Oxidative stress in children with kidney disease

Kılıç

Clinical Laboratory Analysis

et al. 2010

It is well known that antioxidants and reactive oxygen species play an important role in carcinogenesis. In this study, we attempted to evaluate antioxidant enzyme activities and lipid peroxidation levels in cancerous bladder tissue and to determine their relationship with bacterial infection. Bacterial culture was made from all urine samples using Blood and Eosin Methylene Blue agars for checking the presence of bacterial infections. We measured thiobarbituric acid reactive substances (TBARs) and activities of xanthine oxidase (XO), superoxide dismutase (SOD), glutathione peroxidase (GSH-PX), and catalase (CAT) in cancerous tissues of 25 bladder cancer patients, in noncancerous adjacent bladder tissues of 13 out of these 25 patients, and in control bladder tissues of 15 patients with a non-neoplastic genitourinary disease. TBARs levels increased and XO, SOD, GSH-PX, and CAT activities decreased significantly in cancerous bladder tissues. TBARS, XO, and SOD levels were not significantly different between noncancerous adjacent tissue and control bladder tissue. Statistically significantly lower GSH-PX and higher CAT activities were observed in noncancerous adjacent bladder tissue compared with cancerous tissue. GSH-PX level of tumor tissue was correlated significantly with tumor grade (r=-0.425, P=0.034). Results suggested that pathway activity of free radicals were accelerated in the cancerous human bladder tissues via increased TBARs levels and decreased enzyme activities of XO, SOD, GSH-PX, and CAT, which implicated a severe exposure of cancerous tissues to oxidative stress.

Section: Discussionmentioning

confidence: 99%

Lipid peroxidation and antioxidant enzyme activities in cancerous bladder tissue and their relation with bacterial infection: a controlled clinical study

Kılıç

Clinical Laboratory Analysis

et al. 2010

“…In addition, similar to adults, AGE levels are higher in children with CKD and ESKD [20]. Finally, oxidative stress, assessed by lipid peroxidation, is upregulated in children with CKD; interestingly, this enhanced oxidation stimulates antioxidant activity (as assessed by serum catalase activity), which may reflect a compensatory mechanism [21].…”

Section: Mediators Of Inflammation In Children With Ckd or Eskdmentioning

confidence: 94%

Inflammation in chronic kidney disease: role in the progression of renal and cardiovascular disease

2009

Inflammation is the response of the vasculature or tissues to various stimuli. An acute and chronic proinflammatory state exists in patients with chronic kidney disease (CKD), contributing substantially to morbidity and mortality. There are many mediators of inflammation in adults with CKD and end-stage kidney disease (ESKD), including hypoalbuminemia/malnutrition, atherosclerosis, advanced oxidation protein products, the peroxisome proliferators-activated receptor, leptin, the thiobarbituric acid reactive system, asymmetric dimethyl arginine, iron, fetuin-A, and cytokines. Inflammation contributes to the progression of CKD by inducing the release of cytokines and the increased production and activity of adhesion molecules, which together contribute to T cell adhesion and migration into the interstitium, subsequently attracting pro-fibrotic factors. Inflammation in CKD also causes mortality from cardiovascular disease by contributing to the development of vascular calcifications and endothelial dysfunction. Similar to the situation in adults, cardiovascular disease in pediatric CKD is linked to inflammation: abnormal left ventricular wall geometry is positively associated with markers of inflammation. This review focuses on traditional and novel mediators of inflammation in CKD and ESKD, and the deleterious effect inflammation has on the progression of renal and cardiovascular disease.

“…[21] In another study, the concentration of MDA has been found to be increased four-fold and antioxidant enzyme catalase activity decreased 2.5-fold in seven children with glomerulonephritis in comparison to 13 healthy subjects. [12] However, neither of the above studies had investigated oxidative stress in remission phase of AGN, as we did in the present study.…”

Section: Discussionmentioning

confidence: 62%

“…[1][2][3] Although renal experimental studies on oxidative injury have been carried out in glomerular diseases and vasculitis, [4][5][6][7][8][9] oxidative stress has not been adequately evaluated in children with acute glomerulonephritis (AGN), and clinical investigations on this issue are scarce. [10][11][12] Acute glomerulonephritis is an inflammatory and proliferative glomerular disease that is generally triggered by an infectious agent, such as group A beta hemolytic streptococci. Histologically, AGN is characterized by marked proliferation of mesangial and endothelial cells in glomerulus, together with infiltration by hematogenous cells, most notably neutrophils.…”

Section: Introductionmentioning

confidence: 99%

“…[3] Some studies have shown decreased antioxidant enzyme activities of erythrocytes and increased plasma MDA levels in acute stage of acute poststreptococcal GN compared to healthy controls. [10][11][12] However, in previous studies, oxidative stress has been measured only at the acute stage of the disease, and an evaluation of the same patients at follow-up period has never been performed. Furthermore, although AGN patients had been included in previous studies for which the study groups consisted of miscellaneous renal diseases, [10,12] their numbers have been few (i.e., seven or eight).…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Oxidative Stress in Children with Acute Glomerulonephritis

et al. 2008

Background. Oxidative stress has not been adequately investigated in acute glomerulonephritis (AGN); therefore, we aimed to evaluate the oxidative stress (OS) status in children with AGN both at acute and remission stages. Patients and methods. Seventeen children (mean ± SEM, age 9.0 ± 0.5 years) with AGN and 17 healthy controls were included. In addition to routine laboratory investigations, two blood samples were obtained from patients, at admission and after 6-10 weeks, to measure erythrocyte superoxide dismutase (SOD) activity and plasma malondialdehyde (MDA) level. Results. Significantly elevated MDA levels (5.11 ± 0.28 vs. 3.15 ± 0.25 nmol/mL; p < 0.001) were found in acute stage of AGN compared with the controls; however there was no significant difference in SOD activities (3732 ± 193 vs. 4035 ± 142 U/gHb; p > 0.05) between acute stage-AGN and control subjects. Significantly elevated SOD activities (3985 ± 195 U/gHb, p = 0.034) and decreased MDA levels (4.01 ± 0.38 nmol/mL, p = 0.001) were found at remission stage when compared with the acute stage. MDA levels and SOD activities of remission phase were similar to those of controls (p > 0.05). A significantly positive correlation was found between MDA levels and SOD activities in remission period (r = 0.654, p = 0.004). Patients with and without impaired renal functions had similar MDA levels and SOD activities (p >0.05). No significant correlation was found between glomerular filtration rates (GFR) and MDA levels (p > 0.05) and between GFR and SOD (p > 0.05) activities in acute stage-AGN. Conclusions. Oxidative stress may play important role in the pathogenesis of AGN and not be correlated with renal functions. Further research is needed to determine magnitude of OS and indications for antioxidants in other glomerulopathies.