Abstract: TH-PO078
Urinary Apoptosis Inhibitor of Macrophage Reflects the Severity of Tubular Damage in Patients with ANCA-Associated Vasculitis
Session Information
- AKI: Clinical, Outcomes, and Trials - Epidemiology and Pathophysiology
October 24, 2024 | Location: Exhibit Hall, Convention Center
Abstract Time: 10:00 AM - 12:00 PM
Category: Acute Kidney Injury
- 102 AKI: Clinical, Outcomes, and Trials
Authors
- Takahashi, Shunsuke, Department of Nephrology and Hypertension, Saitama Medical Center, Saitama Medical University, Kawagoe, Saitama, Japan
- Takei, Yoshinori, Department of Nephrology, Fukaya Red Cross Hospital, Fukaya, Saitama, Japan
- Takayanagi, Kaori, 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
- Hasegawa, Hajime, 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
Background
Apoptosis inhibitor of macrophage (AIM) produced by tissue macrophages has been implicated in a variety of pathological conditions, including acute kidney injury (AKI). AIM protects renal cells from apoptosis, modulating inflammation, and promotes tissue repair. AIM helps in maintaining kidney function by preventing excessive cell death and supporting the regeneration of damaged renal tissue in AKI. However, the role of AIM in ANCA-associated vasculitis (AAV) remains unknown. In the present study, we investigated whether AIM can be detected in the urine and kidneys of patients with AAV to evaluate the potential of urinary AIM as a marker for AAV.
Methods
AAV patients (n=34) who were treated in our departments (December 2011 to December 2022) and healthy adults (n=16) were enrolled in this study. Serum and urinary AIM were measured by ELISA. The correlation of urinary AIM with renal function, urinary protein level, clinical parameters and various AKI biomarkers were analyzed. Localization of AIM in the kidney of AAV patients was examined by immunostaining using the renal biopsy specimens. This study was approved by the Ethics Committee on Human Research of our institutions (Approval number 855, 2487). Written informed consent was obtained from all patients.
Results
Compared to healthy subjects, urinary AIM was significantly increased in AAV (0.00 ± 0.0 vs. 19.2 ± 3.6 μg/gCr, p<0.01). Urinary AIM levels significantly decreased following immunosuppressive therapy. We found a significant correlation between urinary AIM and serum creatinine, urinary protein, urinary NAG, urinary β2-microglobulin, MPO-ANCA, and C-reactive protein. However, no significant correlation was observed between urinary AIM and either urinary kidney injury molecule-1 or serum AIM. AIM was absent in normal kidney but was detected in renal tubules of the kidney of AAV patients. AIM-producing cells were positive for aquaporin-1, but was negative for uromodulin, and aquaporin-2.
Conclusion
Urinary AIM, which was produced by proximal tubules, might be useful as a marker reflecting the severity of tubular damages in patients with AAV.