Document Detail


The pathogenesis of IgA nephropathy.
MedLine Citation:
PMID:  21301336     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
PURPOSE OF REVIEW: This review will analyze contemporary information concerning the possible pathogenetic mechanisms involved in IgA nephropathy, emphasizing studies in humans rather than experimental animals.
RECENT FINDINGS: Deposition of IgA in the glomeruli, the hallmark of IgA nephropathy, may be a quite common phenomenon. Aberrant O-linked galactosylation of IgA subclass (IgA1) appears to play a central role and 'auto-immunity' to a conformational epitope related to glycans at the hinge region of IgA1 is apparently required. Both a circulating immune complex and an in-situ immune complex mechanism have been advanced. Mediator systems, such as complement activation and engagement of innate immune system, also play prominent roles in determining the clinical onset and severity of disease. Genetic influences are evident but the fine details of genetic predisposition and its impact on outcomes still need to be further elucidated.
SUMMARY: Progress in understanding the details of the pathogenesis of IgA nephropathy will lead to a better means of diagnosis (including noninvasive tests for diagnosis), more accurate individualized prognosis and personalized treatment regimens for this globally distributed and very common primary glomerular disease.
Authors:
Richard J Glassock
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Publication Detail:
Type:  Journal Article; Review    
Journal Detail:
Title:  Current opinion in nephrology and hypertension     Volume:  20     ISSN:  1473-6543     ISO Abbreviation:  Curr. Opin. Nephrol. Hypertens.     Publication Date:  2011 Mar 
Date Detail:
Created Date:  2011-02-10     Completed Date:  2011-05-26     Revised Date:  2013-05-02    
Medline Journal Info:
Nlm Unique ID:  9303753     Medline TA:  Curr Opin Nephrol Hypertens     Country:  England    
Other Details:
Languages:  eng     Pagination:  153-60     Citation Subset:  IM    
Affiliation:
David Geffen School of Medicine at UCLA, Los Angeles, California, USA. glassock@cox.net
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MeSH Terms
Descriptor/Qualifier:
Animals
Antigen-Antibody Complex / blood
Complement Activation
Glomerulonephritis, IGA / etiology*,  genetics,  immunology
Glycosylation
Humans
Immunity, Innate
Immunoglobulin A / metabolism
Chemical
Reg. No./Substance:
0/Antigen-Antibody Complex; 0/Immunoglobulin A

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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