Molecular Insights into Gene Expression Changes in Apoptosis Immune Response and Cellular Regulation Pathways in Chronic Kidney Disease Patients

Abstract Background : Chronic kidney disease (CKD) is a complex, multifactorial disease characterized by the overlapping pathways of apoptosis, immune regulation, and fibrosis, which play a pivotal role in disease progression. However, the molecular integration of these pathways remains incompletely understood, particularly regarding their combined impact on the deterioration of renal function. Methods : The study included 60 participants: 30 patients with CKD and 30 healthy individuals as a control group. Hematological and biochemical parameters, including hemoglobin, hematocrit, urea, creatinine, and glucose, were assessed. Gene expression of CASP8, CASP9, PDCD1, CTLA4, and TGFB3 was analyzed using RT-qPCR, with the 2-ΔΔCt method employed to calculate relative variability. Statistical analyses were performed using comparison tests and correlation analysis. Results : a significant decrease in hemoglobin levels (9.37±0.50 vs. 14.18±0.64 g/dL) and hematocrit (28.63±1.40 vs. 40.69±1.91), compared to a significant increase in urea (124.38±17.39 vs. 29.64±2.25 mg/dL) and creatinine (8.16±0.63 vs. 0.75±0.03 mg/dL) (p<0.001). At the molecular level, significant increases in the gene expression of CASP8 (46.09±6.70 folds) and CASP9 (13.59±1.51 folds) were observed, along with elevated levels of PDCD1 (25.66±4.19), CTLA4 (34.69±8.43), and TGFB3 (15.29±2.83). Conclusion : These findings suggest a complex regulatory network involving apoptosis activation, immunosuppression, and fibrosis in patients with renal failure. These results highlight an integrated molecular axis that may represent a promising target for future therapeutic interventions and provide a foundation for a deeper understanding of the pathogenic mechanisms underlying disease progression.