Open AccessAKI on CKD: heightened injury, suppressed repair, and the underlying mechanisms
Author(s) -
Liyu He,
Qingqing Wei,
Jing Liu,
Mixuan Yi,
Yu Liu,
Hong Liu,
Lin Sun,
Youming Peng,
Fuyou Liu,
Manjeri A. Venkatachalam,
Zheng Dong
Publication year - 2017
Publication title -
kidney international
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.499
H-Index - 276
eISSN - 1523-1755
pISSN - 0085-2538
DOI - 10.1016/j.kint.2017.06.030
Subject(s) - kidney disease , acute kidney injury , medicine , oxidative stress , autophagy , inflammation , hypoxia (environmental) , pathology , cardiology , apoptosis , biology , chemistry , biochemistry , organic chemistry , oxygen
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.
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