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Glomerular endothelial cells and podocytes can express CD80 in patients with minimal change disease during relapse
Gabriel Cara-Fuentes1, Madhusudan Venkatareddy2, Rakesh Verma2
1Division of Pediatric Nephrology, Department of Pediatrics, University of Michigan, MSRB-2, Room 1574, 1500 E Medical Center Dr, Ann Arbor, MI, 48109, USA. gcaraf@gmail.com.
Insights
Urinary CD80 may indicate kidney disease in idiopathic nephrotic syndrome (INS). This study found CD80 expressed on glomerular endothelial cells (GEC) and podocytes in patients with minimal change disease (MCD) during relapse.
Area of Science:
- Nephrology
- Immunology
- Cell Biology
Background:
- Urinary CD80 is a potential biomarker for idiopathic nephrotic syndrome (INS).
- The cellular origin of CD80 in the glomerulus remains unclear.
- Investigating CD80 expression in glomerular cells is crucial for understanding INS pathogenesis.
Purpose of the Study:
- To determine if CD80 is expressed by glomerular cells in INS patients during relapse.
- To investigate CD80 expression in a mouse model of podocyte injury induced by LPS.
- To clarify the cellular source of urinary CD80 in INS.
Main Methods:
- Immunostaining, immunogold labeling, and in situ hybridization were used to detect CD80.
- Human kidney biopsies from minimal change disease (MCD) and focal segmental glomerulosclerosis (FSGS) patients were analyzed.
- A lipopolysaccharide (LPS)-induced mouse model of podocyte injury was employed.
Main Results:
- CD80 was detected on glomerular endothelial cells (GEC) and occasionally on podocytes in MCD patients during relapse.
- CD80 expression was also observed in a subset of FSGS patients.
- In the mouse model, CD80 mRNA and protein were upregulated in GEC and podocytes, mirroring findings in MCD.
Conclusions:
- Glomerular endothelial cells and podocytes can express CD80 in minimal change disease (MCD) during relapse.
- Understanding CD80's role in glomerular cells may elucidate mechanisms of proteinuria in INS.
- This study identifies GEC and podocytes as cellular sources of CD80 in INS.
Background:
Urinary CD80 has emerged as potential biomarker in idiopathic nephrotic syndrome (INS). However, its cellular source remains controversial. The aim of the study was to assess whether CD80 is truly expressed by glomerular cells in INS patients during relapse and in the LPS mouse model of podocyte injury.
Methods:
The presence of CD80 in glomeruli was evaluated by combining immunostaining, immunogold labeling, and in situ hybridization techniques.
Results:
CD80 was present along the surface of glomerular endothelial cells (GEC) and rarely in podocytes in six of nine minimal change disease (MCD) patients in relapse, two of eleven patients with focal segmental glomerulosclerosis in relapse, and absent in controls. In mice, CD80 was upregulated at mRNA and protein level in GEC and podocytes, in a similar pattern to that seen in MCD patients.
Conclusions:
Glomerular endothelial cells and podocytes can express CD80 in patients with MCD during relapse. A better understanding of the role of CD80 in glomerular cells may provide further insights into the mechanisms of proteinuria in INS.
