Sepsis-induced acute kidney injury (SAKI) is a serious perioperative complication and a common clinical syndrome characterized by a rapid deterioration in renal function with a high incidence of 70%. The causes of SAKI include impaired mitochondrial function of renal tubular epithelial cells, oxidative stress, inflammatory reaction and renal microcirculation disorder. Chlorogenic acid, as a natural product of plant origin, has various biological activities, such as antibacterial, antiviral, and anti-tumor, and plays a significant role in the treatment of SAKI. This article reviews the pharmacological activities of chlorogenic acid and the signaling pathways involved in relieving SAKI, in order to provide a theoretical basis for in-depth study of the mechanisms underlying the alleviation of SAKI and the confirmation of potential therapeutic targets.