Kidney Week

Abstract: TH-PO0266

Cell-Bound CD93 Impairs Glomerular Endothelial-Cell Functionality in Idiopathic Nephrotic Syndrome

Session Information

• Glomerular Diseases: Cell Biology
  October 22, 2026 | Location: Exhibit Hall A, Convention Center
  Abstract Time: 10:00 AM - 12:00 PM

Category: Glomerular Diseases

• 1401 Glomerular Diseases: Mechanisms, including Podocyte Biology

Authors

• Fetsko, Audrey Rose, Nationwide Children's Hospital, Columbus, Ohio, United States

Audrey Rose Fetsko, PhD

• Cummins, Timothy, University of Louisville School of Medicine, Louisville, Kentucky, United States

Timothy Cummins, PhD

• Islam, Md Imtiazul, Nationwide Children's Hospital, Columbus, Ohio, United States

Md Imtiazul Islam, PhD

• Nargis, Nelofar, Nationwide Children's Hospital, Columbus, Ohio, United States

Nelofar Nargis, PhD

• Patel, Rishil H., Nationwide Children's Hospital, Columbus, Ohio, United States

Rishil H. Patel

• Wang, Xin, Nationwide Children's Hospital, Columbus, Ohio, United States

Xin Wang, PhD

• Annesi, Lorenzo, Nationwide Children's Hospital, Columbus, Ohio, United States

Lorenzo Annesi, MD

• Johnson, Richard J., University of Colorado System, Denver, Colorado, United States

Richard J. Johnson, MD

• Cara-Fuentes, Gabriel M., Nationwide Children's Hospital, Columbus, Ohio, United States

Gabriel M. Cara-Fuentes, MD, PhD

Background

Idiopathic nephrotic syndrome (INS) is considered an autoimmune podocytopathy. There is also growing recognition that glomerular endothelial cells (GEnC) may contribute to the pathogenesis. Our group recently showed that GEnC overexpress and release CD93. While soluble CD93 contributes to podocyte injury, it remains untested whether endothelial-bound CD93 plays a role in the disease.

Methods

To test the role of endothelial-bound CD93 in INS, we generated CD93-knock-in GEnC (CD93-KI-GEnC) and performed RNAseq, phosphoproteomics, and several functional assays (scratch assays, impedance sensing, etc.) comparing CD93 overexpression to wildtype.

Results

By RNAseq and phosphoproteomics, top biological processes associated with CD93 overexpression in GEnC included extracellular matrix organization and cell adhesion (not shown due to space limitations). Consistently, CD93-KI-GEnC showed a loss of VE-cadherin by immunofluorescence (Fig. 1a), impaired barrier integrity by impedance sensing (Fig. 1b), and increased cell migration (Fig. 1c). Additional studies, including permeability assays and mechanistic studies, are ongoing.

Conclusion

High expression of CD93 impairs GEnC integrity and alters cell behavior. This indicates that the endothelium, and more specifically cell-bound CD93, is involved in the pathogenesis of INS.

Funding

• NIDDK Support