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Updated: May 24, 2026
06:39
Glomerular Outgrowth as an Ex Vivo Assay to Analyze Pathways Involved in Parietal Epithelial Cell Activation
Published on: August 19, 2020
Pathobiology of focal segmental glomerulosclerosis: new developments
1Department of Pathology, College of Physicians and Surgeons, Columbia University, New York, New York 10032, USA. vdd1@columbia.edu
Current Opinion in Nephrology and Hypertension
|February 24, 2012
Summary
Focal segmental glomerulosclerosis (FSGS) involves podocyte injury and depletion. New insights reveal genetic factors and external toxins contribute to this kidney disease, impacting podocyte function and leading to scarring.
Area of Science:
- Nephrology
- Pathology
- Genetics
Background:
- Focal segmental glomerulosclerosis (FSGS) is a leading cause of nephrotic syndrome and kidney failure.
- Podocyte injury and depletion are central to all forms of FSGS.
Purpose of the Study:
- To review new insights into FSGS pathogenesis.
- Focus on extrinsic toxins, permeability factors, and genetic causes.
Main Methods:
- Analysis of experimental toxin models for podocyte injury dynamics.
- Identification of permeability factors in human FSGS.
- Exome capture to identify genetic causes of familial FSGS.
Main Results:
- Toxin models elucidate podocyte injury thresholds and secondary mediators.
- Novel permeability factors affecting podocyte function identified.
- New monogenic causes and APOL1 risk alleles implicated in FSGS.
Conclusions:
- FSGS results from interplay between genetic susceptibility and external injurious factors.
- Podocyte stress leads to depletion, scarring, and glomerular epithelial cell hyperplasia.
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