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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.

30 patients on hemodialysis or peritoneal dialysis have been investigated by computerized tomographic (CT) scan. To evaluate possible cerebral alterations induced by dialysis, CT examinations were carried out before, immediately after and 6 h after the end of dialysis with an Evaluskop, which provides an objective precise evaluation of even slight variations in brain density. No morphological variations were noted after dialysis, while the brain density fell significantly during and after the treatment. A decrease in density was not observed in normal subjects or in patients on continuous peritoneal dialysis. The changes in the densitometric values of brain tissue suggest that there is a postdialysis gain in cerebral water linked to the intermittent treatment. CT may represent a simple reliable method for studying uremic encephalopathy and investigating the pathogenesis of the dialysis disequilibrium syndrome.

Plasma B-type natriuretic peptide (BNP) concentration was evaluated in end-stage renal disease patients to verify if measurements before or after the session could furnish different information. BNP levels in plasma from 52 hemodialysis (HD) patients were measured both before and after the first session of the week. Echocardiographic studies were also performed and patients were followed over a period of 28 months. BNP removal from plasma was influenced by equilibrated Kt/V and patient characteristics. Initial plasma BNP concentration was correlated both with cardiac systolic function (LVEF) and mortality rate, independent of blood sample timing (before or after HD). A relative risk of death of 2.67 was found for plasma BNP levels above 335 pg/mL or 232 pg/mL, before and after HD, respectively. Higher BNP levels were observed in patients with higher burden of comorbidity, as measured by the Charlson Comorbidity Index; however, statistical significance was obtained only for BNP measured before HD. In conclusion, measurement of plasma BNP could give a valuable risk stratification of HD patients while cutting costs, by confining echocardiographic studies only to cases with BNP levels above the established cutoff values.

Summary:The kidney is a major source of the plasma enzyme glutathione peroxidase. We measured plasma glutathione peroxidase activity in 130 patients affected with difFerent renal diseases at various stages, and compared it with the following indices of kidney function: serum creatinine, creatinine clearance, and urinary excretion of a 1 -microglobulin, ß 2 -microglobulin, albumin and N-acetyl-ß-D-glucosaminidase. Plasma glutathione peroxidase activity appeared significantly reduced in most of the renal diseases considered, and showed a significant correlation with most of the renal function indices. Linear discriminant analysis showed that the set of indices composed of plasma glutathione peroxidase activity, serum creatinine and creatinine clearance allowed the best classification of renal diseases. During treatment with the nephrotoxic aminoglycoside, tobramycin, plasma glutathione peroxidase activity showed an early and progressive decrease. We suggest the measurement of plasma glutathione peroxidase activity äs an adjunctive index for the assessment of kidney alterations.

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We postulate that lower than expected PON1 enzyme activity within specific genotypes might explain the reported association between R and L alleles and the risk of developing AIS.