TGF1/Smad, Wnt/-catenin and snail1 are preferentially activated in renal tubular epithelia after injury, leading to epithelial-mesenchymal transition (EMT). The stress response is coupled to EMT and kidney injury; however, the underlying mechanism of the stress response in EMT remains elusive. AMP-activated protein kinase (AMPK) signalling is responsive to stress and regulates cell energy balance and differentiation. We found that knockdown of AMPK, especially AMPK2, enhanced EMT by up-regulating -catenin and Smad3 in vitro. AMPK2 deficiency enhanced EMT and fibrosis in a murine unilateral ureteral obstruction (UUO) model. AMPK2 deficiency also increased the expression of chemokines KC and MCP-1, along with enhanced infiltration of inflammatory cells into the kidney after UUO. CK2 interacted physically with AMPK and enhanced AMPK Thr172 phosphorylation and its catalytic activity. Thus, activated AMPK signalling suppresses EMT and secretion of chemokines in renal tubular epithelia through interaction with CK2 to attenuate renal injury. Copyright (c) 2015 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd.