The long-term outcome of patients with IgA nephropathy treated with fish oil in a controlled trial

It was reported previously that dietary fish oil supplementation retarded t he progression of renal disease in patients with IgA nephropathy in a multi center, placebo-controlled, randomized, 2-yr clinical trial. The aim of thi s study was to determine the long-term influence of fish oil treatment on r enal progression in observations on the study cohort of 106 patients extend ing beyond the 2-yr trial. Renal function was assessed by serial serum crea tinine and 24-h urine protein measurements. Vital, end-stage renal disease (ESRD), and BP status and treatment beyond completion of the 2-yr trial wer e 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. Aft er 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 p atients-eight in the fish oil group versus 19 in the placebo group-develope d 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 suppl ements, switch original placebo-assigned patients to fish oil, and continue fish oil in original fish oil-assigned patients, A significantly greater n umber of nonsupplemented placebo patients developed the primary end point ( P = 0.02) and ESRD (P = 0.003) compared with Long-term supplemented fish oi l patients. Conversely, more fish oil-supplemented patients had stable rena l function than nonsupplemented patients (P = 0.02). By intention, BP contr ol, primarily treated with angiotensin-converting enzyme inhibition, was eq ual 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.