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The complex interplay between kidney injury and inflammation.
McWilliam, Stephen J; Wright, Rachael D; Welsh, Gavin I; Tuffin, Jack; Budge, Kelly L; Swan, Laura; Wilm, Thomas; Martinas, Ioana-Roxana; Littlewood, James; Oni, Louise.
Afiliación
  • McWilliam SJ; Department of Paediatric Pharmacology, Alder Hey Children's Hospital, Liverpool, UK.
  • Wright RD; Department of Women and Children's Health, Institute of Translational Medicine, University of Liverpool, Liverpool, UK.
  • Welsh GI; Department of Women and Children's Health, Institute of Translational Medicine, University of Liverpool, Liverpool, UK.
  • Tuffin J; Bristol Renal, Bristol Medical School, University of Bristol, Bristol, UK.
  • Budge KL; Bristol Renal, Bristol Medical School, University of Bristol, Bristol, UK.
  • Swan L; Department of Women and Children's Health, Institute of Translational Medicine, University of Liverpool, Liverpool, UK.
  • Wilm T; Department of Cellular and Molecular Physiology, Institute of Translational Medicine, University of Liverpool, Liverpool, UK.
  • Martinas IR; Department of Cellular and Molecular Physiology, Institute of Translational Medicine, University of Liverpool, Liverpool, UK.
  • Littlewood J; Department of Cellular and Molecular Physiology, Institute of Translational Medicine, University of Liverpool, Liverpool, UK.
  • Oni L; Department of Cellular and Molecular Physiology, Institute of Translational Medicine, University of Liverpool, Liverpool, UK.
Clin Kidney J ; 14(3): 780-788, 2021 Mar.
Article en En | MEDLINE | ID: mdl-33777361
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.
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Idioma: En Revista: Clin Kidney J Año: 2021 Tipo del documento: Article Pais de publicación: Reino Unido
Texto completo
Añadir a Mi BVS
Imprimir
XML
PubMed Links
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Idioma: En Revista: Clin Kidney J Año: 2021 Tipo del documento: Article Pais de publicación: Reino Unido