Abstract: SA-PO0081
AKI Is Associated with Elevated Urinary Endotrophin
Session Information
- AKI: Clinical Diagnostics and Biomarkers
November 08, 2025 | Location: Exhibit Hall, Convention Center
Abstract Time: 10:00 AM - 12:00 PM
Category: Acute Kidney Injury
- 102 AKI: Clinical, Outcomes, and Trials
Authors
- Vu, Kyle Q., The University of Texas Southwestern Medical Center, Dallas, Texas, United States
- Clark, Amanda J., The University of Texas Southwestern Medical Center, Dallas, Texas, United States
- Mendoza Flores, Brenda, Texas College of Osteopathic Medicine, Fort Worth, Texas, United States
- Saade, Marie Christelle, The University of Texas Southwestern Medical Center, Dallas, Texas, United States
- Pence, Isaac, The University of Texas Southwestern Medical Center, Dallas, Texas, United States
- Bu, Dawei, The University of Texas Southwestern Medical Center, Dallas, Texas, United States
- Scherer, Philipp, The University of Texas Southwestern Medical Center, Dallas, Texas, United States
- Parikh, Samir M., The University of Texas Southwestern Medical Center, Dallas, Texas, United States
Background
Acute Kidney Injury (AKI) affects nearly 20% of hospitalized patients. Diagnostic criteria for AKI depend on incremental changes in serum creatinine and urine output, which lead to inaccurate and delayed diagnosis. Novel biomarkers are needed to diagnose AKI more accurately and target AKI therapies. Endotrophin (ETP) is a signaling molecule released during the formation of collagen type VI. In certain settings, it acts as a pathogenic growth factor and fibrogenic stimulus. Serum ETP is elevated in patients with AKI and is associated with acute and chronic outcomes. Urinary ETP has not been assessed in AKI nor has ETP been evaluated in a pediatric population.
Methods
Discarded urine samples were collected from a tertiary children’s hospital. Medical records were reviewed, and patients who met criteria were sorted into 3 categories: 1. AKI at the time of collection; 2. Hospitalized non-AKI patients who were admitted but did not have AKI; and 3. Outpatient controls who had urine samples sent for routine screening. Demographic variables were collected from the medical record, and eGFR was calculated using the Bedside Schwartz equation. ETP was measured using ELISA, and results were corrected to urine creatinine measured with a commercial assay. Urine ETP:creatinine ratios (uETP:Cre) were compared using Mann-Whitney test. A multivariate linear regression was used to assess whether demographic variables independently associated with uETP:Cre. Odds of AKI were assessed in serial uETP:Cre tertiles using multivariate logistic regression models to adjust for patient variables.
Results
uETP:Cre was elevated in patients with AKI compared to hospitalized patients without AKI (p=0.016) and outpatient controls (p<0.0001) but did not correlate with eGFR. Linear regression revealed that age, but not sex, race, or ethnicity correlated with uETP:Cre (p=0.0025). When correcting for all variables, odds ratio of AKI increased with serial uETP:Cre tertiles.
Conclusion
Non-invasive measurement of urine ETP may deliver clinically meaningful information to aid in AKI diagnosis. Given that ETP may be both a biomarker and an actionable stimulus of inflammation and fibrosis, future studies are needed to understand the role of elevated ETP in AKI and if existing ETP neutralizing antibodies could represent a new avenue for AKI therapy.
Funding
- NIDDK Support