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Acute kidney injury

IL-34 promotes persistent ischaemia-induced AKI

Nature Reviews Nephrology volume 11, page 504 (2015)Cite this article

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Given that CSF-1 is a mediator of kidney fate during injury, the investigators questioned whether IL-34 promoted or inhibited renal repair. They first noted that expression of IL-34 was robustly induced in renal tubule epithelial cells (TECs) acutely after I/R-induced injury in mice. Conversely, both IL-34 receptors (c-FMS and PTP-ζ), were maximally induced in the chronic phase after I/R. The researchers claim these findings provide the first evidence of PTP-ζ expression in the kidney.

The investigators next evaluated the phenotype of Il-34−/− and wild-type mice following I/R-induced AKI and CKD. Following I/R, wild-type mice exhibited dramatically decreased kidney weight, increased tubular pathology, leucocyte infiltration in the interstitium, and elevated loss of tubules compared to Il-34−/− mice. In addition, kidney injury molecule 1 was more robustly expressed in wild-type TECs than in Il-34−/− TECs during the acute phase after I/R. The researchers propose that these data implicate IL-34 in the initiation of macrophage-mediated tubule injury.

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References

  1. Baek, J. H. et al. IL-34 mediates acute kidney injury and worsens subsequent chronic kidney disease. J. Clin. Invest. 10.1172/JCI81166

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  1. Jessica K. Edwards
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Edwards, J. IL-34 promotes persistent ischaemia-induced AKI. Nat Rev Nephrol 11, 504 (2015). https://doi.org/10.1038/nrneph.2015.116

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