Inflammation is an important mediator of most forms of acute kidney injury (AKI). Although neutrophils are prominent components of the inflammatory cascade, the precise role of neutrophils in AKI and the mechanisms by which they contribute to AKI remain controversial. In this issue, Deng et al. identify an important cross talk between renal epithelial cells and neutrophils involving the production and action of leukotriene B4 in mediating cisplatin AKI. We discuss the possible explanations for the discrepant findings that have been reported for neutrophils in cisplatin AKI.
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