The percentages of non-switched memory B cells (R = 0.8399, <i>P</i> < .0001), plasmablasts (R = 0.4486, <i>P</i> = .0318) and the levels of serum IL-6 (R = 0.5461, <i>P</i> = .0070) were positively correlated with the values of 24-h urine proteins in IgAN patients.
Dendritic cells, Toll-like receptor (TLR), interleukin-6 (IFN-α), interferon-alpha (IFN-α) and tumor necrosis factor-alpha (TNF-α) play an important role in the pathogenesis of IgA nephropathy (IgAN).
IgG-ddIgA1 complexes from both patients with IgA nephropathy (IgAN-IgG-dd-IgA1) and healthy controls (HC-IgG-dd-IgA1) could induce the proliferation of mesangial cells and up-regulate expression of MCP-1, IL-6 and CXCL1.
Furthermore, we investigated the influence of IgA1-containing CIC from sera of children with IgAN with clinically active disease (i.e., abnormal urinalysis and/or serum creatinine concentration) or inactive disease (i.e., normal urinalysis and serum creatinine concentration) on the expression of IL-6 and IL-8 genes by mesangial cells.
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).
We evaluated the impact of TGF-beta1 gene Arg(25)-->Pro, TNFalpha gene G-308A and IL-6 gene G-174C polymorphisms on the clinical manifestations of IgA nephropathy.Patients and methods.
We measured mRNA levels of adrenomedullin (AM), C-type natriuretic peptide (CNP), vascular endothelial growth factor (VEGF), interleukin 1beta (IL-1beta) and interleukin 6 (IL-6) in peripheral blood mononuclear cells (PBMC) of patients with IgA nephropathy.
In the present study we have defined renal gene and protein expression of IL-6 and EGF in 10 normal, 10 nonproliferative glomerulonephritis (NPGN) and 30 IgA nephropathy (IgAN) human kidneys by RT-PCR, in situ hybridization and immunohistochemical techniques.
Cytokines IL-4 and IL-6 mRNAs were absent in normals, with IL-4 detectable throughout renal substance in disease; IL-6 gene transcription was intense in glomerular and vascular endothelial sites in IgA nephropathy.
Using RT-PCR methods, IL-6 mRNA was detected in the glomeruli of renal biopsy specimens obtained from patients with IgA nephropathy and lupus nephritis.
IL-6 transcripts were identified in 37% (13 of 35) of patients with active IgA nephropathy, compared with 6% (1 of 17) normal controls (P = 0.015), with no significant increase in IgA remission, or disease control groups.