Abstract: Objective To investigate the expression of protein kinase D(PKD) in the kidneys of mice with acute kidney injury(AKI) and its effect.Methods A total of 27 C57/B6J mice were divided into three groups: a Control group, a Cisplatin group and a Cisplatin+CID group. Then, an AKI model was induced by intraperitoneal injection of cisplatin in mice. The mice were sacrificed 72 h after modeling to collect renal tissue and serum. Meanwhile, another 23 C57/B6J mice were divided into three groups: a Sham group, a bilateral renal ischemia-reperfusion injury(BIR) group and a BIR+CID group. Then, an AKI model was established through clipping the bilateral renal roots of mice for 30 min, and renal tissues and serum were collected 24 h after modeling. The expression of PKD in the kidneys was detected by immunohistochemical staining. Renal function was evaluated through measurement of serum creatinine and blood urea nitrogen(BUN), as well as PAS staining. The mRNA expression of PKD, neutrophil gelatinase-associated lipocalin(NGAL), kidney injury molecule-1(KIM-1), apoptotic markers(Bax), interleukin(IL)-1β, IL-6 and monocyte chemoattractant protein-1(MCP1) was detected by real-time qPCR. The protein expression of PKD, NGAL, KIM-1, Bax and cleaved caspase3 was detected by Western blot.Results After cisplatin treatment or ischemia-reperfusion injury, the expression of PKD in the kidneys of AKI mice was remarkably elevated(P<0.05). Inhibition of PKD significantly aggregated the renal dysfunction and renal tubular epithelial damage in AKI mice after cisplatin treatment or ischemia-reperfusion injury, and aggregated the apoptosis of tubular epithelial cells and inflammation.Conclusions PKD is significantly up-regulated in mice with AKI, and inhibition of PKD significantly aggravats renal injury, which provides a new target for the prevention and treatment of AKI.