Abstract: FR-PO1188
Urinary Biomarkers Are Associated with Distinct Functional and Histologic Patterns of Kidney Allograft Injury
Session Information
- Transplantation: Clinical - Rejection, Biomarkers, and Pharmacology
October 23, 2026 | Location: Exhibit Hall A, Convention Center
Abstract Time: 10:00 AM - 12:00 PM
Category: Transplantation
- 2002 Transplantation: Clinical
Authors
- Lee, Hojin, Korea University Anam Hospital, Seoul, Korea (the Republic of)
- Koo, Tai yeon, Korea University Anam Hospital, Seoul, Korea (the Republic of)
- Yu, Jinyoung, Korea University Anam Hospital, Seoul, Korea (the Republic of)
- Oh, Sewon, Korea University Anam Hospital, Seoul, Korea (the Republic of)
- Kim, Myung-Gyu, Korea University Anam Hospital, Seoul, Korea (the Republic of)
Background
Protein tyrosine phosphatase 1B (PTP1B) has recently been identified as a regulator of the ER stress–oxidative stress–inflammatory axis in ischemic kidney injury. However, its clinical relevance in kidney transplant recipients (KTRs) remains unclear. We investigated whether urinary PTP1B measured at 1 year post-transplant reflects subclinical graft injury and predicts long-term graft function. Liver-type fatty acid-binding protein (L-FABP) and uromodulin were also evaluated for comparison.
Methods
Urine samples were collected at 1 year post-transplant from 80 KTRs enrolled in the KNOW-KT cohort. Urinary PTP1B, L-FABP, and uromodulin levels were quantified by ELISA and normalized to urine creatinine. Recipients were stratified by median biomarker levels. eGFR was assessed annually up to 9 years post-transplant. Longitudinal graft function, graft outcomes, and histopathologic findings from protocol or indication biopsies were analyzed.
Results
Recipients with high urinary L-FABP levels demonstrated persistently lower eGFR during follow-up, with significant differences observed at years 2, 4, 6, and 8 post-transplant. Higher L-FABP levels were also associated with greater tubular atrophy on biopsy, consistent with chronic tubular injury and progressive graft dysfunction.
In contrast, recipients with high urinary PTP1B levels showed lower eGFR at year 2, although differences attenuated thereafter. Histologic analyses demonstrated increased interstitial inflammation in the PTP1B high group, suggesting that elevated urinary PTP1B reflects ongoing inflammatory injury preceding overt graft dysfunction.
Urinary uromodulin was not associated with longitudinal eGFR differences but was associated with higher glomerulosclerosis scores, suggesting a relationship with chronic structural remodeling. Kaplan–Meier analyses showed no significant differences in graft failure or overall survival between groups.
Conclusion
Urinary biomarkers measured at a clinically stable time point reflect distinct aspects of kidney allograft injury. Urinary L-FABP was associated with long-term graft dysfunction and tubular injury, whereas PTP1B reflected inflammatory activity within the allograft. These findings support the potential role of urinary biomarkers as non-invasive tools for identifying subclinical graft injury after kidney transplantation.
Funding
- Government Support – Non-U.S.