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

32 Citations (Scopus)

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 1 2017

Fingerprint

Chronic Renal Insufficiency
Acute Kidney Injury
Wounds and Injuries
Autophagy
Transforming Growth Factors
Blood Vessels
Oxidative Stress
Inflammation
Kidney

Keywords

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

ASJC Scopus subject areas

  • Nephrology

Cite this

AKI on CKD : heightened injury, suppressed repair, and the underlying mechanisms. / He, Liyu; Wei, QingQing; Liu, Jing; Yi, Mixuan; Liu, Yu; Liu, Hong; Sun, Lin; Peng, Youming; Liu, Fuyou; Venkatachalam, Manjeri A.; Dong, Zheng.

In: Kidney International, Vol. 92, No. 5, 01.11.2017, p. 1071-1083.

Research output: Contribution to journalReview article

He, L, Wei, Q, Liu, J, Yi, M, Liu, Y, Liu, H, Sun, L, Peng, Y, Liu, F, Venkatachalam, MA & Dong, Z 2017, 'AKI on CKD: heightened injury, suppressed repair, and the underlying mechanisms', Kidney International, vol. 92, no. 5, pp. 1071-1083. https://doi.org/10.1016/j.kint.2017.06.030
He, Liyu ; Wei, QingQing ; Liu, Jing ; Yi, Mixuan ; Liu, Yu ; Liu, Hong ; Sun, Lin ; Peng, Youming ; Liu, Fuyou ; Venkatachalam, Manjeri A. ; Dong, Zheng. / AKI on CKD : heightened injury, suppressed repair, and the underlying mechanisms. In: Kidney International. 2017 ; Vol. 92, No. 5. pp. 1071-1083.
@article{7c54d275f5944eda95cc6bce966ef1d5,
title = "AKI on CKD: heightened injury, suppressed repair, and the underlying mechanisms",
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",
author = "Liyu He and QingQing Wei and Jing Liu and Mixuan Yi and Yu Liu and Hong Liu and Lin Sun and Youming Peng and Fuyou Liu and Venkatachalam, {Manjeri A.} and Zheng Dong",
year = "2017",
month = "11",
day = "1",
doi = "10.1016/j.kint.2017.06.030",
language = "English (US)",
volume = "92",
pages = "1071--1083",
journal = "Kidney International",
issn = "0085-2538",
publisher = "Nature Publishing Group",
number = "5",

}

TY - JOUR

T1 - AKI on CKD

T2 - heightened injury, suppressed repair, and the underlying mechanisms

AU - He, Liyu

AU - Wei, QingQing

AU - Liu, Jing

AU - Yi, Mixuan

AU - Liu, Yu

AU - Liu, Hong

AU - Sun, Lin

AU - Peng, Youming

AU - Liu, Fuyou

AU - Venkatachalam, Manjeri A.

AU - Dong, Zheng

PY - 2017/11/1

Y1 - 2017/11/1

N2 - 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.

AB - 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.

KW - acute kidney injury

KW - cell signaling

KW - chronic kidney disease

KW - fibrosis

KW - inflammation

KW - mitochondria

UR - http://www.scopus.com/inward/record.url?scp=85031018816&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=85031018816&partnerID=8YFLogxK

U2 - 10.1016/j.kint.2017.06.030

DO - 10.1016/j.kint.2017.06.030

M3 - Review article

VL - 92

SP - 1071

EP - 1083

JO - Kidney International

JF - Kidney International

SN - 0085-2538

IS - 5

ER -