Anti-oxidant status in relation to lipoproteins, leptin and pro-inflammatory cytokines in children with steroid-sensitive nephrotic syndrome.
BACKGROUND
Reactive oxygen species and cytokines are reported to play a role in the proteinuria of nephrotic syndrome. The aim of this study was to investigate indirect evidence of oxidant activity together with leptin, lipoproteins and pro-inflammatory cytokines in children with steroid-sensitive nephrotic syndrome.


METHODS
A total of 40 children with steroid-sensitive nephrotic syndrome (20 with newly onset or relapse comprised group I and 20 in remission while receiving steroids comprised group II) and 20 sex and age matched healthy control children were included. The following indirect parameters of oxidant activity were determined: serum malondialdehyde, erythrocyte superoxide dismutase, catalase and whole-blood-reduced glutathione. Serum leptin, lipids and lipoproteins were also determined.


RESULTS
Similar glutathione, increased malondialdehyde levels and decreased superoxide dismutase and catalase activity were observed in group I patients compared with controls. There was no significant difference in these variables between group I and group II (P >0.05). Tumour necrosis factor-alpha and interleukin-6 concentrations were similar in patients and controls. Concentrations of interleukin-1beta and interleukin-8 were higher in the active phase of nephrotics compared with controls (P <0.05). Significant positive correlations were found between malondialdehyde and interleukin-1beta, interleukin-6, leptin and lipoprotein (a) (P <0.05). There were significant negative correlations between anti-oxidants and leptin, lipoprotein (a) and several cytokines (P <0.05).


CONCLUSIONS
Changes in the concentrations of malondialdehyde, superoxide dismutase, catalase and glutathione are compatible with increased amounts of oxidation in steroid-sensitive nephrotic syndrome. Leptin and pro-inflammatory cytokines may be related to excessive protein permeability in nephrotic syndrome.
Ece
Aydin
A
Department of Paediatrics, Faculty of Medicine, Dicle University, Turkey. aydece@dicle.edu.tr
Atamer
Yildiz
Y
Gürkan
Fuat
F
Bilici
Meki
M
Koçyiğit
Yüksel
Y
D000975:Antioxidants / Q000032:analysis*; D002374:Catalase / Q000097:blood; D002648:Child; D016207:Cytokines / Q000097:blood*; D004912:Erythrocytes / Q000378:metabolism; D005260:Female; D005938:Glucocorticoids / Q000627:therapeutic use*; D005978:Glutathione / Q000097:blood; D006801:Humans; D018836:Inflammation Mediators / Q000097:blood*; D007378:Interleukins / Q000097:blood; D020738:Leptin / Q000097:blood*; D015227:Lipid Peroxidation; D008074:Lipoproteins / Q000097:blood*; D008297:Male; D008315:Malondialdehyde / Q000097:blood; D009404:Nephrotic Syndrome / Q000097:blood* / Q000188:drug therapy; D011241:Prednisone / Q000627:therapeutic use*; D013482:Superoxide Dismutase / Q000097:blood; D014409:Tumor Necrosis Factor-alpha / Q000032:analysis
D000975:Antioxidants; D016207:Cytokines; D005938:Glucocorticoids; D018836:Inflammation Mediators; D007378:Interleukins; D020738:Leptin; D008074:Lipoproteins; D014409:Tumor Necrosis Factor-alpha; D008315:Malondialdehyde; D002374:Catalase; D013482:Superoxide Dismutase; D005978:Glutathione; D011241:Prednisone