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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.
Growth differentiation factor-15 (GDF-15) is a stress-responsive cytokine belonging to the transforming growth factor-β (TGF-β) superfamily. Under physiological conditions, GDF-15 is highly expressed in the placenta, prostate, and bladder. Elevated circulating GDF-15 levels have been reported in various chronic inflammatory and metabolic disorders. In the kidney, GDF-15 is mainly expressed in tubular epithelial cells, and its expression increases during renal injury, suggesting potential renoprotective effects. Although serum GDF-15 has been identified as an early diagnostic and prognostic biomarker in acute kidney injury (AKI), the clinical significance of urinary GDF-15 remains largely unknown. This study aimed to clarify the role of urinary GDF-15 in the renal stress response and its potential involvement in the pathogenesis of human AKI.
We studied 129 patients with AKI treated in our department between December 2020 and March 2025, along with 18 healthy adults as controls. Written informed consent was obtained from all participants. Serum and urinary GDF-15 concentrations were measured by enzyme-linked immunosorbent assay (ELISA). Correlations between urinary GDF-15 and renal function, urinary protein excretion, and established AKI biomarkers were analyzed. In addition, immunohistochemical staining was performed on renal biopsy specimens from AKI cases to determine the localization of GDF-15 expression within renal tissue. The study protocol was approved by the institutional ethics committee (Approval No. 2487).
Urinary GDF-15 was detectable at trace levels in healthy subjects but was markedly elevated in AKI patients (4.4 ± 0.8 pg/mL vs. 17.8 ± 1.0 pg/mL, p < 0.001). Subgroup analyses revealed significant increases in both prerenal and intrinsic AKI (p < 0.001 for each). Etiological analyses demonstrated that urinary GDF-15 was significantly higher in ischemic, glomerulonephritis-related, drug-induced, and hypertensive AKI compared with controls. Patients with higher urinary GDF-15 levels showed a significantly lower rate of eGFR improvement during hospitalization. Receiver operating characteristic (ROC) curve analysis demonstrated that urinary GDF-15 had diagnostic performance comparable to kidney injury molecule-1 (KIM-1) (AUC = 0.8928, p < 0.0001) with a cutoff of 9.87 pg/mL (sensitivity 73.6%, specificity 94.4%). Urinary GDF-15 did not correlate with serum GDF-15, indicating a renal origin. Moreover, urinary GDF-15 levels showed positive correlations with urinary protein, β2-microglobulin, N-acetyl-β-D-glucosaminidase (NAG), neutrophil gelatinase-associated lipocalin (NGAL), and KIM-1. Immunohistochemical analyses revealed marked GDF-15 expression in proximal tubular epithelial cells of renal tissue from AKI patients.
Urinary GDF-15 reflects tubular stress and injury in AKI. It shows strong diagnostic performance comparable to KIM-1 and may serve as a useful early biomarker for AKI involving tubular damage. Urinary GDF-15 thus represents a promising tool for the early detection and prognostic evaluation of AKI.
