Levels of FPN, the only iron export protein in mammals, were down-regulated in the CKD group and the down-regulation was remarkably aggravated and reversed by CDDP and DFO treatment, respectively (Fig. 4a, h), indicating that iron deposition in the remnant kidney of CKD rats may be attributable to FPN down-regulation, and that DFO can ease tissue iron overload by up-regulating FPN. Here, PROS1 is linked to chronic kidney disease.