Immune System Dysfunction and Inflammation in Hemodialysis Patients: Two Sides of the Same Coin.
Susanna CampoAntonio LacquanitiDomenico TrombettaAntonella SmeriglioPaolo MonardoPublished in: Journal of clinical medicine (2022)
Biocompatibility in hemodialysis (HD) has considerably improved in recent decades, but remains an open issue to be solved, appearing essential to reduce systemic inflammation and enhance patients' clinical outcomes. Clotting prevention, reduction in complement and leukocyte activation, and improvement of antioxidant effect represent the main goals. This review aims to analyze the different pathways involved in HD patients, leading to immune system dysfunction and inflammation. In particular, we mostly review the evidence about thrombogenicity, which probably represents the most important characteristic of bio-incompatibility. Platelet activation is one of the first steps occurring in HD patients, determining several events causing chronic sub-clinical inflammation and immune dysfunction involvement. Moreover, oxidative stress processes, resulting from a loss of balance between pro-oxidant factors and antioxidant mechanisms, have been described, highlighting the link with inflammation. We updated both innate and acquired immune system dysfunctions and their close link with uremic toxins occurring in HD patients, with several consequences leading to increased mortality. The elucidation of the role of immune dysfunction and inflammation in HD patients would enhance not only the understanding of disease physiopathology, but also has the potential to provide new insights into the development of therapeutic strategies.
Keyphrases
- oxidative stress
- end stage renal disease
- chronic kidney disease
- ejection fraction
- newly diagnosed
- peritoneal dialysis
- prognostic factors
- immune response
- coronary artery disease
- risk assessment
- public health
- induced apoptosis
- cardiovascular disease
- type diabetes
- diabetic rats
- climate change
- cardiovascular events
- peripheral blood
- heat shock protein