Title:Decrypting the Pathological Pathways in IgA Nephropathy
Volume: 18
Issue: 1
Author(s): Rajiv Jash*, Kousik Maparu, Sanket Seksaria and Saptarshi Das
Affiliation:
- Department of Pharmacology, Sanaka Educational Trust’s Group Of Institutions, Malandighi, Durgapur, 713212, West
Bengal, India
- Department of Pharmacy, JIS University, Kolkata, 700109, West Bengal, India
Keywords:
IgAN, fibrosis, inflammation, ESRD, TGFβ, TBRI.
Abstract: IgAN is the most common form of glomerulonephritis affecting 2000000 people annually.
The disease ultimately progresses to chronic renal failure and ESRD. In this article, we
focused on a comprehensive understanding of the pathogenesis of the disease and thus identifying
different target proteins that could be essential in therapeutic approaches in the management
of the disease. Aberrantly glycosylated IgA1 produced by the suppression of the enzyme β-1, 3
galactosyltransferase ultimately triggered the formation of IgG autoantibodies which form complexes
with Gd-IgA1. The complex gets circulated through the blood vessels through monocytes
and ultimately gets deposited in the glomerular mesangial cells via CD71 receptors present locally.
This complex triggers the inflammatory pathways activating the alternate complement
system, various types of T Cells, toll-like receptors, cytokines, and chemokines ultimately recruiting
the phagocytic cells to eliminate the Gd-IgA complex. The inflammatory proteins cause
severe mesangial and podocyte damage in the kidney which ultimately initiates the repair process
following chronic inflammation by an important protein named TGFβ1. TGF β1 is an important
protein produced during chronic inflammation mediating the repair process via various
downstream transduction proteins and ultimately producing fibrotic proteins which help in the
repair process but permanently damage the glomerular cells.
