Does Dialysis Modality Influence the Oxidative Stress of Uremic Patients?

ArticleinKidney and Blood Pressure Research 35(4):220-5 · January 2012with13 Reads
DOI: 10.1159/000331560 · Source: PubMed
Since peritoneal membrane is more compatible and residual renal function better preserved during peritoneal dialysis, we questioned whether the oxidative burden in chronic kidney disease (CKD) is influenced by dialysis modality. 49 stable CKD patients, 17 on continuous ambulatory peritoneal dialysis (CAPD), 16 on hemodialysis (HD), and 16 non-dialyzed, and 13 healthy subjects were enrolled. Plasma thiobarbituric acid-reactive substances (TBARS; nmol/g protein), serum total antioxidant activity (TAA), total plasma-free thiols (Pt-SH; μmol/g protein), albumin and uric acid were measured by spectrophotometry. Serum residual antioxidant activity (RAA) was calculated. TBARS were higher in HD (78.3 ± 20.3) versus both non-dialyzed (53.1 ± 27.9, p = 0.007) and CAPD groups (58.3 ± 19.8, p = 0.008). Pt-SH was reduced in CKD patients, but showed comparable values between dialysis groups. TAA and RAA were similarly increased in HD and CAPD patients than in the other two groups. Oxidative stress occurs in all CKD patients and worsens as renal function declines. Lipid peroxidation seems more augmented during chronic HD as compared to CAPD, but the plasma antioxidant status did not differ between the investigated dialysis methods. Therefore, dialysis modality appears to influence lipid peroxidation without changing the extracellular antioxidant defense of CKD patients.
    • "Dialysis modality influences oxidative stress marker patterns and magnitude. For example, plasma thiobarbituric acid reactive substances, oxidised LDL, asymmetric dimethylarginine and homocysteine levels have been reported to be higher in HD patients than in PD patients and both modalities have higher levels of these compounds than healthy controls (49,53–55). There are, however, some studies where the difference was in the opposite direction (PD > HD) when markers like homocysteine, plasma hydroperoxides, total antioxidant defence and erythrocyte plasma membrane fluidity were measured (56,57). "
    [Show abstract] [Hide abstract] ABSTRACT: Patients with chronic kidney disease (CKD) have signs of genomic instability and, as a consequence, extensive genetic damage, possibly due to accumulation of uraemic toxins, oxidative stress mediators and other endogenous substances with genotoxic properties. We explored factors associated with the presence and background levels of genetic damage in CKD. A cross-sectional study was performed in 91 CKD patients including pre-dialysis (CKD patients; n = 23) and patients undergoing peritoneal dialysis (PD; n = 33) or haemodialysis (HD; n = 35) and with 61 healthy subjects, divided into two subgroups with the older group being in the age range of the patients, serving as controls. Alkaline comet assay and cytokinesis-block micronucleus assay in peripheral blood lymphocytes were used to determine DNA and chromosome damage, respectively, present in CKD. Markers of oxidative stress [malondialdehyde (MDA), advanced glycation end products (AGEs), thiols, advanced oxidation protein products and 8-hydroxy-2'-deoxyguanosine] and markers of inflammation (C-reactive protein, interleukin-6 and tumour necrosis factor alpha) were also measured. Micronucleus (MN) frequency was significantly higher (P < 0.05) in the CKD group (46±4‰) when compared with the older control (oC) group (27.7±14). A significant increase in MN frequency (P < 0.05) was also seen in PD patients (41.9±14‰) versus the oC group. There was no statistically significant difference for the HD group (29.7±15.6‰; P = NS) versus the oC group. Comet assay data showed a significant increase (P < 0.001) of tail DNA intensity in cells of patients with CKD (15.6±7%) with respect to the total control (TC) group (11±1%). PD patients (14.8±7%) also have a significant increase (P < 0.001) versus the TC group. Again, there was no statistically significant difference for the HD group (12.5±3%) compared with the TC group. Patients with MN values in the upper quartile had increased cholesterol, triglycerides, AGEs and MDA levels and lower albumin levels. Multiple logistic regression analysis showed that male gender, diabetes and treatment modality were independently associated with higher levels of DNA damage. Our results suggest that oxidative stress, diabetes, gender and dialysis modality in CKD patients increased DNA and chromosome damage. To confirm these data, prospective clinical trials need to be performed.
    Full-text · Article · Mar 2013
  • [Show abstract] [Hide abstract] ABSTRACT: Patients on peritoneal dialysis experience inflammation associated with advanced chronic kidney disease and the therapy itself. An important consequence of the inflammation may be acceleration of the rate of decline in residual renal function. The decline in residual renal function has been associated with an increased mortality for patients in this population. Bardoxolone methyl is a synthetic triterpenoid. To date, the effects of bardoxolone methyl on kidney function in humans have been studied in patients with type 2 diabetes mellitus. A large-scale event-driven study of bardoxolone methyl in patients with type 2 diabetes mellitus with stage 4 chronic kidney disease is underway. The safety of bardoxolone methyl has not been evaluated in patients with more advanced (stage 5) chronic kidney disease or patients on dialysis. This report describes a proposed double blind, prospective evaluation of bardoxolone methyl in patients with type 2 diabetes mellitus receiving peritoneal dialysis. In addition to assessing the safety of bardoxolone methyl in this population, the study will evaluate the effect of bardoxolone methyl on residual renal function over 6 months as compared to placebo.
    Full-text · Article · May 2012
  • [Show abstract] [Hide abstract] ABSTRACT: Aim: In chronic kidney disease (CKD) cardiovascular risk is increased. Oxidative stress is strictly involved in the pathophysiology of this enhanced risk as well as leukocytes' activation. To better elucidate these phaenomena we evaluated some parameters of leukocyte activation and oxidative state on fasting blood samples obtained from CKD patients on conservative or hemodialysis (HD) treatment, compared to those obtained from control subjects. Methods: We enrolled 41 patients (25 men and 16 women, mean age 64.7 ± 11.1 years) with CKD and 42 patients (21 men and 21 women, mean age 66.83 ± 14.8 years) with CKD on hemodialysis (HD) treatment. Hemodialyzed patients were evaluated before and after a standard HD session. Leukocyte activation was evaluated by determining plasma elastase and myeloperoxidase level employing ELISA methods. Lipid peroxidation was evaluated as thiobarbituric acid-reactive substances (TBARS), total antioxidant status using spectrophotometry. Results: Elastase was higher in CKD on conservative and on HD treatment and its value increased after the HD session. Myeloperoxidase did not show any variation in CKD on conservative and HD treatment while after HD its value was increased. Lipid peroxidation was increased in CKD on conservative and on HD therapy and its value after dialysis showed no significant variation. Total antioxidant status was increased in CKD on HD treatment and significantly decreased after the HD session; no variation between normal controls and CKD subjects on conservative therapy was observed. Conclusion: Several aspects derive from these data considering the role of oxidative stress in the cardiovascular events that accompany CKD.
    Article · Mar 2013
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