The EAT-Lancet planetary health diet and risk of incident chronic kidney disease.

Abstract

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. 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. 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 (<i>p</i> for interaction = 0.008) and those with the rs2010352 GG genotype (<i>p</i> 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. 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.