Abstract: The effects of hepcidin treatment on mitigating ischemia reperfusion injury (IRI) and acute kidney injury (AKI) by decreasing iron availability and ROS-mediated cell death were tested. Wild type (WT) C57Bl/6 and hepcidin knock out (Hamp?/?) mice were treated with saline or 50 ?g of hepcidin i.p. prior to bilateral renal IRI. Renal function, injury markers, histopathology, and inflammation were examined after 24 hours of reperfusion. In WT mice, IRI induced increases in serum and kidney non-theme iron levels, but hepcidin treatment induced sequestration of iron in the spleen and liver and prevented IRI-associated increases in serum and kidney non-heme iron. Kidney function was significantly better in hepcidin-treated mice, accompanied by less acute tubular necrosis and reduced infiltration of immune cells. Hepcidin treatment decreased kidney ferroportin expression and induced the expression of cytoprotectant, H-Ferritin, and was associated with less ROS and tubular epithelial apoptosis.

Abstract: The effects of hepcidin treatment on mitigating IRI and acute kidney injury by decreasing iron availability and ROS-mediated cell death were tested. C57Bl/6 (WT) and hepcidin knock out (Hamp?/?) mice were treated with saline or 50 ?g of hepcidin i.p. prior to bilateral renal IRI. Renal function, injury markers, histopathology, and inflammation were examined after 24 hours of reperfusion. In WT mice, IRI induced increases in serum and kidney non-theme iron levels, but hepcidin treatment induced sequestration of iron in the spleen and liver and prevented IRI-associated increases in serum and kidney non-heme iron. Kidney function was significantly better in hepcidin-treated mice, accompanied by less acute tubular necrosis and reduced infiltration of immune cells. Hepcidin treatment decreased kidney ferroportin expression and induced the expression of cytoprotectant, H-Ferritin, and was associated with less ROS and tubular epithelial apoptosis.

Abstract: The effects of hepcidin treatment on mitigating renal ischemiareperfusion injury (IRI) and acute kidney injury (AKI) by decreasing iron availability and ROS-mediated cell death were tested. C57Bl/6 (WT) and hepcidin knock out (Hamp?/?) mice were treated with saline or 50 ?g of hepcidin i.p. prior to bilateral renal IRI. Renal function, injury markers, histopathology, and inflammation were examined after 24 hours of reperfusion. In WT mice, IRI induced increases in serum and kidney non-heme iron levels, but hepcidin treatment induced sequestration of iron in the spleen and liver and prevented IRI-associated increases in serum and kidney non-theme iron. Kidney function was significantly better in hepcidin-treated mice, accompanied by less acute tubular necrosis and reduced infiltration of immune cells. Hepcidin treatment decreased kidney ferroportin expression and induced the expression of cytoprotectant, H-Ferritin, and was associated with less ROS and tubular epithelial apoptosis.

Abstract: The effects of hepcidin treatment on mitigating IRI and acute kidney injury by decreasing iron availability and ROS-mediated cell death were tested. C57Bl/6 (WT) and hepcidin knock out (Hamp?/?) mice were treated with saline or 50 ?g of hepcidin i.p. prior to bilateral renal IRI. Renal function, injury markers, histopathology, and inflammation were examined after 24 hours of reperfusion. In WT mice, IRI induced increases in serum and kidney non-heme iron levels, but hepcidin treatment induced sequestration of iron in the spleen and liver and prevented IRI-associated increases in serum and kidney non-heme iron. Kidney function was significantly better in hepcidin-treated mice, accompanied by less acute tubular necrosis and reduced infiltration of immune cells. Hepcidin treatment decreased kidney ferroportin expression and induced the expression of cytoprotectant, H-Ferritin, and was associated with less ROS and tubular epithelial apoptosis.

Abstract: The present invention relates to novel methods of treating or reducing the likelihood of developing gadolinium toxicity by administering to a patient a metal chelator before, concurrently with, or after exposure to gadolinium. The novel methods comprise, inter alia, the use of iron chelators to aid patients at increased risk of developing a gadolinium-induced condition, such as nephrogenic systemic fibrosis, acute kidney injury, cardiovascular disease and accelerated senescence.