European journal of clinical nutrition · 2026
Sulfur microbial diet, genetical predisposition, and the risk of chronic kidney disease: a cohort study.
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Yang Honghao, Zhang Yixiao, Ma Zheng, Li Liuxin, Zheng Gang, Chang Qing, Ji Chao, Xia Yang, Zhao Yuhong
Аннотация
BACKGROUND/OBJECTIVES: Our study evaluated the prospective association between the sulfur microbial diet (SMD), a diet associated with sulfur-metabolizing bacteria in stool, and the chronic kidney disease (CKD) risk, and further investigated whether genetic risk modified this association.
METHODS: This study involved 98,491 UK Biobank participants who had completed at least two 24-hour dietary recall measurements. SMD scores were computed by summing the product of β-coefficients for each food group and their corresponding intake values. Incident CKD was identified using UK Biobank algorithms. The polygenic risk score (PRS) for CKD was constructed based on 263 single-nucleotide polymorphisms. Hazard ratios (HRs) with 95% confidence intervals (CIs) and population attributable fractions (PAFs) were calculated using Cox proportional hazard regression models.
RESULTS: During a median follow-up of 9.38 years, we documented 2,032 incident CKD cases. We observed a dose-response association between the SMD score and increased CKD risk (P for non-linearity = 0.78). Participants in the highest tertile of the SMD score had a significantly higher risk of developing CKD compared to those in the lowest tertile (HR: 1.24, 95% CI: 1.11-1.39, PAF: 6.81, 95% CI: 3.29-10.34). No significant multiplicative or additive interactions between PRS and the SMD score were found (all P > 0.05). The positive associations between the SMD and the CKD risk were similar across low or high genetic risk groups.
CONCLUSION: Higher adherence to SMD was associated with an increased risk of CKD, regardless of genetic risk. Future studies are needed to validate our findings.
METHODS: This study involved 98,491 UK Biobank participants who had completed at least two 24-hour dietary recall measurements. SMD scores were computed by summing the product of β-coefficients for each food group and their corresponding intake values. Incident CKD was identified using UK Biobank algorithms. The polygenic risk score (PRS) for CKD was constructed based on 263 single-nucleotide polymorphisms. Hazard ratios (HRs) with 95% confidence intervals (CIs) and population attributable fractions (PAFs) were calculated using Cox proportional hazard regression models.
RESULTS: During a median follow-up of 9.38 years, we documented 2,032 incident CKD cases. We observed a dose-response association between the SMD score and increased CKD risk (P for non-linearity = 0.78). Participants in the highest tertile of the SMD score had a significantly higher risk of developing CKD compared to those in the lowest tertile (HR: 1.24, 95% CI: 1.11-1.39, PAF: 6.81, 95% CI: 3.29-10.34). No significant multiplicative or additive interactions between PRS and the SMD score were found (all P > 0.05). The positive associations between the SMD and the CKD risk were similar across low or high genetic risk groups.
CONCLUSION: Higher adherence to SMD was associated with an increased risk of CKD, regardless of genetic risk. Future studies are needed to validate our findings.