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Abstract: SA-PO0760

Single-Cell Profiling of Peripheral Immune Changes in Minimal Change Disease

Session Information

Category: Glomerular Diseases

  • 1401 Glomerular Diseases: Mechanisms, including Podocyte Biology

Authors

  • Ku, Hyunah, Seoul National University College of Medicine, Jongno-gu, Seoul, Korea (the Republic of)
  • Kang, Minji, Seoul National University College of Medicine, Jongno-gu, Seoul, Korea (the Republic of)
  • Lee, Jinsun, Seoul National University College of Medicine, Jongno-gu, Seoul, Korea (the Republic of)
  • Oh, Jae-ik, Seoul National University College of Medicine, Jongno-gu, Seoul, Korea (the Republic of)
  • Cho, Semin, Chung Ang University Hospital, Dongjak-gu, Seoul, Korea (the Republic of)
  • Kim, Hyun Je, Seoul National University College of Medicine, Jongno-gu, Seoul, Korea (the Republic of)
  • Park, Sehoon, Seoul National University Hospital Department of Internal Medicine, Jongno-gu, Seoul, Korea (the Republic of)
  • Kim, Dong Ki, Seoul National University Hospital Department of Internal Medicine, Jongno-gu, Seoul, Korea (the Republic of)
Background

Minimal Change Disease (MCD) is a primary glomerulonephritis characterized by massive proteinuria due to podocyte foot process effacement. While it generally responds well to immunosuppressive therapy, further investigation is needed to elucidate the alterations in systemic immune cells, which are presumed to change between the active baseline and the resolved state. We aimed to identify transcriptomic biomarkers and immune features associated with MCD using single cell multiome data.

Methods

PBMCs were obtained from 11 MCD patients (5 baseline, 6 follow-up), 12 membranous nephropathy patients, 8 diabetic nephropathy patients, and 7 healthy controls (HC). Single-cell Multiome data (scRNA-seq + scATAC-seq) were generated. Using Seurat and R packages, we conducted cell type annotation, proportion analysis, and DEG analysis. GO enrichment was performed via ToppGene and STRINGdb.

Results

After QC, we retained 16,764 cells from MCD and 15,592 from HC. Among MCD cells, 5,038 were from the baseline group and 11,726 from follow-up. The MCD baseline group showed a higher proportion of CD14+ monocytes compared to both HC and MCD follow-up. These cells expressed high levels of inflammatory cytokines such as IL1B, TNFAIP6, CCL3, and CXCL8, suggesting acute inflammation and immune cell recruitment. Conversely, CD16+ monocytes were decreased in MCD patients compared to HC but tended to increase in the follow-up group, indicating a potential shift toward immune resolution.

Conclusion

MCD baseline group is marked by increased CD14+ monocytes and pro-inflammatory signals, with reduced anti-inflammatory CD16+ monocytes. This supports the observed effectiveness of immunosuppressive therapy in early disease. In contrast, follow-up group indicates a transition toward adaptive immunity and partial recovery of anti-inflammatory responses, which may explain reduced responsiveness in relapsing cases. Our findings suggest immune cell composition and cytokine expression may serve as potential biomarkers for disease activity and therapeutic guidance in MCD.

Digital Object Identifier (DOI)