IL-10, TGF-β, IL-4, IL-27, and EBI3 are cytokines that regulate inflammation, tissue repair, and fibrosis in the kidney and other organs. These cytokines may contribute to different aspects of chronic Show more
IL-10, TGF-β, IL-4, IL-27, and EBI3 are cytokines that regulate inflammation, tissue repair, and fibrosis in the kidney and other organs. These cytokines may contribute to different aspects of chronic kidney disease (CKD), end-stage renal disease (ESRD), and systemic lupus erythematosus (SLE), which are associated with renal dysfunction and aberrant immune regulation. This study investigates the role of these cytokines in patients with concurrent kidney disease and SLE to understand their contribution to the pathogenesis and progression of this complex condition. Cytokine levels were measured in five groups of CKD/ESRD patients with concurrent SLE, CKD/ESRD patients without SLE, and healthy controls. We conducted a cross-sectional modest size study with 78 patients and 40 healthy controls (n = 118 total). Serum levels of IL-10, TGF-β, IL-4, IL-27, and EBI3 were measured using the ELISA. The data were analyzed and compared using theKruskal-Wallis test. Significant differences in cytokine patterns were observed. IL-10, IL-4, and EBI3 levels were elevated in CKD/ESRD patients with SLE compared to healthy controls, indicating immune dysregulation. TGF-β levels were significantly lower, suggesting a deficiency in immune regulation. IL-27 levels were found to be increased in ESRD patients with SLE compared to those without SLE, indicating its potential role in disease activity. Our study suggests that cytokines like IL-27 may be associated with disease status in patients with both ESRD and SLE. However, its utility for monitoring disease activity or guiding treatment requires validation in larger, prospective cohorts to establish sensitivity, specificity, and a causal role. Show less
Coronary artery disease (CAD) is a devastating illness and a leading cause of death worldwide, primarily caused by atherosclerosis resulting from a genetic-environmental interaction. This study aimed Show more
Coronary artery disease (CAD) is a devastating illness and a leading cause of death worldwide, primarily caused by atherosclerosis resulting from a genetic-environmental interaction. This study aimed to investigate the relationship between the ESR1 (rs9340799), OLR1 (rs3736234), LIPC (rs2070895), VDR (rs2228570), and CETP (rs708272) polymorphisms, lipid profile parameters, and CAD risk in a southeast Iranian population. A total of 400 subjects (200 CAD patients with hyperlipidemia and 200 healthy controls) were enrolled in this case-control study. Five selected polymorphisms were genotyped using the polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) technique. For all single nucleotide polymorphisms (SNPs), the population under study was in the Hardy-Weinberg equilibrium. The T-risk allele frequency of rs2228570 was associated with an increased risk of CAD. The TT and CT genotypes of rs2228570 had also been associated with the risk of CAD. Additionally, the TT genotype was associated with higher serum low-density lipoprotein cholesterol (LDL-c) and high-density lipoprotein cholesterol (HDL-c) levels. The GG genotype of the rs3736234 was associated with higher body mass index (BMI) and triglyceride (TG) levels, and the AA genotype of the rs708272 was associated with higher HDL-c levels. Based on these findings, we propose that the VDR (rs2228570) polymorphism was associated with serum HDL-c and LDL-c levels and may serve as potential risk factors for CAD within the Iranian population. Moreover, rs3736234 and rs708272 influence the concentrations of TG and HDL-c, respectively. These findings provided insights into the complex interplay between genetic variations, cardiovascular risk, and lipid metabolism. Show less