BACKGROUND: Damages to subcellular organelles, such as mitochondria and endoplasmic reticulum, are well recognized in tubular cell injury and death in AKI. However, the changes and involvement of Golgi apparatus are much less known. In this study, we report the regulation and role of METHODS: AKI was induced in mice by renal ischemia–reperfusion injury or cisplatin. RESULTS: GALNT3 was significantly decreased in both CONCLUSIONS: GALNT3 protected kidney tubular cells in AKI at least partially through O-glycosylation of EGFR.