Abstract
BACKGROUND: Diet may be an important modifiable risk factor for chronic kidney disease (CKD). We explored the association between the EAT-Lancet planetary health diet and the risk of incident CKD.</p>
METHODS: We obtained data from the UK Biobank cohort on dietary intake, assessed via 24-hour dietary recall questionnaires, for 179 508 participants without CKD at baseline. We evaluated adherence to the EAT-Lancet diet using 4 scoring methods and analyzed its association with incident CKD. We further identified metabolic and proteomic signatures of the EAT-Lancet diet and mediators linking the EAT-Lancet diet to CKD risk.</p>
RESULTS: During a median follow-up of 12.1 years, 4819 participants developed incident CKD. Higher EAT-Lancet adherence was inversely associated with CKD risk across all 4 scoring methods: Stubbendorff (adjusted hazard ratio [HR] 0.91, 95% confidence interval [CI] 0.88 to 0.94), Kesse-Guyot (adjusted HR 0.92, 95% CI 0.90 to 0.95), Yi-Xiang (adjusted HR 0.94, 95% CI 0.91 to 0.97), and Knuppel (adjusted HR 0.94, 95% CI 0.92 to 0.97). This association was stronger in participants with low residential green space exposure (p for interaction = 0.008) and those with the rs2010352 GG genotype (p for interaction < 0.001). Metabolic and proteomic signatures (122 metabolites and 143 proteins) of the EAT-Lancet diet were significantly inversely associated with CKD risk and mediated the inverse association between the EAT-Lancet index and incident CKD by 18.0% and 27.2%, respectively. Key mediators included degree of fatty acid unsaturation, glycoprotein acetyls, interleukin-18 receptor 1, and kidney injury molecule 1.</p>
INTERPRETATION: The EAT-Lancet diet was associated with lower risk of incident CKD. The related genetic, environmental, proteomic, and metabolic factors identified could inform personalized nutrition strategies.</p>