Pathology Discussion Forum

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Role of Hepcidin in iron regulation:
The main regulator of iron absorption is the protein hepcidin, encoded by the HAMP gene and produced and secreted by the liver. Transcription of HAMP is increased by inflammatory cytokines and iron, and decreased by iron deficiency, hypoxia, and erythroferrone, a hormone produced by marrow erythroblasts. These inputs are integrated to regulate the synthesis and plasma levels of hepcidin. Hepcidin binds to the cellular iron efflux channel ferroportin, causing its internalization and proteolysis, thereby inhibiting the release of iron from intestinal cells and macrophages. Due to these activities, an increase in hepcidin lowers plasma iron levels. Conversely, an abnormal deficiency of hepcidin causes iron overload.
Other proteins involved in iron metabolism do so by regulating hepcidin levels. Decreased hepcidin synthesis or activity may be caused by loss of function mutations in the genes HAMP, HJV, TFR2, and HFE, all of which are associated with hereditary forms of hemochromatosis. Deficiencies of hepcidin also occur when erythroferrone levels are chronically elevated, as occurs in disorders marked by ineffective hematopoiesis, such as β-thalassemia and myelodysplastic syndrome.

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Calcific uremic arteriolopathy (calciphylaxis) is a devastating condition seen almost exclusively in patients with advanced CKD.

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