Shahrzad Alimohammadi
1,2 
, Nahid Moradi
3 , Nabiha Midhat Ansari
4 , Ali Shirbacheh
5 , Kamran Shirbache
6* 1 Doctoral School of Molecular Medicine, University of Debrecen, 4032 Debrecen, Hungary.
2 Department of Immunology, Faculty of Medicine, University of Debrecen, 4032 Debrecen, Hungary.
3 School of Medicine, Isfahan University of Medical Sciences, Isfahan, Iran.
4 Faculty of Medicine, Medical University - Plovdiv, Plovdiv, Bulgaria.
5 Urgences, Centre Hospitalier de l’Agglomération de Nevers, Nevers, France.
6 Hôpital Robert Debré, Groupe Hospitalier Universitaire AP-HP Nord-Université Paris-Cité, France.
Abstract
Hemochromatosis is a genetic disorder that results in excessive iron absorption, followed by iron overload in various organs including the kidneys. IgA nephropathy, on the other hand, is the immunoglobulin A (IgA) deposition in the glomeruli mesangium. Hemochromatosis-associated IgA nephropathy is a condition described as both hemochromatosis and IgA nephropathy in an individual. Recently, there has been growing evidence suggesting a potential association between IgA nephropathy and hemochromatosis. Previous studies have indicated that individuals with hemochromatosis may have an increased risk of developing IgA nephropathy. Some studies suggest a higher prevalence of hemochromatosis-associated gene mutations particularly HFE gene mutations, in IgA nephropathy patients. These gene mutations may affect iron metabolism and contribute to the development of both conditions. Excessive iron in the kidney may also be associated with increasing inflammatory response and IgA deposition in the glomeruli. Treatment options for hemochromatosis-associated IgA include corticosteroids, RAS blockade, immunosuppressive agents, and supportive care for chronic kidney disease.