Background Anti-angiotensin II type 1 receptor antibodies (AT1R-Abs) have been recognized as non-HLA antibodies associated with allograft rejection and poor allograft outcomes after kidney transplantation. The aim of this study was to assess the risk anti-AT1R-Abs pose for rejection and graft loss among kidney transplant populations. Methods We systematically searched PubMed, EMBASE, and the Cochrane Library databases for relevant articles published from inception until June 2021 to identify all studies concerning the role AT1R-Abs play in the clinical outcome after kidney transplantation. Two reviewers independently identified studies, abstracted outcome data, and assessed the quality of the studies. The meta-analysis was summarized using the fixed-effects models or random-effects models, according to heterogeneity. The major outcomes included delayed graft function, acute rejection, graft loss, or patient death after transplantation. Results Twenty-one eligible studies involving a total of 4,023 kidney transplantation recipients were included in the evaluation to identified. Meta-analysis results showed that the AT1R-Ab positive kidney transplant (KT) group had a greater incidence of antibody-mediated rejection (RR = 1.94, 95%CI: 1.61-2.33, P < 0.00001) and graft loss (RR = 2.37, 95%CI: 1.50-3.75, P = 0.0002) than did the AT1R-Abs negative KT group. There was no significant statistical difference in delayed graft function rate, T-cell mediated rejection, mixed rejection, acute cellular rejection, acute rejection, and patient death rate between AT1R-Ab positive KT and AT1R-Ab negative KT groups. Conclusions Our study shows that the presence of anti-AT1R-Abs was associated with a significantly higher risk of antibody-mediated rejection and graft loss in kidney transplantation. Future studies are still needed to evaluate the importance of routine anti-AT1R monitoring and therapeutic targeting. These results shows that assessment of anti-AT1R-Abs would be helpful in determining immunologic risk and susceptibility to immunologic events for recipients.

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The aim of this study was to investigate the potential correlation between the human leukocyte antigen (HLA)-B*27 subtypes in patients with ankylosing spondylitis (AS) and the clinical features of AS. The prevalence of HLA-B*27 subtypes was investigated in 132 healthy donors recruited from our center and in 143 patients with AS. We investigated the differences in HLA-B27 subtype status for the patients and healthy donors by using a PCR-SSP (polymerase chain reaction with sequence-specific primer) method. The clinical outcomes of the patients, including lower back pain, uveitis, peripheral arthritis, stiffness, joints, erythrocyte sedimentation rate (ESR), Anti-streptolysin O (ASO) and C-reactive protein (CRP), were recorded. The male-to-female ratio was 2.5, and the mean age at diagnosis was 29.3 years. HLA-B*27 positivity was detected in 111 patients (77.6%) of patients with AS. The rate of HLA-B*27 positivity was significantly higher in the AS group than patients without AS. The subtypes observed in patients with AS were HLA-B*2704 (55.9%, 62/111), HLA-B*2705 (39.6%, 44/111), HLA-B*2702 (1.80%, 2/111), HLA-B*2707 (0.90%, 1/111), and HLA-B*2704/05(1.80%, 2/111). The main genotypes were HLA-B*2704 and HLA-B*2705. There were no significant differences in clinical manifestations. Multivariate analysis showed statistically significant differences in sex (P=0.01), disease duration (P=0.023), hematocrit (P=0.01), and CRP (P=0.01) between patients in the HLA-B*27(+) AS group and the HLA-B*27(-) AS group. In addition, HLA-B*15, HLA-B*40, HLA-B*13, and HLA-B*46 were the major alleles with associated HLA-B types in patients with HLA-B*27(+) AS. Therefore, we conclude that HLA-B*27 is highly correlated with AS and can be used as an early predictor of AS. In addition, sex, disease duration, ESR, and CRP were significantly different in the HLA-B*27(+) AS group and HLA-B*27(-) AS group. Finally, our study also found a correlation between HLA-B*15, HLA-B*40, HLA-B*13, and HLA-B*46 subtypes and the development of AS.

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