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Pathogenesis of IgA nephropathy

Chee Kay Cheung, PhD, MRCP
Jonathan Barratt, PhD, FRCP
Section Editors
Richard J Glassock, MD, MACP
Fernando C Fervenza, MD, PhD
Deputy Editor
Albert Q Lam, MD


Immunoglobulin A (IgA) nephropathy is the most common lesion found to cause primary glomerulonephritis throughout most developed countries of the world [1-4]. IgA deposits may also be seen on kidney biopsy in individuals with no evidence of renal disease [5]. The reported incidence of mesangial IgA deposition in apparently healthy individuals ranges from 3 to 16 percent [5,6]. These cases had no clinical features of nephritis, but their renal biopsy was consistent with IgA nephropathy.

This observation raises three important points:

There is a large cohort of undiagnosed "latent" IgA nephropathy in the general population.

This must be taken into account when genetic studies are undertaken comparing gene polymorphisms in IgA nephropathy with normal "healthy" populations.

It raises an important consideration for the pathogenesis of IgA nephropathy: The process of mesangial IgA deposition is likely to be separate from the induction of glomerular injury, and IgA deposition does not necessarily need to be followed by nephritis. Identifying the factors common to both processes is essential to our overall understanding of the pathogenesis of IgA nephropathy.

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Literature review current through: Nov 2017. | This topic last updated: Oct 05, 2017.
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