Nephrol Dial Transplant (2003) 18: 463-466
© 2003 European Renal Association-European Dialysis and Transplant Association
Editorial Comments
Uraemic toxins and cardiovascular disease
Nephrology Section, Department of Internal Medicine, University Hospital, Ghent, Belgium
Keywords: cardiovascular disease; uraemic toxins
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Definitions
When renal failure develops, uraemic retention solutes are retained which are normally excreted by the healthy kidneys. If these retention solutes exert biochemical/biological activity, they are called uraemic toxins. According to their physico-chemical characteristics, they can be subdivided into [1]: (i) small water-soluble compounds (<500 Da, prototype urea); (ii) the larger so-called middle molecules (>500 Da, prototype ß2-microglobulin); and (iii) the protein bound solutes.
The retention of these uraemic solutes results in the progressive failure of virtually every organ system, in parallel with the failing function of the kidneys. The resulting clinical picture is the uraemic syndrome.
Cardiovascular disease as an integral part of the uraemic syndrome
The incidence of vascular disease and the morbidity and mortality related to it are extremely high in the population of uraemic patients [2]. Atheromatosis frequently causes ischaemic problems such as angina pectoris, myocardial infarction, cerebrovascular accidents and ischaemia of the lower limbs. Vascular disease occurs much earlier than
Cardiovascular disease as an inflammatory disorder
Uraemic toxins as potential culprits
The calcium–phosphate–parathyroid hormone axis
Phosphate
Parathyroid hormone
Vitamin D
Homocysteine
Advanced glycation end products (AGEs)
Advanced oxidation protein products (AOPP)
Cytokines
Asymmetric dimethylarginine (ADMA)
Pitfalls of research
Therapeutic/preventive options
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