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| ==Causes== | | ==Causes== |
| ===Primary IgA Nephropathy=== | | ===Primary IgA Nephropathy=== |
| The cause of primary IgA nephropathy is unknown. Additionally there are no known infectious or environmental associated factors. However, some studies had associated some genetic mutations and familial clustering as postulated cause of IgAN <ref name="pmid10792601">{{cite journal| author=Hsu SI, Ramirez SB, Winn MP, Bonventre JV, Owen WF| title=Evidence for genetic factors in the development and progression of IgA nephropathy. | journal=Kidney Int | year= 2000 | volume= 57 | issue= 5 | pages= 1818-35 | pmid=10792601 | doi=10.1046/j.1523-1755.2000.00032.x | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=10792601 }} </ref>. These studies are inconclusive and there are more ongoing researches in this area. | | The cause of primary IgA nephropathy is unknown. Additionally there are no known infectious or environmental associated factors. However, IgA nephropathy is associated with some genetic mutations and familial clustering as a postulated cause of primary IgAN <ref name="pmid10792601">{{cite journal| author=Hsu SI, Ramirez SB, Winn MP, Bonventre JV, Owen WF| title=Evidence for genetic factors in the development and progression of IgA nephropathy. | journal=Kidney Int | year= 2000 | volume= 57 | issue= 5 | pages= 1818-35 | pmid=10792601 | doi=10.1046/j.1523-1755.2000.00032.x | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=10792601 }} </ref>. These genetic associations are poorly studied and are largely inconclusive. There are ongoing studies in this field. |
| Primary IgA nephropathy is caused by a genetic predisposition in patients who typically present immediately following a respiratory or gastrointestinal tract infectious organisms or virus. The environmental exposure to these infectious agents may thus facilitate the subsequent pathogenesis of the disease. | | Primary IgA nephropathy is caused by a genetic predisposition in patients who typically present immediately following a respiratory or gastrointestinal tract infections. The environmental exposure to these infectious agents may thus facilitate the subsequent pathogenesis of the disease. |
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| ===Secondary IgA Nephropathy=== | | ===Secondary IgA Nephropathy=== |
| Common primary etiologies associated with glomerular IgA deposits and thus secondary IgA nephropathy are shown below.
| | The most common etiologies associated with glomerular IgA deposits and thus secondary IgA nephropathy include: |
| | * Liver cirrhosis<ref name="pmid22895519">{{cite journal| author=Radhakrishnan J, Cattran DC| title=The KDIGO practice guideline on glomerulonephritis: reading between the (guide)lines--application to the individual patient. | journal=Kidney Int | year= 2012 |volume= 82 | issue= 8 | pages= 840-56 | pmid=22895519 | doi=10.1038/ki.2012.280 | pmc=|url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=22895519 }} </ref> |
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| <u>The most important 3 causes are:</u>
| | * Celiac disease<ref name="pmid22895519">{{cite journal| author=Radhakrishnan J, Cattran DC| title=The KDIGO practice guideline on glomerulonephritis: reading between the (guide)lines--application to the individual patient. | journal=Kidney Int | year= 2012 |volume= 82 | issue= 8 | pages= 840-56 | pmid=22895519 | doi=10.1038/ki.2012.280 | pmc=|url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=22895519 }} </ref> |
| * '''Liver cirrhosis'''<ref name="pmid22895519">{{cite journal| author=Radhakrishnan J, Cattran DC| title=The KDIGO practice guideline on glomerulonephritis: reading between the (guide)lines--application to the individual patient. | journal=Kidney Int | year= 2012 |volume= 82 | issue= 8 | pages= 840-56 | pmid=22895519 | doi=10.1038/ki.2012.280 | pmc=|url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=22895519 }} </ref> | |
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| * '''Celiac disease'''<ref name="pmid22895519">{{cite journal| author=Radhakrishnan J, Cattran DC| title=The KDIGO practice guideline on glomerulonephritis: reading between the (guide)lines--application to the individual patient. | journal=Kidney Int | year= 2012 |volume= 82 | issue= 8 | pages= 840-56 | pmid=22895519 | doi=10.1038/ki.2012.280 | pmc=|url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=22895519 }} </ref> | | * HIV infection<ref name="pmid22895519">{{cite journal| author=Radhakrishnan J, Cattran DC| title=The KDIGO practice guideline on glomerulonephritis: reading between the (guide)lines--application to the individual patient. | journal=Kidney Int | year= 2012 |volume= 82 | issue= 8 | pages= 840-56 | pmid=22895519 | doi=10.1038/ki.2012.280 | pmc=|url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=22895519 }} </ref> |
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| * '''HIV infection'''<ref name="pmid22895519">{{cite journal| author=Radhakrishnan J, Cattran DC| title=The KDIGO practice guideline on glomerulonephritis: reading between the (guide)lines--application to the individual patient. | journal=Kidney Int | year= 2012 |volume= 82 | issue= 8 | pages= 840-56 | pmid=22895519 | doi=10.1038/ki.2012.280 | pmc=|url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=22895519 }} </ref>
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| <u>IgA nephropathy has also been associated with the following diseases, but to a much less extent:</u>
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| *Dermatitis herpetiformis<ref name="pmid22895519">{{cite journal| author=Radhakrishnan J, Cattran DC| title=The KDIGO practice guideline on glomerulonephritis: reading between the (guide)lines--application to the individual patient. | journal=Kidney Int | year= 2012 |volume= 82 | issue= 8 | pages= 840-56 | pmid=22895519 | doi=10.1038/ki.2012.280 | pmc= |url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=22895519 }} </ref>
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| *Seronegative arthritis, especially as ankylosing spondylitis<ref name="pmid22895519">{{cite journal| author=Radhakrishnan J, Cattran DC| title=The KDIGO practice guideline on glomerulonephritis: reading between the (guide)lines--application to the individual patient. |journal=Kidney Int | year= 2012 | volume= 82 | issue= 8 | pages= 840-56 | pmid=22895519 |doi=10.1038/ki.2012.280 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=22895519 }} </ref>
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| *Small-cell carcinoma<ref name="pmid22895519">{{cite journal| author=Radhakrishnan J, Cattran DC| title=The KDIGO practice guideline on glomerulonephritis: reading between the (guide)lines--application to the individual patient. | journal=Kidney Int | year= 2012 |volume= 82 | issue= 8 | pages= 840-56 | pmid=22895519 | doi=10.1038/ki.2012.280 | pmc= |url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=22895519 }} </ref>
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| *Hodgkin’s lymphoma<ref name="pmid22895519">{{cite journal| author=Radhakrishnan J, Cattran DC| title=The KDIGO practice guideline on glomerulonephritis: reading between the (guide)lines--application to the individual patient. | journal=Kidney Int | year= 2012 |volume= 82 | issue= 8 | pages= 840-56 | pmid=22895519 | doi=10.1038/ki.2012.280 | pmc= |url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=22895519 }} </ref>
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| *T-cell lymphoma, such as mycosis fungoides<ref name="pmid22895519">{{cite journal|author=Radhakrishnan J, Cattran DC| title=The KDIGO practice guideline on glomerulonephritis: reading between the (guide)lines--application to the individual patient. | journal=Kidney Int| year= 2012 | volume= 82 | issue= 8 | pages= 840-56 | pmid=22895519 | doi=10.1038/ki.2012.280| pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=22895519 }} </ref>
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| *Disseminated tuberculosis<ref name="pmid22895519">{{cite journal| author=Radhakrishnan J, Cattran DC| title=The KDIGO practice guideline on glomerulonephritis: reading between the (guide)lines--application to the individual patient. | journal=Kidney Int | year= 2012 |volume= 82 | issue= 8 | pages= 840-56 | pmid=22895519 | doi=10.1038/ki.2012.280 | pmc= |url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=22895519 }} </ref>
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| *Bronchiolitis obliterans<ref name="pmid22895519">{{cite journal| author=Radhakrishnan J, Cattran DC| title=The KDIGO practice guideline on glomerulonephritis: reading between the (guide)lines--application to the individual patient. | journal=Kidney Int | year= 2012 |volume= 82 | issue= 8 | pages= 840-56 | pmid=22895519 | doi=10.1038/ki.2012.280 | pmc= |url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=22895519 }} </ref>
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| *Inflammatory bowel disease (Crohn’s disease and ulcerative colitis)<ref name="pmid22895519">{{cite journal| author=Radhakrishnan J, Cattran DC| title=The KDIGO practice guideline on glomerulonephritis: reading between the (guide)lines--application to the individual patient. | journal=Kidney Int | year= 2012 | volume= 82 | issue= 8 | pages= 840-56| pmid=22895519 | doi=10.1038/ki.2012.280 | pmc= |url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=22895519 }} </ref>
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| ==References== | | ==References== |
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]Ali Poyan Mehr, M.D. [2] Associate Editor(s)-in-Chief: Olufunmilola Olubukola M.D.[3]
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Overview
Causes
Primary IgA Nephropathy
The cause of primary IgA nephropathy is unknown. Additionally there are no known infectious or environmental associated factors. However, IgA nephropathy is associated with some genetic mutations and familial clustering as a postulated cause of primary IgAN [1]. These genetic associations are poorly studied and are largely inconclusive. There are ongoing studies in this field.
Primary IgA nephropathy is caused by a genetic predisposition in patients who typically present immediately following a respiratory or gastrointestinal tract infections. The environmental exposure to these infectious agents may thus facilitate the subsequent pathogenesis of the disease.
Secondary IgA Nephropathy
The most common etiologies associated with glomerular IgA deposits and thus secondary IgA nephropathy include:
References
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