The complex interplay between kidney injury and inflammation

McWilliam, Stephen J ORCID: 0000-0002-0509-7425, Wright, Rachael D ORCID: 0000-0002-7606-2297, Welsh, Gavin I, Tuffin, Jack, Budge, Kelly L, Swan, Laura ORCID: 0000-0002-6312-6263, Wilm, Thomas, Martinas, Ioana-Roxana, Littlewood, James and Oni, Louise ORCID: 0000-0002-1532-2390 (2021) The complex interplay between kidney injury and inflammation. Clinical Kidney Journal, 14 (3). pp. 780-788.

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Official URL: http://dx.doi.org/10.1093/ckj/sfaa164

Abstract

<jats:title>Abstract</jats:title> <jats:p>Acute kidney injury (AKI) has gained significant attention following patient safety alerts about the increased risk of harm to patients, including increased mortality and hospitalization. Common causes of AKI include hypovolaemia, nephrotoxic medications, ischaemia and acute glomerulonephritis, although in reality it may be undetermined or multifactorial. A period of inflammation either as a contributor to the kidney injury or resulting from the injury is almost universally seen. This article was compiled following a workshop exploring the interplay between injury and inflammation. AKI is characterized by some degree of renal cell death through either apoptosis or necrosis, together with a strong inflammatory response. Studies interrogating the resolution of renal inflammation identify a whole range of molecules that are upregulated and confirm that the kidneys are able to intrinsically regenerate after an episode of AKI, provided the threshold of damage is not too high. Kidneys are unable to generate new nephrons, and dysfunctional or repeated episodes will lead to further nephron loss that is ultimately associated with the development of renal fibrosis and chronic kidney disease (CKD). The AKI to CKD transition is a complex process mainly facilitated by maladaptive repair mechanisms. Early biomarkers mapping out this process would allow a personalized approach to identifying patients with AKI who are at high risk of developing fibrosis and subsequent CKD. This review article highlights this process and explains how laboratory models of renal inflammation and injury assist with understanding the underlying disease process and allow interrogation of medications aimed at targeting the mechanistic interplay.</jats:p>

Item Type:	Article
Uncontrolled Keywords:	acute kidney injury, glomerulonephritis, inflammation, renal fibrosis
Depositing User:	Symplectic Admin
Date Deposited:	26 Nov 2020 08:34
Last Modified:	18 Jan 2023 23:20
DOI:	10.1093/ckj/sfaa164
Open Access URL:	https://doi.org/10.1093/ckj/sfaa164
Related URLs:	Author Publisher
URI:	https://livrepository.liverpool.ac.uk/id/eprint/3108207