Polyploid tubular cells and chronic kidney disease

Letizia De Chiara; Paola Romagnani

doi:10.1016/j.kint.2022.08.017

Polyploid tubular cells and chronic kidney disease

Kidney Int. 2022 Nov;102(5):959-961. doi: 10.1016/j.kint.2022.08.017.

Authors

Letizia De Chiara¹, Paola Romagnani²

Affiliations

¹ Department of Experimental and Clinical Biomedical Sciences "Mario Serio", University of Florence, Florence, Italy. Electronic address: letizia.dechiara@unifi.it.
² Department of Experimental and Clinical Biomedical Sciences "Mario Serio", University of Florence, Florence, Italy; Nephrology and Dialysis Unit, Meyer Children's University Hospital, Florence, Italy. Electronic address: paola.romagnani@unifi.it.

PMID: 36272751
DOI: 10.1016/j.kint.2022.08.017

Abstract

Defective DNA repair drives chronic kidney disease (CKD), but mechanisms are unclear. Airik and colleagues use a genetic model of defective DNA repair mimicking karyomegalic nephritis, a form of CKD characterized by tubular epithelial cells (TEC) with large nuclei and tubulointerstitial nephritis. They show that DNA damage in TEC triggers endoreplication leading to polyploid TEC and CKD. Blocking endoreplication preserved kidney function, suggesting that DNA damage triggers CKD via TEC polyploidization, questioning the concept of G2/M-arrest.

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MeSH terms

Epithelial Cells
Humans
Kidney Tubules
Nephritis*
Nephritis, Interstitial* / genetics
Polyploidy
Renal Insufficiency, Chronic* / genetics