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2016 ; 17
(ä): 40
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Mesangial cells from patients with IgA nephropathy have increased susceptibility
to galactose-deficient IgA1
#MMPMID27044423
Ebefors K
; Liu P
; Lassén E
; Elvin J
; Candemark E
; Levan K
; Haraldsson B
; Nyström J
BMC Nephrol
2016[Apr]; 17
(ä): 40
PMID27044423
show ga
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?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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