Hemosiderosis is focal deposition of iron that does not cause tissue damage.
(See also Overview of Iron Overload.)
Focal hemosiderosis can result from hemorrhage within an organ. Iron liberated from extravasated red blood cells is deposited within that organ, and significant hemosiderin deposits may eventually develop. Iron loss due to hemorrhage can still occur and cause iron deficiency anemia because iron stored in nonhematopoietic tissues cannot be reused.
Chronic inflammatory syndromes, such as nonalcoholic fatty liver disease and the metabolic syndrome, can also lead to hemosiderosis. In affected patients, abdominal MRI may show excess iron in the liver and spleen. Liver biopsies of these patients may show iron accumulation in hepatocytes and reticuloendothelial cells.
When the lungs are affected, the cause usually is recurrent pulmonary hemorrhage, either idiopathic (eg, Goodpasture syndrome) or due to chronic pulmonary hypertension (eg, as a result of primary pulmonary hypertension, pulmonary fibrosis, or severe mitral stenosis).
Another common site of accumulation is the kidneys, where hemosiderosis can result from extensive intravascular hemolysis. Free hemoglobin is filtered at the glomerulus, resulting in iron deposition in the kidneys. The renal parenchyma is not damaged, but severe hemosiderinuria may result in iron deficiency.