Please use this identifier to cite or link to this item: http://hdl.handle.net/2381/8094
Title: Is progression of IgA nephropathy conditioned by genes regulating atherosclerotic damage?
Authors: Coppo, Rosanna
Feehally, John
First Published: Dec-2009
Publisher: Oxford University Press (OUP)
Citation: Nephrology Dialysis Transplantation, 2009, 24 (12), pp. 3573-3575.
Abstract: Progress has been slow in identifying genetic factors that influence either susceptibility to IgA nephropathy (IgAN) or its progression to end-stage renal disease (ESRD) [1]. Studies of both familial and sporadic IgAN strongly point to clinical and genetic heterogeneity in the entity we presently call IgAN. The human IgAN phenotype does not exhibit classic Mendelian inheritance patterns, but is better considered using the paradigm for genetically complex human autoimmune diseases, for which multiple loci have been identified by family-based genetic studies. In these complex diseases many different types of genetic variations contribute to the final phenotype. Among the many potential mechanisms involved, interest has recently been focused on specific single-nucleotide polymorphism (SNP) alleles that alter the transcriptional activity of genes involved in the pathogenesis. Recently, it has been said that 30–50% of human genes with coding SNPs can present allelic variation in gene expression [2].
DOI Link: 10.1093/ndt/gfp524
ISSN: 0931-0509
1460-2385
Links: http://ndt.oxfordjournals.org/content/24/12/3573
http://hdl.handle.net/2381/8094
Version: Post print
Status: Peer reviewed
Type: Article
Rights: © The Authors 2009. This is a pre-copy-editing, author-produced PDF of an article accepted for publication in 'Nephrology Dialysis Transplantation' following peer review. The definitive publisher-authenticated version, Nephrology Dialysis Transplantation, 2009, 24 (12), pp. 3573-3575, is available online at: http://ndt.oxfordjournals.org/content/24/12/3573. Deposited with reference to the publisher's archiving policy available on the SHERPA/RoMEO website.
Appears in Collections:Published Articles, Dept. of Infection, Immunity and Inflammation

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