Recent advances in the physiopathology of IgA nephropathy - 31/03/18

Doi : 10.1016/j.nephro.2018.02.004

Renato C. Monteiro ^a,^b,^c,^d,^⁎
^a Inserm U1149 centre de recherche sur l’inflammation, 16, rue Henri-Huchard, 75018 Paris, France
^b CNRS ERL8252, 16, rue Henri-Huchard, 75018 Paris, France
^c Laboratoire d’excellence Inflamex, faculté de médecine Bichat, université Paris–Diderot, 16, rue Henri-Huchard, 75018 Paris, France
^d Service d’immunologie, DHU Fire, hôpital Bichat, 16, rue Henri-Huchard, 75018 Paris, France

^⁎Correspondence to: Inserm U1149 centre de recherche sur l’inflammation, 16, rue Henri-Huchard, 75018 Paris, France.Inserm U1149 centre de recherche sur l’inflammation, 16, rue Henri-Huchard, 75018 Paris, France.

Abstract

Immunoglobulin A nephropathy or Berger's disease is the most common type of primary glomerulonephritis, which is characterized by IgA1-containing immune-deposits in the glomerular mesangium. Microscopic haematuria and proteinuria are the most common presentations. Mesangial cell proliferation with IgA deposition is found on renal biopsy. Mechanims of the disease implicate at least four key molecules have been implicated in immune complex formation: galactose-deficient IgA1, autoantibodies anti-galactose-deficient-IgA1, soluble CD89 (Fc receptor for IgA) and the CD71 mesangial IgA receptor (transferrin receptor). These factors associated with environmental factors (antigens, food and microbiota) are correlated with disease progression and recurrence after transplantation. This review exploits recent data on the role of these molecular players of the disease, which may improve future therapeutic management of immunoglobulin A nephropathy.

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Keywords : IgA nephropathy, Glomerulonephritis, Immunoglobulin A, Fc receptor, Glycosylation