Abstract: TH-PO055
Urinary Activin A: A Novel Biomarker for Monitoring the Severity of AKI
Session Information
- AKI: Epidemiology, Risk Factors, Prevention - I
November 07, 2019 | Location: Exhibit Hall, Walter E. Washington Convention Center
Abstract Time: 10:00 AM - 12:00 PM
Category: Acute Kidney Injury
- 101 AKI: Epidemiology, Risk Factors, and Prevention
Authors
- Nagayama, Izumi, Jichi Medical University, Shimotsuke, Tochigi, Japan
- Maeshima, Akito, Jichi Medical University, Shimotsuke, Tochigi, Japan
- Nagata, Daisuke, Jichi Medical University, Shimotsuke, Tochigi, Japan
Background
Acute kidney injury (AKI) is a common but complex condition that is associated with increased morbidity and mortality. There is a need for biomarkers to predict AKI development and severity in critically ill patients. We previously reported that activin A, a member of the TGF-beta superfamily, which was absent in normal kidney, was increased in the ischemic rat kidney and negatively regulates the repair process of the kidney after injury (Maeshima et al. J Am Soc Nephrol 2001). However, the dynamics and significance of urinary activin A have not been clarified in humans. To address this issue, we examined whether urinary activin A can be detectable in human AKI and may serve as a biomarker to predict AKI development and severity.
Methods
Thirty three patients with AKI (renal AKI 22, pre-renal AKI 11) were enrolled in this study approved by the institutional review board of the Jichi Medical University Hospital (Approved number A18-081, A18-089). Written informed consent was obtained from all participants. The Kidney Disease Improving Global Outcomes (KDIGO) classification was used to diagnose and classify patients developing AKI. Serum and urinary activin A was measured by ELISA. Correlations of urinary activin A with other clinical parameters were analyzed.
Results
Urinary activin A, which was almost undetectable in pre-renal AKI, was significantly increased in renal AKI (6.0 ± 3.17 vs. 204.8 ± 96.6 pg/mL, p<0.05). Urinary activin A level in patients with AKI stage III was significantly higher than that in patients with AKI stage I + II (199.4 ± 102.8 vs. 32.8 ± 16.3 pg/mL, p<0.05). There was a significant correlation of urinary activin A level with urinary NGAL, NAG, and alpha-1 microglobulin, but not with L-FABP, urinary protein, serum creatinine, and serum activin A. In one patient with drug-induced AKI who recovered renal function to normal, urinary activin A rapidly decreased before the normalization of serum creatinine, NGAL and L-FABP. In other patient with AKI due to contrast nephropathy, who did not recover renal function, urinary activin A remained at high level at 1 month after the initiation of hemodialysis therapy.
Conclusion
Urinary activin A can be detected in human with AKI and might be a useful and non-invasive biomarker for monitoring the severity of AKI.
Funding
- Government Support - Non-U.S.