Value of urinary levels of interleukin-6, epidermal growth factor, monocyte chemoattractant protein type1 and transforming growth factor β1 in predicting the extent of fibrosis lesions in kidney biopsies of patients with IgA nephropathy.
Transforming growth factor β1 and monocyte chemoattractant protein-1 expression in the renal tissues was significantly greater in the patients with immunoglobulin A nephropathy than in the patients with Henoch-Schönlein purpura nephritis (both p<0.001).
The TGF-β1-509T/C-dominant model for the C allele was significantly associated with proteinuria (≥1.0 g/d) of IgAN patients (P = 0.001, Pc = 0.031 and OR = 1.49).
Subgroup analysis suggests that the TGF-β1 gene -C509T polymorphism would not be a risk factor for IgA nephropathy in Asians but might play a role in Europeans.
Higher transforming growth factor-β1 and severe chronic vasculopathy (but not glomerulosclerosis, interstitial fibrosis or lymphocyte infiltrate) were associated with the IgAN progression 24 months after biopsy.
The aim of this study was to compare genetic variants from the TGFB1, IRF5, STAT4 genes and TRAF1-C5 locus with susceptibility to IgAN and lupus nephritis in two Swedish cohorts.
Our experimental data together with the meta-analysis suggest TGFB1 as an important candidate gene for further biological studies of IgA nephropathy and as a possible target for therapy.
The investigated polymorphisms were not associated with the progression of the IgA nephropathy, as shown by the similar genotype distribution in group A and group B (slow progressors: TGF-beta1, 92.3%; TNFalpha, 25.6%; IL-6, 74.4%; fast progressors: TGF-beta1, 85.7%; TNFalpha, 22.4%; IL-6: 81.6%, ns).
The investigated polymorphisms were not associated with the progression of the IgA nephropathy, as shown by the similar genotype distribution in group A and group B (slow progressors: TGF-beta1, 92.3%; TNFalpha, 25.6%; IL-6, 74.4%; fast progressors: TGF-beta1, 85.7%; TNFalpha, 22.4%; IL-6: 81.6%, ns).
To clarify whether TGF-beta1 contributes to the progression of IgA nephropathy by activating apoptosis in glomerular cells, we examined the expression of TGF-beta1 gene and apoptotic changes in kidney biopsy samples, and assessed those relations to the severity of nephropathy.
Our study suggests that the haplotype reconstruction of TGF-beta1 gene polymorphisms could be more informative than the investigation of single nucleotide polymorphisms for defining the associated risk of developing IgAN.
Although a close relationship between increased renal tissue levels of TGF-beta1 and fibronectin has been reported in IgA nephropathy, no data are available on renal tissue expression of Rho proteins.
These results suggest that TGF-beta1 gene polymorphisms are specifically associated with heavy proteinuria and mesangial cell proliferation in Japanese patients with IgAN, although they do not confer susceptibility to this disease.
These results suggest that TGF-beta1 gene polymorphisms are specifically associated with heavy proteinuria and mesangial cell proliferation in Japanese patients with IgAN, although they do not confer susceptibility to this disease.
Urinary excretion of total and mature TGF-beta1 was reduced in patients with IgA nephropathy after treatment with prednisolone (0.8 mg/kg/d) for 1 month.
These findings suggest that TGF-beta 1 is involved in glomerulosclerosis and the development of tubulointerstitial lesions, indicating its potential importance in the progression and aggravation of immunoglobulin A nephropathy.