pubmed-article:10792601 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:10792601 | lifeskim:mentions | umls-concept:C0017661 | lld:lifeskim |
pubmed-article:10792601 | lifeskim:mentions | umls-concept:C0314603 | lld:lifeskim |
pubmed-article:10792601 | lifeskim:mentions | umls-concept:C0449258 | lld:lifeskim |
pubmed-article:10792601 | lifeskim:mentions | umls-concept:C1527148 | lld:lifeskim |
pubmed-article:10792601 | lifeskim:mentions | umls-concept:C1521761 | lld:lifeskim |
pubmed-article:10792601 | lifeskim:mentions | umls-concept:C0332120 | lld:lifeskim |
pubmed-article:10792601 | pubmed:issue | 5 | lld:pubmed |
pubmed-article:10792601 | pubmed:dateCreated | 2000-6-1 | lld:pubmed |
pubmed-article:10792601 | pubmed:abstractText | IgA nephropathy (IgAN) is the most common glomerulonephritis in the world among patients undergoing renal biopsy. Once considered a relatively benign condition, longitudinal follow-up studies have revealed that in fact 9 to 50% of patients progress to end-stage renal disease within 20 years of disease onset. In the three decades since its first description by Jean Berger and Nicole Hinglais, clinical, epidemiologic, and immunologic studies of the pathogenesis of primary (idiopathic) mesangial glomerulonephritis with predominant IgA deposits have characterized the features of IgAN as a distinct glomerular disease entity. However, the basic molecular mechanism(s) underlying abnormal IgA deposition in the mesangium with ensuing extracellular matrix expansion and mesangial cell proliferation remains poorly understood. The task of elucidating the molecular basis of IgAN is made especially challenging by the fact that both environmental and genetic components likely contribute to the development and progression of IgAN. | lld:pubmed |
pubmed-article:10792601 | pubmed:language | eng | lld:pubmed |
pubmed-article:10792601 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:10792601 | pubmed:citationSubset | IM | lld:pubmed |
pubmed-article:10792601 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:10792601 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:10792601 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:10792601 | pubmed:month | May | lld:pubmed |
pubmed-article:10792601 | pubmed:issn | 0085-2538 | lld:pubmed |
pubmed-article:10792601 | pubmed:author | pubmed-author:NeryRR | lld:pubmed |
pubmed-article:10792601 | pubmed:author | pubmed-author:WongS KSK | lld:pubmed |
pubmed-article:10792601 | pubmed:author | pubmed-author:QUIK HKH | lld:pubmed |
pubmed-article:10792601 | pubmed:author | pubmed-author:BonventreJ... | lld:pubmed |
pubmed-article:10792601 | pubmed:author | pubmed-author:RamirezS BSB | lld:pubmed |
pubmed-article:10792601 | pubmed:issnType | Print | lld:pubmed |
pubmed-article:10792601 | pubmed:volume | 57 | lld:pubmed |
pubmed-article:10792601 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:10792601 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:10792601 | pubmed:pagination | 1818-35 | lld:pubmed |
pubmed-article:10792601 | pubmed:dateRevised | 2005-11-16 | lld:pubmed |
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pubmed-article:10792601 | pubmed:year | 2000 | lld:pubmed |
pubmed-article:10792601 | pubmed:articleTitle | Evidence for genetic factors in the development and progression of IgA nephropathy. | lld:pubmed |
pubmed-article:10792601 | pubmed:affiliation | Departments of Medicine and Pediatrics, Faculty of Medicine, National University of Singapore. mdchsus@nus.edu.sg | lld:pubmed |
pubmed-article:10792601 | pubmed:publicationType | Journal Article | lld:pubmed |
pubmed-article:10792601 | pubmed:publicationType | Review | lld:pubmed |
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