Abstract
Hemodialysis (HD) patient are known to be susceptible to a wide range of early and long-term complication such as chronic inflammation, infections, malnutrition, and cardiovascular disease that significantly affect the incidence of mortality. A large gap between the number of people with end-stage kidney disease (ESKD) and patients who received kidney transplantation has been identified. Therefore, there is a huge need to explore the underlying pathophysiology of HD complications in order to provide treatment guidelines. The immunological dysregulation, involving both the innate and adaptive response, plays a crucial role during the HD sessions and in chronic, maintenance treatments. Innate immune system mediators include the dysfunction of neutrophils, monocytes, and natural killer (NK) cells with signaling mediated by NOD-like receptor P3 (NLRP3) and Toll-like receptor 4 (TLR4); in addition, there is a significant activation of the complement system that is mediated by dialysis membrane-surfaces. These effectors induce a persistent, systemic, pro-inflammatory, and pro-coagulant milieu that has been described as inflammaging. The adaptive response, the imbalance in the CD4+/CD8+ T cell ratio, and the reduction of Th2 and regulatory T cells, together with an altered interaction with B lymphocyte by CD40/CD40L, have been mainly implicated in immune system dysfunction. Altogether, these observations suggest that intervention targeting the immune system in HD patients could improve morbidity and mortality. The purpose of this review is to expand our understanding on the role of immune dysfunction in both innate and adaptive response in patients undergoing hemodialysis treatment.
Highlights
End-stage renal disease (ESRD) is an extremely serious condition, recognized as a public health priority and affecting more than 2.6 million people worldwide.A large part of patients affected by ESRD are dialysis-dependent for the rest of their life and have an increased risk of cardiovascular morbidity and mortality, and a higher susceptibility to infections and malignancies [1]
Most of these elderly patients employ HD as dialysis treatment [10] and their mortality and survival is strongly influenced by comorbidities such as vascular and cardiac disease, whose mechanisms are linked to inflammation and microvascular damage [11], which are related to a progressive accumulation of advanced glycation endfluid (AGE), with increased levels of C reactive protein (CRP), PTX3, IL-6 [12,13], and FGF-23 [14,15]
Short-Term Effect of Hemodialysis Treatment on Complement Activation In HD, the short-term effectors functions of complement activation are the induction of inflammation, promoting coagulation, and impaired host defense owing to accelerated consumption of complement proteins [68]
Summary
End-stage renal disease (ESRD) is an extremely serious condition, recognized as a public health priority and affecting more than 2.6 million people worldwide. Chronic inflammation, andsenescence, the establishment of cellular senescence are Most of these elderly patients employ HD as dialysis treatment [10] and their mortality and survival is strongly influenced by comorbidities such as vascular and cardiac disease, whose mechanisms are linked to inflammation and microvascular damage [11], which are related to a progressive accumulation of AGEs, with increased levels of CRP, PTX3, IL-6 [12,13], and FGF-23 [14,15] These are all large middle uremic toxins difficult to remove with standard dialyzers and responsible for chronic inflammation
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