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<p>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, thereby contributing to the maintenance of kidney function in AKI. However, the role of AIM in anti-neutrophil cytoplasmic antibody-associated vasculitis (AAV) remains unknown. In this study, whether AIM could be detected in the urine and kidneys of patients with AAV was investigated, and the potential of urinary AIM as a biomarker for AAV-related kidney injury was evaluated. A total of 57 patients with AAV treated in our departments between December 2011 and March 2024, together with 16 healthy adults, were enrolled. Serum and urinary AIM levels were measured by ELISA. The correlations of urinary AIM levels with renal function, urinary protein levels, clinical parameters, and established AKI biomarkers were analyzed. The intrarenal localization of AIM was examined by immunostaining using renal biopsy specimens from patients with AAV. Urinary AIM levels were significantly higher in patients with AAV than in healthy controls (18.8 ± 2.8 vs. 0.00 ± 0.0&#xa0;μg/gCr, <i>p</i> &lt; 0.01). Urinary AIM levels decreased significantly after immunosuppressive therapy. Patients with higher urinary AIM levels tended to show limited improvement in renal function. Urinary AIM levels were significantly correlated with serum creatinine, estimated glomerular filtration rate, urinary protein excretion, urinary kidney injury molecule-1, and urinary neutrophil gelatinase-associated lipocalin. In contrast, no significant correlations were observed between urinary AIM levels and urinary <i>N</i>-acetyl-β-<span>d</span>-glucosaminidase, MPO-ANCA titers, or C-reactive protein levels. AIM was not detected in normal kidneys, but it was detected in renal tubules of patients with AAV. AIM-positive cells expressed aquaporin-1, but not uromodulin or aquaporin-2. AIM-positive cells were partially colocalized with KIM-1-positive tubules and CD68-positive cells. These findings suggest that urinary AIM may serve as a non-invasive biomarker reflecting the severity of tubular injury in patients with AAV.</p>

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Urinary apoptosis inhibitor of macrophage reflects renal inflammation and tubular damage in ANCA-associated vasculitis

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年7月31日

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  • Shunsuke Takahashi,
  • Yoshinori Takei,
  • Mari Okada,
  • Kaori Takayanagi,
  • Keiju Hiromura,
  • Hajime Hasegawa,
  • Akito Maeshima

摘要

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, thereby contributing to the maintenance of kidney function in AKI. However, the role of AIM in anti-neutrophil cytoplasmic antibody-associated vasculitis (AAV) remains unknown. In this study, whether AIM could be detected in the urine and kidneys of patients with AAV was investigated, and the potential of urinary AIM as a biomarker for AAV-related kidney injury was evaluated. A total of 57 patients with AAV treated in our departments between December 2011 and March 2024, together with 16 healthy adults, were enrolled. Serum and urinary AIM levels were measured by ELISA. The correlations of urinary AIM levels with renal function, urinary protein levels, clinical parameters, and established AKI biomarkers were analyzed. The intrarenal localization of AIM was examined by immunostaining using renal biopsy specimens from patients with AAV. Urinary AIM levels were significantly higher in patients with AAV than in healthy controls (18.8 ± 2.8 vs. 0.00 ± 0.0 μg/gCr, p < 0.01). Urinary AIM levels decreased significantly after immunosuppressive therapy. Patients with higher urinary AIM levels tended to show limited improvement in renal function. Urinary AIM levels were significantly correlated with serum creatinine, estimated glomerular filtration rate, urinary protein excretion, urinary kidney injury molecule-1, and urinary neutrophil gelatinase-associated lipocalin. In contrast, no significant correlations were observed between urinary AIM levels and urinary N-acetyl-β-d-glucosaminidase, MPO-ANCA titers, or C-reactive protein levels. AIM was not detected in normal kidneys, but it was detected in renal tubules of patients with AAV. AIM-positive cells expressed aquaporin-1, but not uromodulin or aquaporin-2. AIM-positive cells were partially colocalized with KIM-1-positive tubules and CD68-positive cells. These findings suggest that urinary AIM may serve as a non-invasive biomarker reflecting the severity of tubular injury in patients with AAV.