Vitamin E therapy in IgA nephropathy: a double-blind, placebo-controlled study

James C. M. Chan1,2,3, John D. Mahan4, Howard Trachtman5, Jon Scheinman6, Joseph T. Flynn7,8, Uri S. Alon9, Marc B. Lande10, Robert A. Weiss11, Edward P. Norkus12
1The Barbara Bush Children’s Hospital, Maine Medical Center, Portland, USA
2Virginia Commonwealth University, Richmond, USA
3University of Vermont College of Medicine, Burlington, USA
4Ohio State University, Columbus, USA
5Long Island Jewish Hospital, New Hyde Park, USA
6University of Kansas, Kansas City, USA
7University of Michigan, Ann Arbor, USA
8Montefiore Medical Center, Albert Einstein College of Medicine, Bronx, USA
9Mercy Children’s Hospital, Kansas City, USA
10University of Rochester, Rochester, USA
11New York Medical College, Valhalla, USA
12Our Lady of Mercy Medical Center, Bronx, USA

Tóm tắt

IgA nephropathy is the world's most common primary glomerulonephropathy. Recent evidence in a rat model implicated excessive production of oxygen-free radicals in the pathogenesis and suggested that vitamin E-treatment ameliorated progression. We studied this antioxidant therapy on the glomerular filtration rate (GFR), proteinuria and hematuria in biopsy-proven IgA nephropathy in children. The duration of treatment or placebo was 2 years, with vitamin E treatment consisting of 400 IU/day in children weighing <30 kg, and twice that dose for those >30 kg. We measured GFR at entry, midpoint and exit. At baseline and at 4-month intervals after randomization, urinary protein/creatinine ratios and urinalysis were examined. The mixed model procedure with log transformation was used in data analysis to test treatment difference as well as the potential time effect. Fifty-five patients were randomized and 38 completed at least 1 year of follow-up. At entry, the clinical characteristics were not different between the treatment and placebo groups. There was a trend toward better preservation of GFR in vitamin E-treated versus placebo patients, 127±50 vs. 112±31 ml/min/1.73 m2, respectively (P=0.09). The urinary protein/creatinine ratio was significantly lower in the vitamin E-treated group vs. placebo; 0.24±0.38 vs. 0.61±1.37 (P<0.013). However, there was no difference in the prevalence of hematuria between the groups. Vitamin E treatment in our study patients was associated with significantly lower proteinuria, but no effect on hematuria. While there was a trend toward stabilization of GFR in the vitamin E-treated patients, long-term treatment and follow-up are needed to determine whether antioxidant therapy is associated with preservation of renal function in IgA nephropathy.

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