The effect of alpha-tocopherol on the oxidative stress and antioxidants in idiopathic IgA nephropathy.
OBJECTIVE
Nearly 25% of IgA nephropathy patients progress to end-stage renal disease over a 20-25 year follow-up period. IgA containing immune complex stimulates oxygen free radical production by mesangial cells in vitro, which may mediate glomerular injury in this disorder. Therefore, we studied whether dietary supplementation with the antioxidant agent, vitamin E, attenuates renal damage in patients with IgA nephropathy.


METHODS
Twenty-eight patients with idiopathic IgA nephropathy were supplemented with vitamin E 400 mg/day for 6 months. Antioxidant enzymes, glutathione, plasma malondialdehyde (MDA), and renal function were studied after 3 and 6 months therapy.


RESULTS
The result of the study showed high plasma MDA and significant reduction after therapy (1.15 +/- 0.45 VS 0.86 +/- 0.30 microM, p < 0.0001). The RBC vitamin E was also elevated statistically significantly (5.07 +/- 2.42 VS 15.70 +/- 3.37 microM, p < 0.001). Glutathione peroxidase activities were decreased (38.52 +/- 15.53 VS 23.97 +/- 7.63 U/gHb, p < 0.001). Glutathione was also decreased (44.80 +/- 9.70 VS 32.45 +/- 6.74 mg/dl, p < 0.05) but there were no changes in red cell catalase and superoxide dismutase activities. Creatinine clearance, proteinuria, urine N-acetyl glucosaminidase and beta2-microglobulin also showed no improvement.


CONCLUSIONS
Our data demonstrated the particular group of IgA nephropathy patients with low vitamin E level and high oxidative stress had significant reduction of oxidative stress after vitamin E therapy.
Ong-ajyooth
Leena
L
Renal Division, Department of Medicine, Faculty of Medicine Siriraj Hospital, Mahidol University, Bangkok, Thailand.
Ong-ajyooth
Sompong
S
Parichatikanond
Paisal
P
D000975:Antioxidants / Q000494:pharmacology* / Q000627:therapeutic use; D016022:Case-Control Studies; D005260:Female; D005922:Glomerulonephritis, IGA / Q000188:drug therapy*; D005979:Glutathione Peroxidase / Q000187:drug effects; D006801:Humans; D008297:Male; D008315:Malondialdehyde / Q000097:blood; D018384:Oxidative Stress / Q000502:physiology*; D011446:Prospective Studies; D013997:Time Factors; D024502:alpha-Tocopherol / Q000494:pharmacology* / Q000627:therapeutic use
D000975:Antioxidants; D008315:Malondialdehyde; D005979:Glutathione Peroxidase; D024502:alpha-Tocopherol