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[Proatherogenic changes induced by hemodialysis; probably a result of bio-incompatibility]
1Medisch Centrum Alkmaar, afd. Nefrologie en Dialyse, Wilhelminalaan 12, 1815 JD Alkmaar. nube.grooteman@wxs.nl
Insights
Chronic hemodialysis patients face high cardiovascular disease risk. The hemodialysis procedure itself may accelerate atherosclerosis through inflammatory processes, contributing to this risk.
Area of Science:
- Cardiovascular Medicine
- Nephrology
- Immunology
Context:
- Chronic hemodialysis patients exhibit a significantly elevated risk of cardiovascular disease (CVD).
- Traditional risk factors inadequately explain the full extent of CVD in this population.
- Atherosclerosis, a key contributor to CVD, is increasingly understood as an inflammatory condition.
Purpose:
- To investigate the potential role of the hemodialysis procedure itself in accelerating atherosclerosis.
- To explore the inflammatory mechanisms linking hemodialysis to enhanced cardiovascular risk.
Summary:
- Hemodialysis involves blood-dialyzer contact, stimulating humoral and cellular systems, initiating an inflammatory response.
- This process leads to repeated exposure of the vascular endothelium to inflammatory mediators, cytokines, oxidative stress, and activated blood components.
- These factors contribute to endothelial dysfunction and accelerated atherosclerosis in chronic hemodialysis patients.
Impact:
- Findings suggest hemodialysis treatment may be an independent contributor to cardiovascular risk in patients with chronic kidney disease.
- Highlights the need for strategies to mitigate the inflammatory effects of hemodialysis to improve cardiovascular outcomes.
- Provides a mechanistic link between hemodialysis and accelerated atherosclerosis, informing future research and clinical practice.
Abstract:
Chronic haemodialysis patients have a disproportionately high risk for developing cardiovascular disease, which can only in part be explained by known risk factors such as dyslipidaemia, hypertension, hyperhomocysteinemia, diabetes mellitus and chronic volume expansion. A possible cause is that the haemodialysis treatment itself contributes to the accelerated atherosclerosis, observed in these patients. Nowadays, atherosclerosis is considered an inflammatory process, mediated by a dysfunction of the vascular endothelium. As a result, blood cells adhere to the vascular surface and release a variety of vasoactive mediators, cytokines, growth factors and free radicals. Due to the contact between blood and dialyzer, humoral systems and cellular elements are stimulated, and this may be viewed as an inflammatory reaction. As a consequence of this, the vascular surface of haemodialysis patients is repeatedly exposed to the influences of cytokines, coagulation products, vasoactive mediators, stimulated leukocytes and thrombocytes, and oxidative stress. It is therefore conceivable that the haemodialysis treatment itself enhances the greatly increased cardiovascular risk in chronic haemodialysis patients.