Volume 18 Supplement 1

34th International Symposium on Intensive Care and Emergency Medicine

Open Access

Human acute kidney injury is associated with a proinflammatory phenotype

  • N Gauge1,
  • M Varrier1,
  • D Boardman1,
  • M Hernandez-Fuentes1 and
  • M Ostermann1
Critical Care201418(Suppl 1):P375

https://doi.org/10.1186/cc13565

Published: 17 March 2014

Introduction

Animal research suggests that acute kidney injury (AKI) is an inflammatory condition [1]. Our aim was to describe the immune phenotype in human AKI.

Methods

We enrolled patients with: AKI grade II/III (defined by KDIGO criteria) and systemic inflammatory response syndrome (SIRS) without sepsis; SIRS without AKI; and AKI II/III without SIRS. A healthy control population was used for baseline comparison. Serial blood samples were taken on days 0, 2 and 7. Cells were separated using Percoll gradients and phenotyped using flow cytometry.

Results

The results from 24 day 0 samples identified statistically significant differences between SIRS, AKI, AKI + SIRS and healthy controls amongst: CD8+ cytotoxic T cells, CD45CD25+++ regulatory T cells, and CD45CD25++ cytokine secreting non-T-regulatory cells (Table 1). The percentage of CD69-positive neutrophils was significantly increased across all three groups relative to controls, with little variation between AKI, SIRS and AKI + SIRS patients.
Table 1

(abstract P375)

 

AKI + SIRS

AKI no SIRS

SIRS alone

Control

% CD8+ cytotoxic T cells

23.3

16.7

11.6

31.1

% Fr. II T-regulatory cells

4.1

2.7

1.6

1.2

% Fr. III cytokine T cell

11.5

21.2

13.9

8.0

% CD69+ neutrophils

83.9

69.7

65.5

7.35

Conclusion

Human AKI is associated with a proinflammatory phenotype.

Authors’ Affiliations

(1)
Guy's St Thomas' Hospital

References

  1. Akcay A, et al.: Mediators of inflammation in acute kidney injury. Mediators Inflamm 2009 2009, 137072.Google Scholar

Copyright

© Gauge et al.; licensee BioMed Central Ltd. 2014

This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.

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