Inflammation and Cardiovascular Disease Associated With Hemodialysis for End-Stage Renal Disease

Abstract

Chronic kidney disease (CKD) and cardiac insufficiency often co-exist, particularly in uremic patients on hemodialysis (HD). The occurrence of abnormal renal function in patients with cardiac insufficiency is often indicative of a poor prognosis. It has long been established that in patients with cardiac insufficiency, poorer renal function tends to indicate poorer cardiac mechanics, including left atrial reserve strain, left ventricular longitudinal strain, and right ventricular free wall strain (Unger et al., Eur J Heart Fail, 2016, 18(1), 103–12). Similarly, patients with chronic kidney disease, particularly uremic patients on HD, often have cardiovascular complications in addition to abnormal endothelial function with volume overload, persistent inflammatory states, calcium overload, and imbalances in redox responses. Cardiac insufficiency due to uremia is therefore mainly due to multifaceted non-specific pathological changes rather than pure renal insufficiency. Several studies have shown that the risk of adverse cardiovascular events is greatly increased and persistent in all patients treated with HD, especially in those who have just started HD treatment. Inflammation, as an important intersection between CKD and cardiovascular disease, is involved in the development of cardiovascular complications in patients with CKD and is indicative of prognosis (Chan et al., Eur Heart J, 2021, 42(13), 1244–1253). Therefore, only by understanding the mechanisms underlying the sequential development of inflammation in CKD patients and breaking the vicious circle between inflammation-mediated renal and cardiac insufficiency is it possible to improve the prognosis of patients with end-stage renal disease (ESRD). This review highlights the mechanisms of inflammation and the oxidative stress that co-exists with inflammation in uremic patients on dialysis, as well as the mechanisms of cardiovascular complications in the inflammatory state, and provides clinical recommendations for the anti-inflammatory treatment of cardiovascular complications in such patients.

Immune System Dysfunction and Inflammation in Hemodialysis Patients: Two Sides of the Same Coin

“…Nevertheless, these patients are still chronically exposed to systemic stress related both to hemodynamic and non-hemodynamic factors, with increased risk for cardiovascular, neoplastic, and infection diseases [3,4].…”

The Correlation of Interleukin-6, Malnutrition Inflammation Score and Asymmetric Dimethylarginine in Chronic Kidney Disease Patients Undergoing Routine Hemodialysis

“…Hemodialysis-related and non-hemodialysis-related factors can cause inflammation by stimulating the synthesis of cytokines such as CRP, IFN-γ, IL-1, IL-6, and TNF-α [26]. Another biomarker related to inflammation is suPAR (soluble urokinase plasminogen activator receptor) [38]. High levels of suPAR and other pro-inflammatory mediators were associated with CKD progression [38], [39].…”

“…Another biomarker related to inflammation is suPAR (soluble urokinase plasminogen activator receptor) [38]. High levels of suPAR and other pro-inflammatory mediators were associated with CKD progression [38], [39]. Pro-inflammatory cytokines that are also increased in prolonged proteinuria include transforming growth factor-ß (TGF-ß), vascular endothelial growth factor (VEGF), and platelet-derived growth factor (PDGF) [40].…”

Renoprotective potentials of small molecule natural products targeting mitochondrial dysfunction

“…Traditional and non-traditional risk factors have a significant effect on the life expectancy of CKD patients. The interconnectivity of molecular mechanisms in oxidative stress, inflammation, and endothelial dysfunction, is the primary shared factor in determining CKD, high blood pressure, CVD, and cardiovascular-renal remodeling (Wang and Gao, 2022). Therefore, summarizing our existing understanding and identifying prospective future research pathways and therapeutic options for intervention and our current state of knowledge would help treat oxidative stress-related CKD.…”