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- Title
Pathogenic role of the IgA molecule in IgA nephropathy.
- Authors
Lai, Kar Neng; Leung, Joseph CK
- Abstract
SUMMARY: Deposits of IgA together with complement in different body tissues support the hypothesis that IgA can trigger inflammatory mechanisms. IgA nephropathy (IgAN) is characterized by predominant mesangial IgA1 deposits of a polymeric nature. So far, the mechanism of polymeric IgA1 deposition in the kidney mesangium is poorly understood in IgAN. The exact pathophysiological sequel preceding renal fibrosis following the mesangial deposition of IgA immune complexes remains speculative. Recent in vitro studies revealed that binding of IgA to mesangial cells led to increased expression of growth factors, cytokines, and integrins. The release of these proinflammatory factors is likely to enhance inflammatory injury. In addition, the local renin–angiotensin system present in renal tissues also contributes to renal fibrosis through the activation of transforming growth factor-β. The question of whether polymeric IgA isolated from patients with IgAN exerted any upregulatory effect on the synthesis of macrophage migration inhibitory factor (MIF) and components of the renin–angiotensin system in human mesangial cells was explored. The in vitro studies revealed that polymeric IgA from IgAN patients upregulated the gene expression of renin and MIF in human mesangial cells in a dose-dependent manner. These findings further support the notion that glomerular deposition of IgA is not only a pathological epiphenomenon of IgAN, but that polymeric IgA exerts a pathophysiologic effect on the mesangial cells leading to renal fibrosis.
- Subjects
IGA glomerulonephritis; IMMUNE complexes
- Publication
Nephrology, 2002, Vol 7, pS86
- ISSN
1320-5358
- Publication type
Article
- DOI
10.1046/j.1440-1797.7.s3.2.x