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Human acute kidney injury is associated with a proinflammatory phenotype


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


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.


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)


Human AKI is associated with a proinflammatory phenotype.


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

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Gauge, N., Varrier, M., Boardman, D. et al. Human acute kidney injury is associated with a proinflammatory phenotype. Crit Care 18 (Suppl 1), P375 (2014).

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