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2015 ; 1
(1
): 8-18
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New Insights into the Pathogenesis of IgA Nephropathy
#MMPMID26568951
Novak J
; Rizk D
; Takahashi K
; Zhang X
; Bian Q
; Ueda H
; Ueda Y
; Reily C
; Lai LY
; Hao C
; Novak L
; Huang ZQ
; Renfrow MB
; Suzuki H
; Julian BA
Kidney Dis (Basel)
2015[May]; 1
(1
): 8-18
PMID26568951
show ga
BACKGROUND: IgA nephropathy, a frequent cause of end-stage renal disease, is an
autoimmune disease wherein immune complexes consisting of IgA1 with
galactose-deficient O-glycans (autoantigen) and anti-glycan autoantibodies
deposit in glomeruli and induce renal injury. Multiple genetic loci associated
with disease risk have been identified. The prevalence of risk alleles varies
geographically, highest in eastern Asia and northern Europe, fewer in other parts
of Europe and North America, and the least in Africa. IgA nephropathy is
diagnosed from pathological assessment of a renal biopsy specimen. Currently,
therapy is not disease-targeted but rather is focused on maintaining control of
blood pressure and proteinuria, ideally with suppression of angiotensin II.
Possible additional approaches differ between countries. Disease-specific therapy
as well as new tools for diagnosis, prognosis, and assessment of responses to
therapy are needed. SUMMARY: Glycosylation pathways associated with aberrant
O-glycosylation of IgA1 and, thus, production of autoantigen, have been
identified. Furthermore, unique characteristics of the autoantibodies in IgA
nephropathy have been uncovered. Many of these biochemical features are shared by
patients with IgA nephropathy and Henoch-Schönlein purpura nephritis, suggesting
that the two diseases may represent opposite ends of a spectrum of a disease
process. Understanding the molecular mechanisms involved in formation of
pathogenic IgA1-containing immune complexes will enable development of
disease-specific therapies as well as diagnostic and prognostic biomarkers. KEY
MESSAGES: IgA nephropathy is an autoimmune disease caused by glomerular
deposition of nephritogenic circulating immune complexes consisting of
galactose-deficient IgA1 (autoantigen) bound by anti-glycan autoantibodies. A
better understanding of the multi-step process of pathogenesis of IgA nephropathy
and the genetic and environmental contributing factors will lead to development
of biomarkers to identify patients with progressive disease who would benefit
from a future disease-specific therapy.
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