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Abstract: FR-PO692

Exogenous Hepcidin Mitigates and Delays Onset of Lupus Nephritis

Session Information

Category: Glomerular

  • 1001 Glomerular: Basic/Experimental Immunology and Inflammation


  • Scindia, Yogesh M., Univerisity of Virginia, Charlottesville, Virginia, United States
  • Mandziak, Ewa U., University of Virginia, Charlottesville, Virginia, United States
  • Loi, Valentina, AO Brotzu Cagliari, Cagliari, Italy
  • Mohammad, Saleh, University of Virginia, Charlottesville, Virginia, United States
  • Swaminathan, Sundararaman, University of Virginia, Charlottesville, Virginia, United States

Lupus nephritis (LN) is an end-organ manifestation of systemic lupus erythematosus (SLE) with a strong gender bias and affects mostly pre-menopausal women. Current interventions are imprecise and broadly immunosuppressive and hence there is a constant need for identifying new therapeutic targets. Recent human studies have identified Hepcidin (Hamp), the master regulator of iron metabolism as a biomarker of LN, and renal flares are associated with low Hamp levels. So far there are no mechanistic studies examining the role of hepcidin in the pathogenesis of SLE. We therefore hypothesized that Hamp treatment would mitigate SLE-induced kidney disease.


7-week-old female MRL/lpr mice (a spontaneous model of SLE, n = 4-5) were treated bi-weekly with saline or 50 μg of hepcidin (i.p) for 10 weeks, following which outcomes like microalbuminuria, histopathology, circulating autoantibody levels and other markers of inflammation were examined.


Saline treated mice developed severe LN by 17 weeks of age as indicated by high microalbuminuria, collagen deposition, renal IL-6, CXCL-1 and M-CSF transcripts, and an infiltration of CD45 cells, F4/80+ve macrophages and T cells. There was a concomitant increase in circulating autoantibodies and serum MCP-1, IL-6, GM-CSF and TNFa. Hamp treatment significantly reduced all theses manifestations of LN (Microalbuminuria; PBS, 914.6 ± 64.6 mg/gm vs Hamp 314.2 ± 111.2 mg/gm). Hamp treatment was associated with a systemic decrease in Cox-2, a mediator of inflammation. There was an increase in renal H-ferritin and a concomitant decrease in iron dependent enzymes, Rrm-1 and Rrm-2, both of which are required for DNA synthesis.


This is the first study to demonstrate therapeutic benefit of Hamp in LN. Our results indicate that Hamp protects against LN by decreasing Cox-2 and reducing inflammation as well as by reducing cell proliferation through the induction of cytoprotective H-ferritin. Further studies are required to investigate whether Hamp mediated protection leads to end-organ resistance to LN or through to modulation of immune responses.


  • NIDDK Support