Molecular Insights into the Pathogenesis of IgA Nephropathy.

Abstract

Immunoglobulin IgA nephropathy (IgAN) is the leading form of primary glomerulonephritis associated with end-stage renal failure, requiring either dialysis or renal transplantation. Microscopic hematuria and proteinuria are the most common presentations, and mesangial cell proliferation with IgA deposition are found in renal biopsies. There is growing evidence that IgAN is an immune complex (IC)-mediated disease. To date, three key molecules have been implicated in IC formation, correlating with disease progression/recurrence after transplantation: galactose-deficient IgA1 (Gd-IgA1), IgG anti-Gd-IgA1 antibodies, and soluble CD89 (an Fc receptor for IgA). This review examines recent data on the role of these molecular players in IgAN. Understanding these factors is essential because such knowledge could lead to improved strategies for the future management of patients with IgAN.

• Authors: Thomas Robert, Laureline Berthelot, Alexandra Cambier, Eric Rondeau, Renato C Monteiro
• Journal: Trends in molecular medicine (Trends Mol Med) Vol. 21 Issue 12 Pg. 762-775 (Dec 2015) ISSN: 1471-499X [Electronic] England
• PMID: 26614735 (Publication Type: Journal Article, Review)
• Copyright: Copyright © 2015. Published by Elsevier Ltd.

Chemical References

• Antigen-Antibody Complex
• Immunoglobulin A

Topics

• Antigen-Antibody Complex (metabolism)
• Glomerulonephritis, IGA (immunology, metabolism, pathology, physiopathology)
• Humans
• Immunoglobulin A (metabolism)
• Kidney Diseases (immunology, pathology)
• Kidney Glomerulus (pathology)
• Mesangial Cells (pathology)