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已发表论文
2型糖尿病患者胆红素与慢性肾脏病关联中的炎症效应：一项回顾性队列研究
Authors Chen Y , Wang S, Chen X, Sun B, Cheng Y, Li X, Chen L
Received 6 November 2025
Accepted for publication 20 December 2025
Published 19 January 2026 Volume 2026:19 578233
DOI https://doi.org/10.2147/JIR.S578233
Checked for plagiarism Yes
Review by Single anonymous peer review
Peer reviewer comments 2
Editor who approved publication: Dr Quan Zhang
Yanyan Chen,* Shanshan Wang,* Xiangna Chen,* Bei Sun, Ying Cheng, Xiaoyu Li, Liming Chen
NHC Key Laboratory of Hormones and Development, Tianjin Key Laboratory of Metabolic Diseases, Chu Hsien-I Memorial Hospital & Tianjin Institute of Endocrinology, Tianjin Medical University, Tianjin, 300134, People’s Republic of China
*These authors contributed equally to this work
Correspondence: Liming Chen, NHC Key Laboratory of Hormones and Development, Tianjin Key Laboratory of Metabolic Diseases, Chu Hsien-I Memorial Hospital & Tianjin Institute of Endocrinology, Tianjin Medical University, No. 6 North Huanrui Road, Beichen District, Tianjin, 300134, People’s Republic of China, Tel +8613920979401, Email chenliming@tmu.edu.cn
Background: The associations of bilirubin (BIL) and systemic inflammation with chronic kidney disease (CKD) remain unclear. This study examined associations among BIL, systemic inflammation, and CKD progression in type 2 diabetes patients, assessing systemic inflammation’s mediating role.
Methods: This retrospective cohort study included 1215 subjects. The exposure was baseline BIL concentrations, while inflammation-related indicators including systemic inflammatory response index (SIRI) and systemic immune-inflammation index (SII). The main outcome was the first event of CKD progression, characterized by a decrease in the estimated glomerular filtration rate (eGFR) stage, with a sustained ≥ 25% decline in eGFR from baseline, confirmed by two consecutive measurements ≥ 3 months apart. Cox proportional hazards models assessed associations between BIL, systemic inflammation, and CKD progression. Subgroup and sensitivity analyses were also conducted. Restricted cubic splines (RCS), and mediation analysis were performed to assess the nonlinear associations and mediating role of systemic inflammation.
Results: During a median follow-up duration of 2.00 years (interquartile range: 1.03– 2.84 years), 153 participants exhibited progression of CKD. The RCS analysis indicated nonlinear associations between both total bilirubin (TBIL, P for nonlinear < 0.001) and indirect bilirubin (IBIL, P for nonlinear < 0.001) with CKD progression. Cox regression models showed the adjusted hazard ratios (HRs) and 95% confidence intervals (CIs) for TBIL and IBIL were 0.92 (95% CI: 0.89, 0.96) and 0.90 (95% CI: 0.85, 0.94), respectively. Subgroup and sensitivity analyses reinforced the findings, demonstrating consistent outcomes across demographic groups and under varied analytical conditions. The modest mediating effects were observed for SIRI (5.21%) and SII (5.50%) with TBIL, and for SIRI (7.17%) and SII (6.92%) with IBIL. However, these correlations were not observed with direct bilirubin (DBIL).
Conclusion: Lower BIL levels (especially IBIL) were inversely associated with CKD progression risk in type 2 diabetes, with systemic inflammation partially mediating this relationship.
Keywords: bilirubin, inflammation, chronic kidney disease, type 2 diabetes, cohort study
NHC Key Laboratory of Hormones and Development, Tianjin Key Laboratory of Metabolic Diseases, Chu Hsien-I Memorial Hospital & Tianjin Institute of Endocrinology, Tianjin Medical University, Tianjin, 300134, People’s Republic of China
*These authors contributed equally to this work
Correspondence: Liming Chen, NHC Key Laboratory of Hormones and Development, Tianjin Key Laboratory of Metabolic Diseases, Chu Hsien-I Memorial Hospital & Tianjin Institute of Endocrinology, Tianjin Medical University, No. 6 North Huanrui Road, Beichen District, Tianjin, 300134, People’s Republic of China, Tel +8613920979401, Email chenliming@tmu.edu.cn
Background: The associations of bilirubin (BIL) and systemic inflammation with chronic kidney disease (CKD) remain unclear. This study examined associations among BIL, systemic inflammation, and CKD progression in type 2 diabetes patients, assessing systemic inflammation’s mediating role.
Methods: This retrospective cohort study included 1215 subjects. The exposure was baseline BIL concentrations, while inflammation-related indicators including systemic inflammatory response index (SIRI) and systemic immune-inflammation index (SII). The main outcome was the first event of CKD progression, characterized by a decrease in the estimated glomerular filtration rate (eGFR) stage, with a sustained ≥ 25% decline in eGFR from baseline, confirmed by two consecutive measurements ≥ 3 months apart. Cox proportional hazards models assessed associations between BIL, systemic inflammation, and CKD progression. Subgroup and sensitivity analyses were also conducted. Restricted cubic splines (RCS), and mediation analysis were performed to assess the nonlinear associations and mediating role of systemic inflammation.
Results: During a median follow-up duration of 2.00 years (interquartile range: 1.03– 2.84 years), 153 participants exhibited progression of CKD. The RCS analysis indicated nonlinear associations between both total bilirubin (TBIL, P for nonlinear < 0.001) and indirect bilirubin (IBIL, P for nonlinear < 0.001) with CKD progression. Cox regression models showed the adjusted hazard ratios (HRs) and 95% confidence intervals (CIs) for TBIL and IBIL were 0.92 (95% CI: 0.89, 0.96) and 0.90 (95% CI: 0.85, 0.94), respectively. Subgroup and sensitivity analyses reinforced the findings, demonstrating consistent outcomes across demographic groups and under varied analytical conditions. The modest mediating effects were observed for SIRI (5.21%) and SII (5.50%) with TBIL, and for SIRI (7.17%) and SII (6.92%) with IBIL. However, these correlations were not observed with direct bilirubin (DBIL).
Conclusion: Lower BIL levels (especially IBIL) were inversely associated with CKD progression risk in type 2 diabetes, with systemic inflammation partially mediating this relationship.
Keywords: bilirubin, inflammation, chronic kidney disease, type 2 diabetes, cohort study