Association of C-reactive protein and complement factor H gene polymorphisms with risk of lupus nephritis in Chinese population

Abstract

Background: Complement overactivation is a major driver of lupus nephritis (LN). Impaired interactions of C-reactive protein (CRP) with complement factor H (CFH) have been shown as a pathogenic mechanism that contributes to the overactivation of complement in LN. However, genetic variations of neither CRP nor CFH show consistent influences on the risk of LN.

Aim: To examine whether genetic variations of CRP and CFH in combination can improve the risk stratification in Chinese population.

Methods: We genotyped six CRP single nucleotide polymorphisms (SNPs) (rs1205, rs3093062, rs2794521, rs1800947, rs3093077, and rs1130864) and three CFH SNPs (rs482934, rs1061170, and rs1061147) in 270 LN patients and 303 healthy subjects.

Results: No linkage was found among CRP and CFH SNPs, indicating lack of genetic interactions between the two genes. Moreover, CRP and CFH SNPs, neither individually nor in combination, are associated with the risk or clinical manifestations of LN. Given the unambiguous pathogenic roles of the two genes.

Conclusion: These findings suggest that the biological effects of most genetic variations of CRP and CFH on their expressions or activities are not sufficient to influence the disease course of LN.

Keywords: C-reactive protein; Complement factor H; Lupus nephritis; Single nucleotide polymorphism.; Systemic lupus erythematosus.

Figure 1

Polymorphisms schematic diagram and the clinical characteristics of patients with lupus nephritis. A: Polymorphisms in the C-reactive protein (CRP) and complement factor H (CFH) gene, six single nucleotide polymorphisms (SNPs) in CRP and three SNPs in CFH were selected; B: Clinical characteristics of patients with lupus nephritis. CRP: C-reactive protein; CFH: Complement factor H; SNP: Single nucleotide polymorphisms; UTR: Untranslated regions.