BMI SNPs restricted to SNPs nominally associated with type 2 diabetes (T2D) and WHR, respectively. For details, see Methods. Kidney function outcomes from the CKDGen Consortium were annual eGFR (estimated glomerular filtration rate) decline (based on serum creatinine levels and calculated by the MDRD equation), available in overall population and subpopulation with chronic kidney disease (CKD, NCKDcases=3338 cases, NCKDcontrols=39,653, Noverall=43,008), and UACR (urinary albumin-to-creatinine ratio), available in overall population and subpopulation with diabetes (NDM=11,529, Noverall=118,460). Sensitivity MR analyses are shown in Supplemental Tables 3-4.