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Updated: Jul 16, 2026
Ischemia-reperfusion Model of Acute Kidney Injury and Post Injury Fibrosis in Mice
Published on: August 9, 2013
Systemic inflammation accelerates the development of focal segmental glomerulosclerosis in a mouse model of
Lian Liu1, Qiu Li2, Gaofu Zhang3
1Department of pediatrics, University-town Hospital of Chongqing Medical University, Chongqing, 400014, China.
Abstract:
Research indicates that minimal change disease (MCD) and focal segmental glomerulosclerosis (FSGS) may reflect varying severities of the same underlying condition, with inflammation potentially facilitating the progression from MCD to FSGS. The aim of this study was to determine the whether systemic inflammation accelerated the progression from MCD to FSGS in a mouse model of Adriamycin-induced nephrosis. In this model, systemic inflammation induced transient proteinuria without significant serum biochemical alterations or significant renal histological changes in control mice that did not develop nephrotic syndrome. In contrast, both mice with Adriamycin-induced nephrosis mice and mice with Adriamycin-induced nephrosis with systemic inflammation showed histological features of MCD at week 4 and progressive exacerbation of FSGS. However, the glomerular lesions of mice with Adriamycin-induced nephrosis in a state of systemic inflammation were more obvious than those of mice with Adriamycin-induced nephrosis. These findings suggest that systemic inflammation may hasten histological development from MCD to FSGS in this mouse model.
Insights
Systemic inflammation may accelerate the progression from minimal change disease (MCD) to focal segmental glomerulosclerosis (FSGS). This study in a mouse model showed inflammation worsened glomerular lesions in Adriamycin-induced nephrosis.
Area of Science:
- Nephrology
- Immunology
- Pathology
Background:
- Minimal change disease (MCD) and focal segmental glomerulosclerosis (FSGS) may represent a spectrum of kidney disease.
- Inflammation is hypothesized to drive progression from MCD to FSGS.
Purpose of the Study:
- To investigate if systemic inflammation accelerates MCD to FSGS progression in a mouse model.
- To analyze the impact of inflammation on Adriamycin-induced nephrosis.
Main Methods:
- Utilized a mouse model of Adriamycin-induced nephrosis.
- Induced systemic inflammation in a subset of mice.
- Assessed proteinuria, serum biochemistry, and renal histology at various time points.
Main Results:
- Systemic inflammation caused transient proteinuria in control mice without nephrosis.
- Both nephrotic and inflamed nephrotic mice developed MCD and progressed to FSGS.
- Inflamed nephrotic mice exhibited more severe glomerular lesions compared to non-inflamed nephrotic mice.
Conclusions:
- Systemic inflammation appears to hasten the histological progression from MCD to FSGS in this Adriamycin-induced nephrosis model.
- These findings support a role for inflammation in the pathogenesis of FSGS progression.
