Background: Periostin is in charge of tissue regeneration, fibrosis, and wound healing via interaction with integrin. Major investigations were conducted in various neoplasms and cardiac fibrosis. Recently, the role of periostin in nephrology field is emerging. We investigated the role of periostin in kidney fibrosis. Methods: We investigated the function of periostin using unilateral ureteral obstruction (UUO) model. We used wild type C57BL/6 mice and periostin-deficient mice (Postn-/-). In vitro, primary cultured inner medullary collecting duct (IMCD) cells were used from wild type and POSTN-/-mice. Results: Periostin expression was strongly induced by UUO in wild type mice. Postn-/- mice showed more preserved kidney structure and less fibrous tissue. Other fibrosis genes such as fsp-1, αSMA, collagen 1α1, and fibronectin were increased in wild type mice and were significantly decreased in POSTN-/- mice. Messenger RNA expressions of inflammatory cytokine (IL-6, IFN-γ, and MCP-1) were also decreased in Postn-/-mice. Invitro, administration of TGF-β1 increased periostin expression in wild type IMCD cells. Also, fsp-1, αSMA, collagen 1α1, and fibronectin expressions were increased by administration of periostin along with cellular morphology change even though the intensity was lower than TGF-β1. Periostin potentiated TGF-β1-induced fibrosis when it administered together with TGF-β1. Anti- periostin polyclonal antibody and integrin blockade peptides decreased fibrosis gene expression. Conclusion: Periostin is not only one of the markers for kidney fibrosis, but also may itself augment the progressionof the fibrosis. Thus,periostin inhibition may be a therapeutic target for the prevention of kidney disease progression.