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Abstract
Oxidative stress is defined as the imbalance between the generation of reactive oxygen species and antioxidant defense mechanisms.
Under normal conditions, there is a steady-state balance between the production of oxygen free radicals and their destruction by the antioxidant systems. In CRF patients, the balance between pro-and anti-oxidant capacity is shifted towards an increased oxidative stress. At the same time, patients on regular haemodialysis are under continuous oxidative stress.
It is generally accepted that renal failure is associated with drastic oxidative stress-i.e an imbalance between antioxidants and prooxidants contribute to the pathogenesis and progression of acute and chronic renal failure. Oxygen free radicals and their secondary products together called reactive oxygen species exert angiotoxic and cardiotoxic effects. Consequently, these compounds contribute to an increased cardiovascular risk. Additionally, dialysis depletes antioxidative defence.
Components of oxidative stress which appear in chronic renal failure are oxidation processes of lipids, peptides, proteins, and nucleic acids. After lipid peroxidation with its biological consequences such as disturbance of membranal organization, secondary lipid peroxidation products are formed. Many of these products are able to exert similar toxic effects which can prolong and potentiate the primary free radical damage. Within those secondary lipid peroxidation products, there are a lot of different aldehydes such as MDA and 4-hydroxyalkenales.