Renal tubular cell injury can enhance calcium oxalate monohydrate (COM) crystal adhesion at the injured site and thus may increase the stone risk. Nevertheless, underlying mechanism of such enhancement remained unclear. In the present study, confluent MDCK renal tubular cell monolayers were scratched to allow cells to proliferate and repair the injured site. At 12-h post-scratch, the repairing cells had significant increases in crystal adhesion capacity and cell proliferation as compared to the control. Cell cycle analysis using flow cytometry demonstrated that the repairing cells underwent cell cycle shift from G0/G1 to S and G2/M phases. Cyclosporin A (CsA) and hydroxyurea (HU) at sub-toxic doses caused cell cycle shift mimicking that observed in the repairing cells. Crystal-cell adhesion assay confirmed the increased crystal adhesion capacity of the CsA-treated and HU-treated cells similar to that of the repairing cells. These findings provide evidence indicating that cell cycle shift from G0/G1 to S and G2/M phases is responsible, at least in part, for the increased adhesion of COM crystals on repairing renal tubular cells at the injured site.