PMID- 27051449 OWN - NLM STAT- PubMed-not-MEDLINE DCOM- 20160407 LR - 20240325 IS - 1741-427X (Print) IS - 1741-4288 (Electronic) IS - 1741-427X (Linking) VI - 2016 DP - 2016 TI - A Transmembrane Polymorphism of Fcgamma Receptor IIb Is Associated with Kidney Deficiency Syndrome in Rheumatoid Arthritis. PG - 3214657 LID - 10.1155/2016/3214657 [doi] LID - 3214657 AB - Objective. The purpose is to investigate the role of kidney deficiency and the association between kidney deficiency and a polymorphism FcgammaRIIb 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). FcgammaRIIb 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 FcgammaRIIb variants. FAU - Mo, Na AU - Mo N AD - Division of Rheumatology and Clinical Immunology, The First Affiliated Hospital of Guangzhou University of Chinese Medicine, Guangzhou 510405, China. FAU - Lai, Ruogu AU - Lai R AD - Division of Rheumatology and Clinical Immunology, The First Affiliated Hospital of Guangzhou University of Chinese Medicine, Guangzhou 510405, China. FAU - Luo, Shizi AU - Luo S AD - Division of Rheumatology and Clinical Immunology, The First Affiliated Hospital of Guangzhou University of Chinese Medicine, Guangzhou 510405, China. FAU - Xie, Jianglin AU - Xie J AD - Division of Rheumatology and Clinical Immunology, The First Affiliated Hospital of Guangzhou University of Chinese Medicine, Guangzhou 510405, China. FAU - Wang, Xizi AU - Wang X AD - Division of Rheumatology and Clinical Immunology, The First Affiliated Hospital of Guangzhou University of Chinese Medicine, Guangzhou 510405, China. FAU - Liu, Lijuan AU - Liu L AD - Division of Rheumatology and Clinical Immunology, The First Affiliated Hospital of Guangzhou University of Chinese Medicine, Guangzhou 510405, China. FAU - Liu, Xiaoling AU - Liu X AD - Division of Rheumatology and Clinical Immunology, The First Affiliated Hospital of Guangzhou University of Chinese Medicine, Guangzhou 510405, China. FAU - Chen, Guangxing AU - Chen G AUID- ORCID: 0000-0002-1102-6965 AD - Division of Rheumatology and Clinical Immunology, The First Affiliated Hospital of Guangzhou University of Chinese Medicine, Guangzhou 510405, China. LA - eng PT - Journal Article DEP - 20160308 PL - United States TA - Evid Based Complement Alternat Med JT - Evidence-based complementary and alternative medicine : eCAM JID - 101215021 PMC - PMC4802036 EDAT- 2016/04/07 06:00 MHDA- 2016/04/07 06:01 PMCR- 2016/03/08 CRDT- 2016/04/07 06:00 PHST- 2015/12/06 00:00 [received] PHST- 2016/02/07 00:00 [revised] PHST- 2016/02/18 00:00 [accepted] PHST- 2016/04/07 06:00 [entrez] PHST- 2016/04/07 06:00 [pubmed] PHST- 2016/04/07 06:01 [medline] PHST- 2016/03/08 00:00 [pmc-release] AID - 10.1155/2016/3214657 [doi] PST - ppublish SO - Evid Based Complement Alternat Med. 2016;2016:3214657. doi: 10.1155/2016/3214657. Epub 2016 Mar 8.