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J Am Soc Nephrol 10:1772-1777, 1999
© 1999 American Society of Nephrology


REGULAR ARTICLES

The Long-Term Outcome of Patients with IgA Nephropathy Treated with Fish Oil in a Controlled Trial

JAMES V. DONADIO, JR.*, JOSEPH P. GRANDE*,{dagger}, ERIK J. BERGSTRALH{ddagger}, RICHARD A. DART§, TIMOTHY S. LARSON*, DOROTHY C. SPENCER* and THE MAYO NEPHROLOGY COLLABORATIVE GROUP,a

* Division of Nephrology, Department of Internal Medicine, Mayo Clinic & Foundation, Rochester, Minnesota
{dagger} Division of Anatomic Pathology, Department of Laboratory Medicine and Pathology, Mayo Clinic & Foundation, Rochester, Minnesota
{ddagger} Section of Biostatistics, Mayo Clinic & Foundation, Rochester, Minnesota
§ Department of Hypertension and Nephrology, Marshfield Clinic, Marshfield, Wisconsin.

Correspondence to Dr. James V. Donadio, Jr., Mayo Foundation, 200 First Street SW, Rochester, MN 55905. Phone: 507-266-1047; Fax: 507-266-7891; E-mail: donadio.james{at}mayo.edu

Abstract

Abstract. It was reported previously that dietary fish oil supplementation retarded the progression of renal disease in patients with IgA nephropathy in a multicenter, placebo-controlled, randomized, 2-yr clinical trial. The aim of this study was to determine the long-term influence of fish oil treatment on renal progression in observations on the study cohort of 106 patients extending beyond the 2-yr trial. Renal function was assessed by serial serum creatinine and 24-h urine protein measurements. Vital, end-stage renal disease (ESRD), and BP status and treatment beyond completion of the 2-yr trial were determined. As in the trial, the primary end point was an increase of 50% or more in the serum creatinine, and the secondary end point was ESRD. After a mean follow-up of 6.4 yr, 46 patients—17 in the fish oil group versus 29 in the placebo group—reached the primary end point (P = 0.002), and 27 patients—eight in the fish oil group versus 19 in the placebo group—developed ESRD (P = 0.009). At the end of the 2-yr trial, 75 patients (45 fish oil, 30 placebo) remained at risk for the primary end point. This is also when the double-blind part of the trial ended, allowing physicians to stop supplements, switch original placebo-assigned patients to fish oil, and continue fish oil in original fish oil-assigned patients. A significantly greater number of nonsupplemented placebo patients developed the primary end point (P = 0.02) and ESRD (P = 0.003) compared with long-term supplemented fish oil patients. Conversely, more fish oil-supplemented patients had stable renal function than nonsupplemented patients (P = 0.02). By intention, BP control, primarily treated with angiotensin-converting enzyme inhibition, was equal in the fish oil and placebo groups. Proteinuria was modestly reduced in both groups. It is concluded that early and prolonged treatment with fish oil slows renal progression for high-risk patients with IgA nephropathy.




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