Human acute kidney injury is associated with a proinflammatory phenotype

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)

Conclusion

Human AKI is associated with a proinflammatory phenotype.