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During the congress, E-Posters will be accessible to all participants on the congress website 24/7, as well as in the E-poster stations in the congress center.
Preparing your E-Poster
Please review the E-Poster format requirements carefully when preparing your E-Poster. Should your E-Poster not meet the mentioned requirements, it may not be displayed as described above.
E-Poster Submission Deadline
Please prepare and upload your E-Poster no later than March 14, 2026 11.59PM CET. After this date, you will no longer be able to prepare and upload your E-poster and it will not be displayed and accessible on the congress website.
Please follow the instructions below to input your abstract title.
Abstract titles should be brief and reflect the content of the abstract.
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 tubular cells from apoptosis, modulates inflammation, and promotes tissue repair. In concert with kidney injury molecule-1 (KIM-1), 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 and evaluated the potential of urinary AIM as a disease and prognostic marker for AAV.
This study enrolled 57 patients with AAV treated in Saitama Medical Center or Gunma University Hospital from October 2011 to March 2024: new-onset AAV (n=46), AAV in remission (n=5) and relapsing AAV (n=6). Healthy adults served as controls (n=16). Serum and urinary AIM were measured by ELISA. Associations between urinary AIM and 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 numbers 855 and 2487). Written informed consent was obtained from all patients.
Twenty-three patients with AAV were male and 34 were female; mean age was 73.3 ± 9.7 years (mean ± SD). All patients had microscopic polyangiitis (MPA). Compared to healthy subjects, urinary AIM was significantly increased in AAV (0.00 ± 0.0 vs. 18.8 ± 2.8 μg/gCr, p<0.01) and significantly decreased following immunosuppressive therapy. We found a significant correlation between urinary AIM and serum creatinine, estimated glomerular filtration rate(eGFR), urinary protein, urinary KIM-1, urinary Neutrophil Gelatinase-Associated Lipocalin (NGAL) and serum AIM. However, no significant correlation was observed between urinary AIM and either urinary N-acetyl-β-D-glucosaminidase (NAG), MPO-ANCA titer of CRP. 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, with partial overlap with CD68 or KIM-1, but were negative for uromodulin, and aquaporin-2. No significant correlation was observed between urinary AIM levels and the extent of interstitial fibrosis or interstitial cell infiltration. Urinary AIM levels were significantly higher in patients with crescentic or sclerotic glomeruli. Limited reduction in urinary AIM was observed predominantly in patients requiring hemodialysis or with insufficient renal recovery (<30% improvement in serum creatinine).
Urinary AIM, produced by proximal tubular cells, reflects the severity of tubular injury in AAV and may serve as a prognostic indicator of renal outcomes. These findings support urinary AIM as a candidate biomarker for disease activity and recovery in ANCA-associated vasculitis.