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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.
Fetuin-A has been reported to attenuate inflammation and fibrosis in the kidney. Production of post-translational modifications-Fetuin-A (PTM-FetA), an abnormal Fetuin-A, represents the loss of kidney protection in response to stress. Urinary PTM-FetA (uPTM-FetA) has recently been reported as an early biomarker to predict renal function decline in type 2 diabetes. Sodium-glucose cotransporter 2 inhibitors (SGLT2i) provide the reno-protection effect to reduce albuminuria, but the longitudinal therapeutic response of SGLT2i on uPTM-FetA in diabetic patients, including those without microalbuminuria, remains unknown.
We prospectively collected urine from diabetic patients before and after SGLT2i, at 3, 6, and 12 months. Clinical, laboratory, and demographic characteristics were also recorded. uPTM-FetA was quantified using the DNlite-DKD assay and normalized to urine creatinine (UCr). Participants were stratified into high- and low-risk groups based on baseline uPTM-FetA/UCr (cutoff: 7.53 ng/mg).
At baseline before SGLT2i, 86 patients were enrolled, with follow-up samples collected at 3, 6, and 12 months (N=50, 53, and 56, respectively). Their age was 60.4 ±10.4 years (male:female=65:21) with a mean eGFR (CKD-EPI) of 83.21 ± 21.95ml/min/1.73m2. There was a significant decrease in HbA1c, fasting glucose, uric acid, and uPTM-FetA/UCr across the four time points. The uPTM-FetA/UCr was significantly correlated with urine albumin creatinine ratio (UACR) at 3, 6, and 12 months after SGLT2i (Figure 1). Compared to low-risk groups with low uPTM-FetA/UCr (N=48), high-risk groups with high uPTM-FetA/UCr (N=38) only had higher HbA1c (8.68±1.56% vs 7.97±1.18%, p=0.026) at baseline, but not in serum creatinine, eGFR, or UACR. Diabetic patients with high-risk exhibited significant improvements in HbA1c, UACR, and uPTM-FetA/UCr over 12 months after SGLT2i compared to those with low-risk (Figure 2). Among diabetic patients without microalbuminuria (UACR <30 mg/g) at baseline (N=52), 35% of them (N=18) still had high uPTM-FetA/UCr. High-risk patients without microalbuminuria had a significant reduction in uPTM-FetA/UCr following SGLT2i at both 6 and 12 months, in comparison with low-risk patients without microalbuminuria (Figure 3).
Our findings highlight that uPTM-FetA provides a sensitive and stable biomarker for monitoring the therapeutic responses after SGLT2i in diabetes patients, even in patients without microalbuminuria, indicating early detection of signaling of kidney damage before microalbuminuria.
