An Overview of Haemodialysis and Oxidant Stress

Abstract

Today’s patient population is increasingly older. Patients with chronic renal failure therefore start extracorporeal substitutive treatment having congestive heart failure, chronic liver disease, diabetes and so forth. In these patients, however, long-term haemodialytic treatment may add further aggravation on their pre-existing pathological conditions. Oxidative stress and alterations in lipid metabolism are caused by haemodialysis mainly due to (1) bioincompatibility type of reactions such as production of reactive oxygen species by inflammatory cells due to complement-mediated or -independent pathways, and (2) the imbalance between oxidants and antioxidants due to the diffusive loss of hydrophilic vitamins such as ascorbic acid. The events related to the oxidant stress may sustain a state of chronic inflammation. Recent advances suggest that atherosclerosis and proliferation of the smooth muscle are initiated and sustained by inflammatory mechanisms. Therefore, attempts to counterbalance the prooxidant effect of haemodialysis and to reduce the chronic inflammatory state will be presented.

Oxidant Stress in Hemodialysis

“…This problem may not have immediate clinical effects, but it may represent a long-term complication derived from the repetitive effects of blood-membrane interaction [1, 2, 3]. …”

“…However, the multifactorial nature of this process [4]might include other factors peculiar to chronic HD, such as the absence of a complete correction of the uremic toxicity, malnutrition and the progressive worsening of the clinical condition due to aging and comorbidity. Altogether these factors trigger oxidative stress by establishing a steadily abnormal production of prooxidant stimuli coupled with a defective or insufficient antioxidant protection [1, 2, 3]. …”

Canine Model of Cardiorenal Failure

“…In addition to these syndromes, the balance between Nitric Oxide (NO) and Radical Oxygen Species (ROS) was shown to shift towards the latter by increased production of ROS, a low antioxidant status and lower availability of NO. These processes connecting with the production of proinflammatory cytokines, might contribute to the formation of cardiorenal syndrome [22]. In conclusion, our canine model with a combination of CHF and RF provides a useful tool for investigating mechanisms of cardiorenal syndrome as well as for research and development of drugs for treatment of patients with cardiorenal syndrome.…”

Cardiotonic Steroids and Cardiac Fibrosis

“…The role of CTS is thus clear in the pathogenesis of cardiac dysfunction with respect to calcium handling and the genesis of fibrosis. The presence of oxidative stress in the ESRD patients has been well documented (Fiorillo, Oliviero et al 1998;Tetta, Biasioli et al 1999). Most of the reactive oxygen species are produced by the mitochondria and a dysfunction in the mitochondria has been discussed above.…”