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Mesangial cells from patients with IgA nephropathy have increased susceptibility to galactose-deficient IgA1

Journal article
Authors Kerstin Ebefors
Peidi Liu
Emelie Lassén
Johannes Elvin
Emma Candemark
Kristina Levan
Börje Haraldsson
Jenny Nyström
Published in Bmc Nephrology
Volume 17
Pages 40
ISSN 1471-2369
Publication year 2016
Published at Institute of Neuroscience and Physiology, Department of Physiology
Institute of Medicine, Department of Molecular and Clinical Medicine
Institute of Clinical Sciences, Department of Obstetrics and Gynecology
Pages 40
Language en
Links dx.doi.org/10.1186/s12882-016-0251-...
Keywords Mesangial cells, IgA nephropathy, PDGF, growth-factor-beta, renal-transplantation, immune-complexes, pdgf-bb, expression, recurrence, glomeruli, glomerulonephritis, immunoglobulin, proliferation, Urology & Nephrology
Subject categories Clinical Medicine

Abstract

Background: IgA nephropathy (IgAN) is the most common glomerulonephritis in the world, affecting close to a million people. Circulating galactose-deficient IgA (gd-IgA), present in patients with IgAN, form immune complex deposits in the glomerular mesangium causing local proliferation and matrix expansion. Intriguing though, individuals having gd-IgA deposits in the kidneys do not necessarily have signs of glomerular disease. Recurrence of IgAN only occurs in less than half of transplanted patients with IgAN, indicating that gd-IgA is not the only factor driving the disease. We hypothesize that, in addition to IgA complexes, patients with IgAN possess a subtype of mesangial cells highly susceptible to gd-IgA induced cell proliferation. Methods: To test the hypothesis, we designed a technique to culture primary mesangial cells from renal biopsies obtained from IgAN patients and controls. The cell response to gd-IgA treatment was then measured both on gene and protein level and the proliferation rate of the cells in response to PDGF was investigated. Results: When treated with gd-IgA, mesangial cells from patients with IgAN express and release more PDGF compared to controls. In addition, the mesangial cells from patients with IgAN were more responsive to treatment with PDGF resulting in an increased proliferation rate of the cells compared to control. Mesangial cells cultured from patients with IgAN expressed and released more IL-6 than controls and had a higher expression of matrix genes. Both mesangial cells derived from patients with IgAN and controls increased their expressed TGF beta 1 and CCL5 when treated with gd-IgA. Conclusion: We conclude that mesangial cells derived from IgAN patients have a mesangioproliferative phenotype with increased reactivity to IgA and that these cellular intrinsic properties may be important for the development of IgA nephropathy.

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