Background/Objectives: This study aimed to evaluate the relationship between sirtuin family members (SIRT1, SIRT3, and SIRT6) and Wnt/β-catenin pathways with inflammation during the rejection process following kidney transplantation, as well as to explore their potential roles as candidate biomarkers. Materials and Methods: Blood samples were collected from 35 kidney transplant rejection patients and 30 healthy controls. The gene expression levels of SIRT1, SIRT3, SIRT6, and Wnt/β-catenin pathway components were measured using real-time PCR, and miRNA and lncRNA expression levels were analyzed. Statistical analyses were performed using SPSS version 23. Results: Significant alterations in SIRT1, SIRT3, and SIRT6 expression levels were observed in rejection patients, suggesting their potential role in disease pathogenesis and as therapeutic biomarkers. Key altered genes included hsa-miR-34c-1, hsa-miR-122b-5b, MALAT1, HOTAIR, LINC00473, TUG, PVT1, SIRT1, SIRT3, SIRT6, WNT1, TCF-LEF, LRP, AXIN1, IL1B, IL6, and IFNB1, all showing significant changes. However, no significant differences were found for miRNAs such as hsa-miR-21-2, hsa-miR-155-5p, and hsa-miR-200b-3p. SIRT1 expression was significantly decreased in the cellular rejection group, with a more pronounced reduction in these patients. Significant differences in SIRT1 expression were observed with interstitial inflammation and glomerulitis. Increased inflammation severity correlated with decreased SIRT1 and increased TCF-LEF, TUG, and miR-21 levels, while tubulitis severity was associated with elevated TCF-LEF and miR-155 expression. Conclusions: Along with the activation of Wnt/β-catenin pathways and increased levels of certain miRNAs and long non-coding RNAs (lncRNAs) associated with TCF-LEF transcription factors, the observed decrease in SIRT1 expression may be related to the severity of inflammation and tubulitis. These findings suggest that SIRT1, Wnt/β-catenin pathways, and non-coding RNAs play a role in the rejection process following kidney transplantation and could be considered as potential biomarkers or therapeutic target candidates for future research.

This prospective cross-sectional study aimed to evaluate leukocyte DNA damage in coronavirus disease (COVID-19) patients. In this study, 50 COVID-19-positive patients attending the Erzurum City Hospital Internal Medicine Outpatient Clinic and 42 control group patients were included. DNA damage was detected in living cells through leukocyte isolation in 50 COVID-19-positive patients using the comet assay method. DNA tail/head (olive) moments were evaluated and compared. White blood cells (WBC), red blood cells (RBC), hemoglobin (HGB), neutrophils (NEU), lymphocytes (LYM), eosinophils (EO), monocytes (MONO), basophils (BASO), platelets (PLT), and the neutrophil/lymphocyte ratio (NLR) were analyzed. The RBC, lymphocyte, eosinophil, and monocyte means were significantly higher in the control group (p < 0.05), whereas the HGB and neutrophile means were significantly higher in the study group (p < 0.05). There were significant negative correlations between COVID-19 and RBC (r = −0.863), LYM (r = −0.542), EO (r = −0.686), and MONO (r = −0.385). Meanwhile, there were significant positive correlations between COVID-19 and HGB (r = 0.863), NEU (r = 0.307), tail moment (r = 0.598), and olive moment (r = 0.582). Both the tail and olive moment mean differences were significantly higher in the study group, with higher ranges (p < 0.05). COVID-19 infection caused statistically significant increases in both the tail and olive damage percentage in patients, causing DNA damage. Lastly, the NLR rate was associated with the presence and progression of COVID-19.

Background and Objectives: The aim of this study was to investigate the changes in the SIRT family, the effects of sirtuins on kidney graft function, and their potential as biomarkers in patients who develop rejection after kidney transplantation. Materials and Methods: Blood samples were collected from 45 kidney transplant patients before and after rejection. Some of these patients experienced T-cell-mediated early rejection (TCMR), while others presented antibody-mediated late rejection (ABMR). The mRNA expression levels of SIRT-1, SIRT-3, and SIRT-7 were measured via real-time PCR, while the protein levels of SIRT-1, SIRT-2, SIRT-3, SIRT-5, and SIRT-7 were assessed using ELISA. Patients were grouped based on rejection type and histological characteristics. Statistical analyses were performed using SPSS software (V23). Results: The mean age of the patient group was 42.22, while the control group had a mean age of 35.23 (p = 0.002). SIRT-1, SIRT-3, and SIRT-7 levels were significantly higher in patients with rejection (p < 0.001). In patients with late-stage rejection, SIRT-3 was found to be associated with interstitial fibrosis and C4d accumulation. SIRT-7 levels showed a weak correlation with potassium levels (p = 0.014). Conclusions: Our findings demonstrate significant changes in the SIRT family during both early- and late-stage rejection processes. Particularly, the role of SIRT-3 in the late stage is highlighted, suggesting the potential use of this gene as a biomarker for managing rejection processes. These findings could provide valuable insights for developing treatment strategies in organ transplantation.

Aim: By creating antibodies, the immune system protects the body from foreign antigens. The immune system may occasionally sustain damage that results in a loss of tolerance to its antigens, which triggers the creation of antibodies directed against those antigens. Another challenge in solid organ transplantation is the existence of these anti-HLA antibodies. Our goal was to find out if common autoimmune disorders such type 1 diabetes (T1D), Behçet's disease (BD), and ankylosing spondylitis (AS) result in the development of anti-HLA antibodies. Materials and Methods: 100 patients with AS, 100 patients with BD, 60 patients with T1D, and 100 healthy people were included in this study. PRA screening tests were performed on serum from blood samples taken from both patients and healthy individuals to look for the presence of anti-HLA antibodies. Results: Of the AS patients, 5 were positive for PRA class II alone, 7 were positive for both PRA class I and class II, and 1 patient was positive for PRA class I. In BD, 3 patients was positive for both PRA class I and II, 7 patients was positive for PRA class II alone, and 1 patient was positive for PRA class I. In T1D, 1 patient were positive for PRA class I, 3 patients were positive for PRA class II alone, and 2 patients were positive for both. In summary: When three patient groups were compared with the control group, there was no statistically significant difference in the detection of anti-HLA antibodies between the patient groups and the control group.

Objectives: Renal allograft rejection diagnosis requires invasive biopsy. We assessed whether peripheral blood mRNA of 14 Hippo, interferon (IFN) and NF-κB pathway genes and 11 serum biomarkers could distinguish acute rejection from stable graft function. Methods: Three groups: biopsy-confirmed acute rejection (n=20), stable graft (n=25), healthy controls (n=30). PBMC mRNA was quantified by qRT-PCR; serum biomarkers by ELISA and spectrophotometry. Statistical analyses used Mann–Whitney U with Benjamini–Hochberg correction; ROC analyses used bootstrap 95 % CIs and 5-fold cross-validation. GEO datasets GSE51675 and GSE145408 provided directional cross-validation. Results: Thirteen of 14 genes were upregulated in rejection vs. controls (pFDR<0.01); TEAD1 (log ₂ FC=+2.44) and TRAF6 (+2.40) led. ISG15 was downregulated in both transplant groups, consistent with calcineurin inhibitor-mediated suppression, while serum free ISG15 protein was unchanged in stable graft but markedly lower in rejection than in both controls and stable graft (pFDR<0.001 and 0.002), discriminating rejection from stable graft in a way the mRNA signal did not. Only TEAD1 (Cohen’s d =1.40) and YAP1 ( d =1.17) discriminated rejection from stable graft with adequate power. TEAD1 mRNA (AUC=0.849) and serum leptin (AUC=0.922) were the strongest single markers; their combination yielded cross-validated AUC=0.990. Conclusions: PBMC YAP1/TEAD1 with serum leptin are promising non-invasive biomarkers for acute renal rejection. ISG15 downregulation is more consistent with calcineurin inhibitor-mediated suppression than with generalized immune impairment, although this interpretation requires direct mechanistic confirmation; notably, serum free ISG15 protein discriminated rejection from stable graft even though PBMC ISG15 mRNA did not, suggesting the protein-level measurement warrants further evaluation as a candidate marker. Prospective multicentre validation is required.

Objective: This study aimed to characterize the immuno-epigenetic role of the YY1–SIRT7–H3K18Ac–PD-L1 axis in renal allograft survival and to identify molecular biomarkers associated with rejection. Materials and Methods: A total of 65 participants were enrolled: 20 patients with biopsy-confirmed allograft rejection, 25 with stable graft function, and 20 healthy controls. Blood samples were collected into EDTA-containing tubes and stored at −80°C. Total RNA was isolated and complementary DNA (cDNA) synthesized for gene expression analysis by real-time polymerase chain reaction (RT-PCR), using glyceraldehyde-3-phosphate dehydrogenase (GAPDH) and U6 small nuclear RNA (snRNA) as reference genes. Serum concentrations of SIRT7, H3K18Ac, and oxidative stress markers — superoxide dismutase (SOD) and glutathione (GSH) — were quantified by enzyme-linked immunosorbent assay (ELISA). Statistical analyses were performed using SPSS v23.0 (p < 0.05). Results: Messenger RNA levels of STAT3, CD274 (PD-L1), H3F3A, SIRT7, and YY1 were significantly elevated in the rejection group, whereas PDCD1 (PD-1) was higher in the survival group (p<0.05). Long non-coding RNAs NEAT1, MALAT1, and GAS5 were upregulated in rejection (p<0.05). Significant alterations were detected in miR-21, miR-34a, miR-125, and miR-155 (p<0.01). SOD and GSH were decreased, while malondialdehyde (MDA) and catalase were elevated (p<0.05). NEAT1 and MALAT1 were predominantly upregulated in humoral rejection, whereas GAS5 was reduced. Conclusion: The YY1–SIRT7 epigenetic axis, in conjunction with PD-L1 signaling, appears to be implicated in immune evasion and inflammatory amplification following renal transplantation, supporting the potential utility of these molecules as immuno-epigenetic biomarkers of allograft rejection. Keywords: kidney transplantation allograft rejection epigenetics PD-L1 non-coding RNA biomarkers