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Review
. 2017 Nov;92(5):1071-1083.
doi: 10.1016/j.kint.2017.06.030. Epub 2017 Sep 8.

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

Liyu He  1 , Qingqing Wei  2 , Jing Liu  3 , Mixuan Yi  3 , Yu Liu  1 , Hong Liu  1 , Lin Sun  1 , Youming Peng  1 , Fuyou Liu  1 , Manjeri A Venkatachalam  4 , Zheng Dong  5
Affiliations
Review

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

Liyu He et al. Kidney Int. 2017 Nov.

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.

Keywords: acute kidney injury; cell signaling; chronic kidney disease; fibrosis; inflammation; mitochondria.

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Figures

Figure 1
Figure 1
Poor prognosis of AKI in patients with CKD and related co-morbidities.
Figure 2
Figure 2
Potential mechanisms underlying AKI sensitivity and non-recovery in CKD patients.
See this image and copyright information in PMC

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