Tubulointerstitial injury plays an important role in the development and progression of chronic kidney disease (CKD). Kidney injury molecule-1 (KIM-1) is induced in damaged proximal tubules both in acute renal injury and in CKD. However, the dynamics of KIM-1 in CKD and effects of KIM-1 expression on disease progression are unknown. Here we aimed to determine the associations between tubular KIM-1 expression level, renal function and inflammation in CKD. The relationships between the levels of KIM-1 and clinicopathological parameters were analyzed in patients with progressive and non-progressive Immunoglobulin A nephropathy (IgAN). KIM-1 expression was increased in IgAN patients and its expression significantly correlated with the decrease of renal function. KIM-1 was particularly evident at the site with reduced capillary density and KIM-1 positive tubules were surrounded by infiltrates of inflammatory cells. Using in vitro cell models, we showed that cellular stressors, including hypoxia induced KIM-1 expression. KIM-1 expressing cells produced more chemokine/cytokine when cultured under hypoxic conditions. Furthermore, we showed that tubular cells with KIM-1 expression can regulate the immune response of inflammatory cells through secretion of chemotactic factors. These data suggest that KIM-1 expressing epithelial cells may play a role in the pathogenesis of tubulointerstitial inflammation during chronic renal injury through secretion of chemokines/cytokines.