Abstract: FR-PO0383
Urinary Amphiregulin Reflects Tubular Injury Severity in Patients with AKI
Session Information
- AKI: Biomarkers, Diagnostics, and Risk Prediction
October 23, 2026 | Location: Exhibit Hall A, Convention Center
Abstract Time: 10:00 AM - 12:00 PM
Category: Acute Kidney Injury
- 102 AKI: Clinical, Outcomes, and Trials
Authors
- Abe, Erika, Saitama Medical Center, Saitama Medical University, Kawagoe, Saitama, Japan
- Okada, Mari, Saitama Medical Center, Saitama Medical University, Kawagoe, Saitama, Japan
- Takahashi, Shunsuke, Saitama Medical Center, Saitama Medical University, Kawagoe, Saitama, Japan
- Maeshima, Akito, Saitama Medical Center, Saitama Medical University, Kawagoe, Saitama, Japan
Background
Acute kidney injury (AKI) is characterized by tubular injury followed by regeneration and repair. Activation of the epidermal growth factor receptor (EGFR) signaling pathway is associated with cell proliferation, inflammation, and fibrosis. Amphiregulin (AREG), an EGFR ligand essential for kidney development, has an unclear role in the adult kidney. In this study, we investigated urinary AREG concentrations in patients with AKI and evaluated their clinical significance.
Methods
Between October 2020 and April 2024, we enrolled 225 patients with AKI treated at our department and 19 healthy controls. Recipients of deceased-donor kidney transplantation were also included because kidney transplantation mimics ischemia–reperfusion injury. Serum and urinary AREG concentrations were measured using ELISA, and their correlations with established AKI biomarkers and clinical parameters were analyzed.
Results
Urinary AREG was undetectable in healthy controls. In contrast, urinary AREG increased significantly in AKI patients (0.0 ± 0.0 vs. 20.0 ± 26.0 ng/mL, p < 0.001), rising in proportion to AKI severity (stage 1: 9.45 ± 10.6 ng/mL, p = 0.27; stage 2: 22.3 ± 22.7 ng/mL, p < 0.01; stage 3: 31.7 ± 26.6 ng/mL, p < 0.001). Urinary AREG showed significant correlations with serum creatinine, eGFR, urinary protein, urinary NAG, urinary NGAL, urinary KIM-1, and urinary β2-microglobulin, but not with urinary L-FABP or serum AREG levels. Among the different etiologies of AKI, deceased-donor kidney transplant recipients exhibited the highest urinary AREG levels. In recipients successfully weaned from dialysis early after transplantation, urinary AREG rapidly became negative and remained undetectable for up to 4 months. Conversely, urinary AREG remained persistently elevated in patients with acute rejection, urinary tract infection, or cytomegalovirus infection associated with delayed recovery from dialysis dependence. Immunostaining showed AREG expression in distal tubular epithelial cells in kidneys with AKI.
Conclusion
AREG is not expressed in normal adult kidneys but is significantly upregulated after AKI. Urinary AREG may reflect the severity of tubular injury and ongoing renal repair processes. Importantly, in kidney transplant recipients, urinary AREG may serve as a promising noninvasive biomarker for predicting rejection, infectious complications, and renal prognosis.