IgA nephropathy classification: Difference between revisions

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[[Category:Nephrology]]
[[Category:Genetic disorders]]

Revision as of 19:53, 3 November 2016

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

When IgA nephropathy occurs in isolation, it is called "primary IgA nephropathy". In converse, if IgA nephropathy is a consequence of a more systemic disease, it is called "secondary IgA nephropathy"

Classification

Primary IgA Nephropathy

When IgA nephropathy occurs alone, it is called "primary IgA nephropathy". It is thus not secondary to any chronic concomitant disease. Before the diagnosis of primary IgA nephropathy is made, secondary causes need to be ruled out.

Secondary IgA Nephropathy

When IgA nephropathy occurs secondary to other chronic or systemic diseases, it is called “secondary IgA nephropathy”. Secondary causes of IgA nephropathy should be ruled out because secondary causes may alter the management plan and probably the prognosis too.


Classification of IgA nephropathy

The pathologic classification of IgA nephropathy has been developed by the International IgA Nephropathy Network together with the Renal Pathology Society. This classification is called “The Oxford classification of IgA nephropathy”. This classification was done after a 5 years retrospective study on clinical data and kidney biopsies were obtained from 265 patients and multiple patho-histological analyses were done on the kidney specimens [1]. IgAN is then histologically classified as:

  • Mesangial hypercellularity
  • Segmental glomerulosclerosis
  • Endocapillary hypercellularity
  • Tubular atrophy/interstitial fibrosis

References

  1. Working Group of the International IgA Nephropathy Network and the Renal Pathology Society. Cattran DC, Coppo R, Cook HT, Feehally J, Roberts IS; et al. (2009). "The Oxford classification of IgA nephropathy: rationale, clinicopathological correlations, and classification". Kidney Int. 76 (5): 534–45. doi:10.1038/ki.2009.243. PMID 19571791.

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