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2018 ; 33
(5
): 763-777
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New insights into the pathogenesis of IgA nephropathy
#MMPMID28624979
Yeo SC
; Cheung CK
; Barratt J
Pediatr Nephrol
2018[May]; 33
(5
): 763-777
PMID28624979
show ga
IgA nephropathy is the most common form of glomerulonephritis in many parts of
the world and remains an important cause of end-stage renal disease. Current
evidence suggests that IgA nephropathy is not due to a single pathogenic insult,
but rather the result of multiple sequential pathogenic "hits". An abnormally
increased level of circulating poorly O-galactosylated IgA1 and the production of
O-glycan-specific antibodies leads to the formation of IgA1-containing immune
complexes, and their subsequent mesangial deposition results in inflammation and
glomerular injury. While this general framework has formed the foundation of our
current understanding of the pathogenesis of IgA nephropathy, much work is
ongoing to try to precisely define the genetic, epigenetic, immunological, and
molecular basis of IgA nephropathy. In particular, the precise origin of poorly
O-galactosylated IgA1 and the inciting factors for the production of
O-glycan-specific antibodies continue to be intensely evaluated. The mechanisms
responsible for mesangial IgA1 deposition and subsequent renal injury also remain
incompletely understood. In this review, we summarize the current understanding
of the key steps involved in the pathogenesis of IgA nephropathy. It is hoped
that further advances in our understanding of this common glomerulonephritis will
lead to novel diagnostic and prognostic biomarkers, and targeted therapies to
ameliorate disease progression.
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