Whilst the inhibition of TNF-α, IL-18, IL-1β and C5a, amongst other inflammatory mediators, has shown to reduce inflammatory injury and preserve renal function (Bonventre and Zuk, 2004; Basile et al., 2012), how these inflammatory mediators may be implicated in the dysregulation of renal blood flow, specifically in the sustained dysregulation of MBF in AKI, is not well characterised. This evidence concerns the gene IL1B and acute kidney injury.