IgA Nephropathy: New Aspects in Pathophysiology and Pathogenesis

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

1. Department of Nephrology, Dialysis, and Renal Transplantation, University North Hospital, Saint-Étienne, France
2. Jean Monnet University, Saint-Étienne, France
*Correspondence to francois.berthoux@wanadoo.fr

Disclosure: The authors have declared no conflicts of interest.
Received: 21.01.15 Accepted: 27.02.15
Citation: EMJ Neph. 2015;3[1]:97-103.


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.

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