title: A Transmembrane Polymorphism of Fcγ Receptor IIb Is Associated with Kidney Deficiency Syndrome in Rheumatoid Arthritis.
abstract: 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.
authors.affiliation: Division of Rheumatology and Clinical Immunology, The First Affiliated Hospital of Guangzhou University of Chinese Medicine, Guangzhou 510405, China.
authors.forename: Na
authors.initials: N
authors.lastname: Mo
authors.affiliation: Division of Rheumatology and Clinical Immunology, The First Affiliated Hospital of Guangzhou University of Chinese Medicine, Guangzhou 510405, China.
authors.forename: Ruogu
authors.initials: R
authors.lastname: Lai
authors.affiliation: Division of Rheumatology and Clinical Immunology, The First Affiliated Hospital of Guangzhou University of Chinese Medicine, Guangzhou 510405, China.
authors.forename: Shizi
authors.initials: S
authors.lastname: Luo
authors.affiliation: Division of Rheumatology and Clinical Immunology, The First Affiliated Hospital of Guangzhou University of Chinese Medicine, Guangzhou 510405, China.
authors.forename: Jianglin
authors.initials: J
authors.lastname: Xie
authors.affiliation: Division of Rheumatology and Clinical Immunology, The First Affiliated Hospital of Guangzhou University of Chinese Medicine, Guangzhou 510405, China.
authors.forename: Xizi
authors.initials: X
authors.lastname: Wang
authors.affiliation: Division of Rheumatology and Clinical Immunology, The First Affiliated Hospital of Guangzhou University of Chinese Medicine, Guangzhou 510405, China.
authors.forename: Lijuan
authors.initials: L
authors.lastname: Liu
authors.affiliation: Division of Rheumatology and Clinical Immunology, The First Affiliated Hospital of Guangzhou University of Chinese Medicine, Guangzhou 510405, China.
authors.forename: Xiaoling
authors.initials: X
authors.lastname: Liu
authors.affiliation: Division of Rheumatology and Clinical Immunology, The First Affiliated Hospital of Guangzhou University of Chinese Medicine, Guangzhou 510405, China.
authors.forename: Guangxing
authors.identifier: 0000-0002-1102-6965
authors.initials: G
authors.lastname: Chen