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. 2023 Apr 8;15:61. doi: 10.1186/s13148-023-01476-y

Table 2.

Findings of individual-level allele score-based MR investigating causal effects of EAA on kidney function and CKD

Genetically predicted exposure Model 1a Model 2b
Effect (95% CI)c P Effect (95% CI)c P
eGFRd
IEAA − 0.001 (− 0.001, − 0.001) < 0.001f − 0.001 (− 0.002, − 0.001) < 0.001f
GrimAA − 0.001 (− 0.002, − 0.001) < 0.001f − 0.001 (− 0.002, − 0.001) < 0.001f
HannumAA − 0.0001 (− 0.001, 0.0004) 0.76 − 0.0002 (− 0.001, 0.0003) 0.44
PhenoAA − 0.0002 (− 0.001, 0.0002) 0.3 − 0.0003 (− 0.001, 0.0002) 0.22
CKDd
IEAA 1.02 (1.00, 1.04) 0.10 1.02 (1.00, 1.04) 0.07
GrimAA 1.02 (1.00, 1.04) 0.13 1.03 (1.00, 1.05) 0.02e
HannumAA 1.00 (0.98, 1.02) 0.91 1.00 (0.98, 1.02) 0.99
PhenoAA 1.00 (0.98, 1.02) 0.78 1.00 (0.98, 1.02) 0.89

CI Confident interval; CKD Chronic kidney disease; eGFR Estimated glomerular filtration rate

aAdjusted for age, sex, and 10 ancestry principal components

bAdjusted for covariables in model 1 + hypertension, diabetes mellitus, lipid profiles, hypercholesterolemia, body mass index (BMI), and smoking

cEffect sizes and CIs correspond to a 1 Z-score increase in EAA allele score (or genetically predicted EAA). Effect sizes are presented as beta estimates for log-transformed eGFR and hazard ratios for CKD

deGFR is based on the combined cystatin C/creatinine-based estimation using CKD-EPI equation. CKD stage 3–5 is defined by eGFR < 60 ml/min per 1.73 m2

eNominally significant

fSignificant after FDR correction