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[Proatherogenic changes induced by hemodialysis; probably a result of bio-incompatibility].
- Source :
-
Nederlands tijdschrift voor geneeskunde [Ned Tijdschr Geneeskd] 2000 Dec 30; Vol. 144 (53), pp. 2540-4. - Publication Year :
- 2000
-
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.
- Subjects :
- Acute-Phase Reaction chemically induced
Anticoagulants therapeutic use
Arteriosclerosis immunology
Arteriosclerosis prevention & control
Chronic Disease
Humans
Kidneys, Artificial
Risk Factors
Acute-Phase Reaction immunology
Arteriosclerosis etiology
Coated Materials, Biocompatible
Dialysis Solutions adverse effects
Renal Dialysis adverse effects
Subjects
Details
- Language :
- Dutch; Flemish
- ISSN :
- 0028-2162
- Volume :
- 144
- Issue :
- 53
- Database :
- MEDLINE
- Journal :
- Nederlands tijdschrift voor geneeskunde
- Publication Type :
- Academic Journal
- Accession number :
- 11191788