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Updated: Jun 3, 2025

Isolation, Characterization, And High Throughput Extracellular Flux Analysis of Mouse Primary Renal Tubular Epithelial Cells
Published on: June 20, 2018
Proteinuria and tubular cells: Plasticity and toxicity
Anna Faivre1,2, Thomas Verissimo1, Sophie de Seigneux1,2
1Department of Medicine, Cell Physiology and Metabolism, University of Geneva, Geneva, Switzerland.
Aim:
Proteinuria is the most robust predictive factors for the progression of chronic kidney disease (CKD), and interventions targeting proteinuria reduction have shown to be the most effective nephroprotective treatments to date. While glomerular dysfunction is the primary source of proteinuria, its consequences extend beyond the glomerulus and have a profound impact on tubular epithelial cells. Indeed, proteinuria induces notable phenotypic changes in tubular epithelial cells and plays a crucial role in driving CKD progression. This comprehensive review aims to elucidate the mechanisms involved in the tubular handling of proteins and explore the potential effects of proteinuria on the function of tubular epithelial cells.
Methods:
This paper is a narrative review. Litterature review was performed on PubMed from its inception until 2024, focusing on the effects of proteinuria on tubular cells.
Results:
The review highlights the toxic effects of plasma proteins on tubular epithelial cells through signal transduction pathways, as well as endoplasmic reticulum stress activation, oxidative stress, and metabolic alterations. Additionally, it provides an updated understanding of the dynamic phenotypic changes occurring within the nephron in response to proteinuria.
Conclusions:
By examining the intricate interplay between proteinuria and tubular epithelial cells, this review sheds light on key factors contributing to CKD progression and unveils potential targets for therapeutic interventions.
Insights
Proteinuria, a key factor in chronic kidney disease (CKD) progression, damages kidney tubular epithelial cells. Understanding these effects reveals new therapeutic targets for CKD.
Area of Science:
- Nephrology
- Cell Biology
- Biochemistry
Background:
- Proteinuria is a primary indicator of chronic kidney disease (CKD) progression.
- While glomerular damage initiates proteinuria, tubular epithelial cells are significantly impacted, driving disease advancement.
- Interventions reducing proteinuria are currently the most effective nephroprotective strategies.
Purpose of the Study:
- To elucidate mechanisms of tubular protein handling.
- To explore the detrimental effects of proteinuria on tubular epithelial cell function.
- To review the dynamic phenotypic changes in nephrons due to proteinuria.
Main Methods:
- This study is a narrative review.
- Literature search conducted on PubMed from inception to 2024.
- Focus on the impact of proteinuria on tubular cells.
Main Results:
- Proteinuria induces toxic effects on tubular epithelial cells via signaling pathways, ER stress, oxidative stress, and metabolic changes.
- Plasma proteins trigger detrimental cellular responses.
- The review details phenotypic alterations in nephrons caused by proteinuria.
Conclusions:
- The interaction between proteinuria and tubular cells is critical for CKD progression.
- Identifying these mechanisms offers potential therapeutic targets for kidney disease.
- This review provides insights into novel therapeutic strategies for managing CKD.
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