A Transmembrane Polymorphism of Fcγ Receptor IIb Is Associated with Kidney Deficiency Syndrome in Rheumatoid Arthritis

Abstract EN

Objective.

The purpose is to investigate the role of kidney deficiency and the association between kidney deficiency and a polymorphism FcγRIIb 695T>C coding for nonsynonymous substitution IIe232Thr (I232T) in rheumatoid arthritis (RA).

Methods.

Clinical parameters and autoantibodies were analyzed and genotyping was performed in 159 kidney deficiency and 161 non-kidney-deficiency RA patients.

Results.

The age of disease onset and disease duration exhibited significant differences between two groups ( P < 0.01 ).

Patients with kidney deficiency tend to have higher activity of disease ( P < 0.05 ).

Anti-cyclic citrullinated peptides antibodies (ACPA) levels of patients with kidney deficiency were higher than the controls ( P = 0.039 ).

125 (78.6%) kidney deficiency and 114 (70.8%) non-kidney-deficiency patients had both ACPA-positive and RF-positive ( P = 0.04 , OR = 3.29).

FcγRIIb I232TT homozygotes were identified in 10 of 159 (6.3%) kidney deficiency subjects and 1 of 161 (0.6%) controls ( P = 0.000 , OR = 16.45).

Furthermore, in pooled genotype analysis, I232IT and I232TT homozygotes were significantly enriched in kidney deficiency individuals compared with the controls ( P = 0.000 , OR = 3.79).

Frequency of T allele was associated with kidney deficiency RA population ( P = 0.000 , OR = 3.18).

Conclusion.

This study confirmed that kidney deficiency was closely associated with disease activity and autoimmune disorder in RA.

Kidney deficiency in RA is first to reveal a strong genetic link to FcγRIIb variants.