Haemodialysis induces mitochondrial dysfunction and apoptosis.

Area of Science:

• Cell Biology
• Nephrology
• Biochemistry

Background:

• Mitochondria are key regulators of apoptosis induced by oxidative stress.
• Nuclear factor-kappaB (NF-kappaB) integrates pro-inflammatory signals and oxidative stress.

Purpose of the Study:

• To investigate the impact of hemodialysis on mitochondrial function, reactive oxygen species (ROS) generation, and peripheral blood mononuclear cell (PBMC) apoptosis in end-stage renal disease (ESRD) patients.

Main Methods:

• PBMCs were isolated from eight ESRD patients before and during hemodialysis (HD).
• Flow cytometry was used to assess intracellular ROS, mitochondrial membrane potential (Δψm), and PBMC apoptosis.
• Levels of IL-6, IL-6 soluble receptor, IL-6 gp130, NF-kappaB, B-cell lymphoma protein-2, and heat shock protein-70 were measured.

Main Results:

• Hemodialysis significantly increased plasma and PBMC-secreted IL-6 levels.
• A higher percentage of lymphocytes showed mitochondrial membrane potential collapse, apoptosis, and increased ROS generation (superoxide and hydrogen peroxide) during HD.
• NF-kappaB activation and expression of anti-apoptotic proteins (Bcl-2, HSP70) were elevated during HD.

Conclusions:

• Intra-dialytic cytokine activation and impaired mitochondrial function during hemodialysis contribute to increased ROS and PBMC apoptosis.
• The body activates compensatory pathways to mitigate cell stress and apoptosis during hemodialysis.