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==Overview==
==Overview==



Revision as of 19:06, 12 January 2017

IgA nephropathy Microchapters

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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]

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:

  • Liver cirrhosis[2]
  • Celiac disease[2]
  • HIV infection[2]

References

  1. Hsu SI, Ramirez SB, Winn MP, Bonventre JV, Owen WF (2000). "Evidence for genetic factors in the development and progression of IgA nephropathy". Kidney Int. 57 (5): 1818–35. doi:10.1046/j.1523-1755.2000.00032.x. PMID 10792601.
  2. 2.0 2.1 2.2 Radhakrishnan J, Cattran DC (2012). "The KDIGO practice guideline on glomerulonephritis: reading between the (guide)lines--application to the individual patient". Kidney Int. 82 (8): 840–56. doi:10.1038/ki.2012.280. PMID 22895519.

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