Acute kidney injury in rats with or without pre-existing chronic kidney disease: Cytokine/chemokine response

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Abstract

Aim:

Evidence suggests the possibility that pre-existing chronic kidney (CKD) disease may result in a more severe outcome of acute kidney injury (AKI). The aim of this study was to examine whether CKD enhances the inflammatory response in the kidney, as well as other organs, in response to AKI in rats.

Methods:

CKD was induced by 5/6 nephrectomy (Nx) and AKI by intestinal ischaemia and reperfusion (IIR).

Results:

For 6 weeks following Nx there was a progressive increase in serum creatinine with associated development of albuminuria. The increment in creatinine above baseline determination 90 min following IIR was comparable in 5/6 Nx and in the sham 5/6 Nx. Similarly, increased levels of serum alanine transaminase and histomorphological changes in the lungs were observed in the rats exposed to IIR compared with those exposed to sham IIR, with no additional significant impact of 5/6 Nx. In kidney tissue the levels of cytokines/chemokines were equally elevated regardless of exposure to sham IIR or IIR. In lung and liver tissue the levels of cytokines/chemokines were equally elevated in the rats that were exposed to IIR, regardless of exposure to sham Nx or Nx.

Conclusion:

We conclude that the immediate severity of AKI induced by IIR in rats with CKD is similar to that induced in rats without CKD. However, the impact of Nx on the cytokine/chemokine response after AKI is not uniform in kidney, lung or liver tissue.

SUMMARY AT A GLANCE

Established a rat model of pre-existing chronic kidney injury and provided evidence that a second acute kidney injury challenge did not alter the immediate cytokine response to the acute injury compared with rats without chronic kidney injury.

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