IgA Nephropathy: New Aspects in Pathophysiology and Pathogenesis - European Medical Journal

IgA Nephropathy: New Aspects in Pathophysiology and Pathogenesis

Download PDF
*Francois Berthoux,1,2 Hesham Mohey,1 Nicolas Maillard,1 Christophe Mariat1

The authors have declared no conflicts of interest.

EMJ Nephrol. ;3[1]:97-103. DOI/10.33590/emjnephrol/10314123. https://doi.org/10.33590/emjnephrol/10314123.
IgA nephropathy, autoimmune disease, IgA1 molecule, glycosylation, genetics, pathogenesis, pathophysiology

Each article is made available under the terms of the Creative Commons Attribution-Non Commercial 4.0 License.


Knowledge of the pathophysiology of immunoglobulin A nephropathy (IgAN) has progressed significantly, with this disease being clearly identified as an autoimmune disease with a peculiar autoantigen (galactosedeficient IgA1 [Gd-IgA1]), specific autoantibodies (IgG and IgA1 anti-glycans), and formation followed by mesangial deposition of circulating immune complexes with the involvement of other players, such as mesangial transferrin receptor (TfR), monocyte Fcα receptor (CD89), and glomerular transglutaminase 2 (TG2). The pathogenesis still requires additional clarifications in order to explain the initiation of the disease and to establish the respective role of genetics, environment, and hazard concordance in the cascade of events/steps. The clinical application of this new knowledge is spreading slowly and includes possible measurement of serum Gd-IgA1, IgG anti-Gd-IgA1, IgA anti-Gd-IgA1, soluble CD89, and soluble TfR in the urine of patients with IgAN.

Please view the full content in the pdf above.

Join our mailing list

To receive the EMJ updates straight to your inbox free of charge, please click the button below.
Join Now