NODding off AKI with Progranulin?

Inflammation is a common feature of murine models of AKI. The endogenous mechanisms which serve to limit inflammation and reduce the severity of AKI are poorly understood. Zhou et al identify progranulin as one such protective mediator. Deficiency of progranulin was associated with increased inflammation and increased injury in both ischemic and nephrotoxic models of AKI. Moreover, administration of exogenous progranulin reduced AKI even when delivered after AKI was established. Interference in NOD2 pathways is suggested as a possible mechanism for protection. PRGN-based therapeutics are under development and might have application in the treatment or prevention of AKI.