Correlation Between Fc γ RⅡB Genetic Polymorphism And Rheumatoid Arthritis Of Kidney Deficiency

ObjectiveTo explore the relationship between FcγRIIB gene polymorphism and rheumatoid arthritis of kidney deficiency, and to provide clinical evidence to reveal the immunological mechanism of the etiology and pathogenesis of the kidney rheumatoid arthritis.MethodThere are201RA patients included in the study, divided into kidney-deficiency group and non-kidney deficiency group. This thesis will analyze the clinical data of the RA patients’sex composition, the age of onset, the course of disease, the number of joint tenderness, the number of swollen joints, the erythrocyte sedimentation rate(ESR), C-reactiveprotein(CRP), RF and DAS28score. There are237cases in the normal control group, divided into gene mutant group and un-mutated group by drawing the peripheral blood, extracting DNA, nested PCR and sequencing the second exon FcγRIIB695TC cites. Then statistically analyze the correlation between FcγRIIB695TC and the clinical data of the disease incidence, the condition assessment (DAS28score), immunological parameters (RF, anti-CCP antibodies) and the kidney condition (kidney deficiency and non-kidney deficiency).Results1. General comparison between kidney-deficiency group and non-kidney deficiency group. The proportion of men to women is1to4.5. The sex composition of both groups has no statistical significance (P>0.05). The age of onset and the course of disease of the kidney-deficiency RA patients are obviously larger than that of non-kidney deficiency group (P<0.05). The average age of onset of kidney-deficiency group is48.98and their average course of disease is141.5months. 2. The disease activity factors (DAS28score, ESR, CRP) of kidney deficiency group and the non-kidney deficiency group are not statistically significant (P>0.05). The disease activity (DAS28score) of both groups has no statistical significance (P>0.05), so does the immunological parameters (RF, anti-CCP antibodies) of both groups (P>0.05).3. Correlation research of FcγRIIB695TC and the onset of rheumatoid arthritis. There is no correlation between the FcγRIIB695TC of the normal control group and that of the RA patients. OR value is0.812.95%of the confidence interval is0.552to1.195. OR value is not statistically significant (P>0,05).4. The disease activity factors (DAS28score, ESR, CRP) of gene mutant group and un-mutated group are not statistically significant (P>0.05). The disease activity (DAS28score) of both groups has no statistical significance (P>0.05), so does the immunological parameters (RF, anti-CCP antibodies) of both groups (P>0.05).5. Risk between FcγR II B695TC and rheumatoid arthritis of kidney deficiency. There is a close correlation between Rheumatoid arthritis of kidney deficiency and FcγRIIB695TC. OR value is12.136,95%of its confidence interval is5.739to25.665. OR value has remarkable statistical significance, P=0.00; Kidney deficiency is also related to FcγRⅡB695CC. OR value is1.208,95%of its confidence interval is0.229to0.390. OR value is statistically significant, P=0.02. In addition, Kidney deficiency is correlated well with FcγRⅡB695TC+695CC. OR value is13.414,95%of its confidence interval is6.370to28.245. OR value has remarkable statistical significance, P=0.00.The age of onset of rheumatoid arthritis of kidney deficiency correlates with the course of disease, but has no significant correlation with the disease activity and the immunological parameters. The rheumatoid arthritis of kidney deficiency is significantly correlated with FcγRⅡB695TC. If FcγRⅡB695TC cites mutate, the risk of the rheumatoid arthritis of kidney deficiency will increase13times.ConclusionThere is no connection between FcγRIIB695TC and human rheumatoid arthritis. Rheumatoid arthritis of kidney deficiency is closely associated with FcγⅡB695TC. RA patients of FcγRⅡB695TC are more prone to kidney deficiency. It can be conjectured that the kidney deficiency of RA patients of FcγRⅡB695TC is in relation to congenital kidney essence deficiency. This study provides immunological mechanism for rheumatoid arthritis of kidney deficiency with clinical bases.