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<p>Renal transplantation is the most effective treatment option for patients with end-stage renal disease. Renal allograft rejection is characterized by infiltration of inflammatory cells, predominantly lymphocytes, monocytes, and macrophages. Monocytes and macrophages play a crucial role in both acute and chronic renal allograft injury. In this study, we analyzed CD68 + and CD163 + renal tissue macrophage infiltration, as well as urinary soluble CD163 (usCD163), in patients with renal allograft dysfunction resulting from antibody-mediated rejection (AMR). Fifty-five renal allograft recipients with for-cause graft biopsies were recruited for the study. CD68 and CD163 macrophage infiltration were assessed using immunohistochemistry (IHC) on renal allograft biopsy samples. usCD163 levels were quantified using enzyme-linked immunosorbent assay (ELISA) and compared with age- and sex-matched healthy controls. We found higher counts of glomerular CD68+ (4.5 ± 4.4) and CD163+ (3.2 ± 3.5) macrophages in graft biopsies with AMR than in those with no evidence of rejection (NER) (1.1 ± 1.7 and 1.8 ± 1.7, respectively). CD163 + macrophage infiltration in the tubulointerstitium was greater in AMR (16.7 ± 9) than in NER (10.5 ± 5). The intratubular and intra-peritubular capillary (PTC) CD163 + cell counts were higher (2.45 ± 3, 0.65 ± 1.2) in AMR than in NER. CD163 + macrophages in the glomerulus and tubulointerstitium were associated with glomerulitis (<i>p</i> &lt; 0.001) and interstitial fibrosis (<i>p</i> &lt; 0.005), respectively. usCD163 correlated with serum creatinine (<i>p</i> = 0.020, <i>r</i> = 0.368) and CD163 + macrophage infiltration in the glomeruli and tubulointerstitium. The decrease in elevated usCD163 levels and tissue macrophage infiltration during follow-up in patients with AMR indicates a response to macrophage-driven allograft injury, suggesting a potential non-invasive biomarker for rejection. Our findings imply that macrophage activation plays a key role in AMR. These results highlight potential avenues for future research and therapeutic strategies.</p>

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Graft Macrophage Infiltration and Urinary Soluble CD163 in Antibody-Mediated Renal Allograft Rejection

  • 期刊论文

  • 发表日期：

    2025年12月12日

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  • Shubhi Kamthan,
  • Snigdha Pratap Singh,
  • Narayan Prasad,
  • Vinita Agrawal,
  • Niharika Bharti

摘要

Renal transplantation is the most effective treatment option for patients with end-stage renal disease. Renal allograft rejection is characterized by infiltration of inflammatory cells, predominantly lymphocytes, monocytes, and macrophages. Monocytes and macrophages play a crucial role in both acute and chronic renal allograft injury. In this study, we analyzed CD68 + and CD163 + renal tissue macrophage infiltration, as well as urinary soluble CD163 (usCD163), in patients with renal allograft dysfunction resulting from antibody-mediated rejection (AMR). Fifty-five renal allograft recipients with for-cause graft biopsies were recruited for the study. CD68 and CD163 macrophage infiltration were assessed using immunohistochemistry (IHC) on renal allograft biopsy samples. usCD163 levels were quantified using enzyme-linked immunosorbent assay (ELISA) and compared with age- and sex-matched healthy controls. We found higher counts of glomerular CD68+ (4.5 ± 4.4) and CD163+ (3.2 ± 3.5) macrophages in graft biopsies with AMR than in those with no evidence of rejection (NER) (1.1 ± 1.7 and 1.8 ± 1.7, respectively). CD163 + macrophage infiltration in the tubulointerstitium was greater in AMR (16.7 ± 9) than in NER (10.5 ± 5). The intratubular and intra-peritubular capillary (PTC) CD163 + cell counts were higher (2.45 ± 3, 0.65 ± 1.2) in AMR than in NER. CD163 + macrophages in the glomerulus and tubulointerstitium were associated with glomerulitis (p < 0.001) and interstitial fibrosis (p < 0.005), respectively. usCD163 correlated with serum creatinine (p = 0.020, r = 0.368) and CD163 + macrophage infiltration in the glomeruli and tubulointerstitium. The decrease in elevated usCD163 levels and tissue macrophage infiltration during follow-up in patients with AMR indicates a response to macrophage-driven allograft injury, suggesting a potential non-invasive biomarker for rejection. Our findings imply that macrophage activation plays a key role in AMR. These results highlight potential avenues for future research and therapeutic strategies.