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During the congress, E-Posters will be accessible to all participants on the congress website 24/7, as well as in the E-poster stations in the congress center.
Preparing your E-Poster
Please review the E-Poster format requirements carefully when preparing your E-Poster. Should your E-Poster not meet the mentioned requirements, it may not be displayed as described above.
E-Poster Submission Deadline
Please prepare and upload your E-Poster no later than March 14, 2026 11.59PM CET. After this date, you will no longer be able to prepare and upload your E-poster and it will not be displayed and accessible on the congress website.
Please follow the instructions below to input your abstract title.
Abstract titles should be brief and reflect the content of the abstract.
Systemic inflammation, a risk factor associated with both the onset and progression of chronic kidney disease (CKD), is commonly defined as a C-reactive protein (CRP) level ≥2 mg/L. This threshold is primarily used in Western populations, whereas Japanese patients generally present with relatively lower CRP levels. It remains unclear if CRP level is associated with CKD progression within these lower ranges. The objective of this study was to evaluate the association between CRP levels and CKD progression in patients with CKD in Japan.
This was an observational secondary data analysis using the Japan Chronic Kidney Disease Database Extension (J-CKD-DB-Ex) registry, a nationwide, multicentre electronic health record-based database of patients with CKD in Japan. Individuals aged ≥18 years with CKD with an estimated glomerular filtration rate (eGFR) of 15–<60 mL/min/1.73 m² were included. Those with a history of inflammatory diseases or a history of using immunosuppressive agents within the 180-day period before the index date were excluded. Eligible individuals were categorized by baseline serum CRP levels: <0.5 mg/L, 0.5–<2.0 mg/L, 2.0–<10.0 mg/L and ≥10.0 mg/L. The index date was defined as the date of the first CRP measurement taken at least six months after the first eGFR measurement following registry enrolment. Individuals were followed up for 2 years. The primary endpoint was time to CKD progression, defined as the composite of end-stage renal disease (defined as eGFR <15 mL/min/1.73 m2) and/or a reduction in eGFR of ≥30%. The cumulative incidence of the composite endpoint was described using the Kaplan–Meier method. Hazard ratios (HRs) and 95% confidence intervals (CIs) were estimated using Cox proportional hazards models adjusted for age, sex and other covariates, with the reference being the CRP level <0.5 mg/L group.
A total of 7062 patients met the eligibility criteria; the median age was 73.0 years and 59.4% were men. Patients were categorized into four groups based on their baseline CRP levels: <0.5 mg/L, n=1092; 0.5–<2.0 mg/L, n=3779; 2.0–<10.0 mg/L, n=1492; and ≥10.0 mg/L, n=699. The cumulative incidence of the composite endpoint during the 2-year follow-up period for each CRP group was 12.1%, 15.0%, 19.2% and 22.0%, respectively (p<0.0001; Figure). Adjusted HRs (95% CIs) for the composite endpoint were 1.23 (1.01–1.48) for the 0.5–<2.0 mg/L group, 1.55 (1.26–1.91) for the 2.0–<10.0 mg/L group and 1.86 (1.47–2.35) for the ≥10.0 mg/L group.
Elevated CRP levels, even within moderately low ranges, were associated with CKD progression among patients with CKD in Japan. Our findings highlight systemic inflammation as an important factor in CKD management, underscoring the need for proactive monitoring and tailored interventions. Future research should aim to establish specific CRP cutoffs for risk stratification to help improve patient outcomes.
