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Ultrastructural podocyte alterations and autophagosome number in pediatric podocytopathies: associations with CD36
Bárbara Rocha Rodrigues1, Ludmila Fonseca Ruy1, Maria Eduarda Gomes da Costa1
1Kidney Research Center, Department of Pathology, Genetics and Evolution, Institute of Biological and Natural Sciences, Federal University of Triângulo Mineiro, Uberaba, Minas Gerais, Brazil.
Insights
Pediatric focal segmental glomerulosclerosis (FSGS) and minimal change disease (MCD) show distinct podocyte changes and altered CD36/NLRP3 expression. These findings suggest different cellular homeostasis disruptions in these pediatric kidney diseases.
Area of Science:
- Pediatric Nephrology
- Cellular Biology
- Kidney Pathology
Background:
- Focal segmental glomerulosclerosis (FSGS) and minimal change disease (MCD) are leading causes of nephrotic syndrome in children.
- Podocytopathies involve podocyte injury, impacting glomerular filtration barrier integrity.
- Understanding ultrastructural podocyte alterations is crucial for characterizing these diseases.
Purpose of the Study:
- To investigate podocyte ultrastructural alterations in pediatric FSGS and MCD.
- To examine autophagosome number and glomerular CD36/NLRP3 expression in these conditions.
- To identify potential differences in cellular homeostasis mechanisms.
Main Methods:
- Retrospective analysis of 37 pediatric renal biopsies (FSGS n=16, MCD n=21).
- Transmission electron microscopy assessed foot process width and autophagosome number.
- Immunohistochemistry evaluated glomerular CD36 and NLRP3 expression.
Main Results:
- Both FSGS and MCD exhibited increased foot process width and reduced autophagosome number.
- CD36 expression was lower in MCD compared to controls and FSGS.
- NLRP3 expression was elevated in FSGS, with distinct correlations in MCD.
Conclusions:
- Pediatric FSGS and MCD display unique podocyte ultrastructural changes and differential CD36/NLRP3 expression.
- These findings indicate heterogeneous cellular homeostasis disruptions in pediatric podocytopathies.
- Further research is needed to elucidate mechanisms of podocyte injury and structural integrity.
Introduction:
Focal segmental glomerulosclerosis (FSGS) and minimal change disease (MCD) are pediatric podocytopathies characterized by podocyte injury and nephrotic syndrome. Podocyte structural integrity depends on tightly regulated mechanisms of cellular homeostasis, including autophagy. However, ultrastructural alterations associated with pediatric podocytopathies remain incompletely characterized. We investigated podocyte ultrastructural alterations, autophagosome number, and glomerular CD36/NLRP3 expression in pediatric podocytopathies.
Methods:
This retrospective cross-sectional study evaluated renal biopsies from 37 children diagnosed with FSGS (n = 16) or MCD (n = 21). Glomerular CD36 and NLRP3 expression were assessed by immunohistochemistry, whereas foot process width and autophagosome number were evaluated by transmission electron microscopy.
Results:
Both FSGS and MCD showed increased foot process width and reduced autophagosome number compared with controls. Autophagosome number correlated negatively with foot process width in both groups. CD36 expression was reduced in MCD compared with controls and FSGS, whereas NLRP3 expression was increased in FSGS compared with controls. In MCD, NLRP3 expression correlated positively with CD36 expression and autophagosome number.
Conclusion:
Pediatric FSGS and MCD exhibited distinct patterns of podocyte ultrastructural alterations accompanied by differences in glomerular CD36/NLRP3 expression. These observations suggest heterogeneous alterations in cellular homeostasis between pediatric podocytopathies and warrant further investigation into mechanisms associated with podocyte structural integrity and injury.
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