Abstract
Monocyte chemoattractant protein-1 (MCP-1) and its receptor CCR2 stimulate inflammation response by activating and recruiting monocytes/macrophages. MCP-1 and CCR2 polymorphisms were reported to be associated with various diseases. To explore the relationship between MCP-1 and CCR2 polymorphisms and IgA nephropathy (IgAN), we conducted this case-control study by enrolling 351 IgAN patients and 310 health controls. Odds ratios (ORs) and 95% confidence intervals (CIs) were calculated to evaluate potential associations of MCP-1 and CCR2 polymorphisms with susceptibility and clinical parameters of IgAN. No statistical differences between IgAN group and the control group in the MCP-1 -2518 and CCR2 +190 genotypic groups were observed (P > 0.05). Individuals with MCP-1 -2518 GG genotypes had a higher blood pressure (GG vs. AA+AG: OR = 1.79, 95% CI = 1.07-2.99, P = 0.026) and Lee's grade (GG vs. AA+AG: OR = 2.05, 95% CI = 1.19-3.54, P = 0.009; GG vs. AA: OR = 2.24, 95% CI = 1.19-4.20, P = 0.01), compared with patients with AA/AG genotypes. A significant association between CCR2 +190 polymorphism and Lee's grades was observed (GA+AA vs. GG: OR = 2.66, 95% CI = 1.63-4.35, P < 0.001; GA vs. AA+GG: OR = 2.27, 95% CI = 1.39-3.70, P = 0.001). Our results indicated that MCP-1 and CCR2 polymorphisms may influence the progression of IgAN, but not increase/decrease its susceptibility.
Highlights
IgA nephropathy (IgAN), which is called Berger’s disease, is the most frequent glomerulonephritis characterized by the deposition of IgA1-based immune complexes in mesangium [1, 2]
An increased number of tubulointerstitial macrophages was significantly associated with a poor prognosis in IgAN patients [25]
IgA1 deposition, as the initiating factor in IgAN, can stimulate mesangial cells to produce MCP1 [30], which eventually leaidng to the activation and accumulation of monocytes/macrophages and contributing to renal interstitial inflammation in kidney [31], Stangou et al found that in IgAN patients, Monocyte chemoattractant protein-1 (MCP-1) was positively associated with severe extracapillary proliferation (P = 0.001) and Th2 and Th17 cytokines were directly involved in renal pathology in IgAN through regulating the MCP-1 production [32]
Summary
IgA nephropathy (IgAN), which is called Berger’s disease, is the most frequent glomerulonephritis characterized by the deposition of IgA1-based immune complexes in mesangium [1, 2]. IgAN patients with mild symptoms often coincide with an upper respiratory tract infection at initial, but 50% of these patients will develop into end-stage renal disease within the 20 years [6]. Low socioeconomic status, and gene are the risk factors for IgAN [7]. In a test including 148 healthy female twins, the heritability of serum undergalactosylated IgA1 and IgA levels were found to be 80% and 46%, respectively, which indicates the importance of genetic factors in pathogenesis of IgAN [8]. Genome-wide association studies reported polymorphisms in gene were strongly correlated with IgAN prevalence and prognosis, but the associations and the magnitude are needed to confirm [9, 10]
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