Review

Immunotherapy for acute kidney injury

Division of Renal Medicine, Department of Medicine, University of Cambridge, Cambridge, UK

* Author for correspondence

Cambridge Institute for Medical Research, University of Cambridge School of Clinical Medicine, Box 139 Addenbrooke’s Hospital, Hills Road, Cambridge CB2 0XY, UK and Lymphocyte Biology Section, National Institute of Allergy & Infectious Diseases, Building 10, Room 11N 308, NIH, Bethesda, MD 20814, USA.

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Email the corresponding author at mrc38@hermes.cam.ac.uk

Published Online:8 Mar 2012https://doi.org/10.2217/imt.11.175

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Abstract

Acute renal failure, now referred to as acute kidney injury, is a common and clinically important problem. Acute kidney injury frequently occurs as a result of acute tubular necrosis (ATN), which is often caused by a reduction in systemic blood pressure or renal blood flow (e.g., as observed in severe sepsis or during renal transplantation). The disease course in ATN is variable, including prolonged dialysis-dependence and chronic renal dysfunction, but there is currently no specific therapy for ATN. There is increasing evidence that the inflammatory response in ATN significantly contributes to disease severity and outcome. In this review, we summarize recent developments in the understanding of how the immune system responds to dying cells, and the relevance of these discoveries to ATN. In particular, NLRP3 inflammasome activation and IL-1β-mediated neutrophil recruitment are likely to play a key role and may provide novel therapeutic targets for immunotherapy in ATN.

Keywords:

Papers of special note have been highlighted as: ▪ of interest ▪▪ of considerable interest

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Published online 8 March 2012

Published in print March 2012

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Financial & competing interests disclosure

The authors have no relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript. This includes employment, consultancies, honoraria, stock ownership or options, expert testimony, grants or patents received or pending, or royalties.

No writing assistance was utilized in the production of this manuscript.

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