Abstract: TH-PO0461
Urinary Activin A as a Prognostic Biomarker in IgAN
Session Information
- Glomerular Diseases: Clinical, Outcomes, and Therapeutics Research - IgAN
October 22, 2026 | Location: Exhibit Hall A, Convention Center
Abstract Time: 10:00 AM - 12:00 PM
Category: Glomerular Diseases
- 1402 Glomerular Diseases: Clinical, Outcomes, and Therapeutics
Authors
- Ikeuchi, Hidekazu, Department of Nephrology and Rheumatology, Gunma University Graduate School of Medicine, Maebashi, Gunma, Japan
- Takei, Yoshinori, Department of Nephrology, Fukaya Red Cross Hospital, Fukaya, Saitama, Japan
- Kinoshita, Masato, Department of Nephrology and Rheumatology, Gunma University Graduate School of Medicine, Maebashi, Gunma, Japan
- Suwa, Junya, Department of Nephrology and Rheumatology, Gunma University Graduate School of Medicine, Maebashi, Gunma, Japan
- Hamatani, Hiroko, Department of Nephrology and Rheumatology, Gunma University Graduate School of Medicine, Maebashi, Gunma, Japan
- Takeuchi, Yoichi, Department of Nephrology and Rheumatology, Gunma University Graduate School of Medicine, Maebashi, Gunma, Japan
- Kaneko, Yoriaki, Department of Nephrology and Rheumatology, Gunma University Graduate School of Medicine, Maebashi, Gunma, Japan
- Takahashi, Shunsuke, Department of Nephrology and Hypertension, Saitama Medical Center, Saitama Medical University, Kawagoe, Saitama, Japan
- Maeshima, Akito, Department of Nephrology and Hypertension, Saitama Medical Center, Saitama Medical University, Kawagoe, Saitama, Japan
- Hiromura, Keiju, Department of Nephrology and Rheumatology, Gunma University Graduate School of Medicine, Maebashi, Gunma, Japan
Background
IgA nephropathy (IgAN) has a variable clinical course, and non-invasive biomarkers that predict long-term kidney outcomes are needed. Activin A, a member of the transforming growth factor-β superfamily, has been implicated in kidney injury and fibrosis, and activin signaling has recently emerged as a therapeutic target in pulmonary arterial hypertension. We investigated whether urinary activin A predicts renal prognosis in IgAN.
Methods
We retrospectively analyzed 91 patients with biopsy-proven IgAN diagnosed between October 2011 and March 2015. Urinary activin A, follistatin, kidney injury molecule-1 (KIM-1), and neutrophil gelatinase-associated lipocalin (NGAL) were measured by ELISA and normalized to urinary creatinine. The primary outcome was the doubling of serum creatinine (Cr) from baseline or the initiation of kidney replacement therapy. The secondary outcome was a 1.5-fold increase in serum Cr. Associations were assessed using Spearman correlation, ROC analysis, Kaplan-Meier curves, and Cox models adjusted for age, sex, eGFR, and proteinuria.
Results
Urinary activin A was higher in patients with impaired kidney function and greater proteinuria. It correlated positively with urinary NGAL (r=0.33, P=0.001), KIM-1 (r=0.27, P=0.010), and proteinuria (r=0.27, P=0.010), and negatively with eGFR (r=-0.312, P=0.003). During a median follow-up of 74 months, 19 patients reached the primary outcome. Baseline urinary activin A was higher in patients with renal function decline than in those without (43.6±47.0 vs. 15.3±27.4 pg/gCr, P=0.001), whereas urinary NGAL, KIM-1, and follistatin did not differ significantly. The predictive value of urinary activin A remained consistent when using the secondary outcome. ROC analysis for the primary outcome showed an AUC of 0.78, with an optimal cutoff of 11.1 pg/gCr. Patients with urinary activin A >11.1 pg/gCr had significantly shorter renal survival (P<0.001). In multivariable Cox analysis, urinary activin A remained independently associated with renal function decline (hazard ratio 1.021 per pg/gCr; 95% CI, 1.01-1.04; P=0.005).
Conclusion
Urinary activin A is a promising non-invasive prognostic biomarker in IgAN. Its association with long-term renal outcomes after adjustment for eGFR and proteinuria suggests that urinary activin A may reflect activin-related kidney injury pathways and provide valuable information for risk stratification in patients with IgAN.