Abstract: FR-OR039
Urinary Fetuin-A Predicts Kidney Outcomes and Identifies Residual Risk Across Treatment Arms in the CREDENCE Trial
Session Information
- Exciting Developments in CKD Research: From Diagnostics to Management and More
October 23, 2026 | Location: Mile High Ballroom 1D, Convention Center
Abstract Time: 04:50 PM - 05:00 PM
Category: CKD (Non-Dialysis)
- 2202 CKD (Non-Dialysis): Clinical, Outcomes, and Trials
Authors
- Tseng, Tzu-Ling, Bio Preventive Medicine, Zhubei City, Taiwan
- Button, Eric, Precision Diabetes, Raleigh, North Carolina, United States
- Rossi, Chiara, University of Pisa, Pisa, Italy
- Raggi, Francesco, University of Pisa, Pisa, Italy
- Solini, Anna, University of Pisa, Pisa, Italy
- Huang, Chi-Hsuan, Bio Preventive Medicine, Zhubei City, Taiwan
- Ferrannini, Ele, University of Pisa, Pisa, Italy
Background
Albuminuria and eGFR incompletely capture risk in diabetic kidney disease (DKD), with substantial heterogeneity in progression. We evaluated whether urinary post-translationally modified fetuin-A (uPTM-FetA; DNlite) predicts renal outcomes independently of standard markers and provides clinically meaningful risk stratification across treatment arms in CREDENCE.
Methods
Baseline uPTM-FetA was measured in 2,429 participants (placebo n=1,466; canagliflozin n=963). The primary endpoint was sustained ≥40% eGFR decline, ESKD, or renal death. Associations were assessed using multivariable Cox models adjusting for UACR, eGFR, age, and LDL-C. Patients were stratified by uPTM-FetA quartiles. Kaplan-Meier analyses evaluated cumulative event risk overall and within each treatment arm.
Results
uPTM-FetA correlated with UACR (ρ=0.49) and eGFR (ρ=-0.22) (p<0.0001). In multivariable analysis, higher uPTM-FetA independently predicted renal outcomes (HR 1.30 [1.12–1.51], p=0.0004), with effect size comparable to established clinical predictors. Risk increased stepwise across quartiles (Q2 HR 1.93, Q3 3.53, Q4 9.33 vs Q1), demonstrating strong risk discrimination.
Within both placebo and canagliflozin arms, uPTM-FetA stratified patients into progressively higher-risk groups (log-rank p<0.0001 for both). Notably, elevated uPTM-FetA identified patients at substantial residual risk despite active treatment, with consistent separation of event curves across treatment arms.
Conclusion
uPTM-FetA is a strong, independent predictor of DKD progression and provides clinically meaningful risk stratification beyond UACR and eGFR. Its ability to identify patients at persistently elevated risk, including those receiving standard-of-care therapy, supports its potential role in risk stratification and therapeutic decision-making in DKD.