AKI on CKD: heightened injury, suppressed repair, and the underlying mechanisms

Liyu He, QingQing Wei, Jing Liu, Mixuan Yi, Yu Liu, Hong Liu, Lin Sun, Youming Peng, Fuyou Liu, Manjeri A. Venkatachalam, Zheng Dong

Research output: Contribution to journalReview article

49 Scopus citations

Abstract

Acute kidney injury (AKI) and chronic kidney disease (CKD) are interconnected. Although AKI-to-CKD transition has been intensively studied, the information of AKI on CKD is very limited. Nonetheless, AKI, when occurring in patients with CKD, is known to be more severe and difficult to recover. CKD is associated with significant changes in cell signaling in kidney tissues, including the activation of transforming growth factor-β, p53, hypoxia-inducible factor, and major developmental pathways. At the cellular level, CKD is characterized by mitochondrial dysfunction, oxidative stress, and aberrant autophagy. At the tissue level, CKD is characterized by chronic inflammation and vascular dysfunction. These pathologic changes may contribute to the heightened sensitivity of, and nonrecovery from, AKI in patients with CKD.

Original languageEnglish (US)
Pages (from-to)1071-1083
Number of pages13
JournalKidney International
Volume92
Issue number5
DOIs
StatePublished - Nov 2017

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Keywords

  • acute kidney injury
  • cell signaling
  • chronic kidney disease
  • fibrosis
  • inflammation
  • mitochondria

ASJC Scopus subject areas

  • Nephrology

Cite this

He, L., Wei, Q., Liu, J., Yi, M., Liu, Y., Liu, H., Sun, L., Peng, Y., Liu, F., Venkatachalam, M. A., & Dong, Z. (2017). AKI on CKD: heightened injury, suppressed repair, and the underlying mechanisms. Kidney International, 92(5), 1071-1083. https://doi.org/10.1016/j.kint.2017.06.030