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Low-dose fish oil therapy effective in IgA nephropathy

 IgA nephropathy is a fairly common kidney disorder. It is caused by an inflammation (glomerulonephritis) in the network of  small blood vessels called capillaries involved in the filtration of waste products from the blood. Specifically, it manifests itself through the deposit of the antibody immunoglobulin A (IgA) in the mesangial cells, which support the walls of the capillaries. The IgA deposits cause swelling due to inflammation due to lesions to the capillaries interfere with proper filtration of waste products from the blood. IgA nephropathy is more common in men than in women and its incidence peaks between the ages of 16 and 35 years. IgA nephropathy is associated with a gradual decline in kidney function leading to end-stage renal disease within 5 to 25 years of diagnosis in 20-40% of patients. The disease is usually diagnosed after blood or excess protein is observed in the urine. Serum creatinine levels are abnormally high in IgA nephropathy because the kidneys are unable to filter creatinine (a waste byproduct of creatine, a protein that supplies energy for muscle contraction) out of the blood and excrete it in the urine. A doubling in serum creatinine level corresponds to a 50% decline in kidney function. There are no pharmaceutical drugs that will slow down or reverse the progression of IgA nephropathy.

Researchers at the Mayo Clinic previously reported that supplementation with 1.9 grams/day of EPA (eicosapentaenoic acid) plus 1.4 grams/day of DHA (docosahexaenoic acid) is effective in retarding the progression of IgA nephropathy. The researchers have now carried out another clinical trial to determine whether doubling the daily dose of fish oil supplement would be even more effective. Their randomized clinical trial involved 73 patients with biopsy-diagnosed IgA nephropathy. Ten of the patients had quite severe disease as indicated by a baseline serum creatinine level of 3.0-4.9 mg/dL while the remaining 63 patients had moderate disease (serum creatinine between 1.5-2.9 mg/dL). The fish oil supplement used in the trial was supplied by Pronova in Norway (trade name Omacor) in the form of highly purified ethyl esters of EPA and DHA.

At the end of the 2-year study period the serum creatinine level in the low-dose group (1.9 g/day of EPA plus 1.5 g/day of DHA) had increased by 0.08 mg/dL per year while patients in the high-dose group (3.8 g/day of EPA plus 3.0 g/day of DHA) saw an average yearly increase of 0.10 mg/dL. Rapid deterioration in kidney function (creatinine increase of more than 0.5 mg/dL per year) was observed in 70% of the patients with severe disease as compared to only 23% in the group with moderate disease. There was no significant difference in the number of patients in the low and high dose groups who developed end-stage renal disease (ESRD). At the end of 2 years 86% in the low-dose group and 80% in the high-dose group were still free of ESRD. The corresponding numbers after 3 years were 73% and 76%. The 2-year number of about 85% ESRD-free compares to only 63% ESRD-free in a previously investigated placebo group.

The Omacor supplement was generally well-tolerated, but two patients (out of 73) did discontinue their treatment as a result of gastrointestinal intolerance. There were no unfavourable effects on serum lipid profiles (cholesterol levels), hematocrits, peripheral blood leucocytes or platelets. The researchers conclude that low- dose and high-dose fish oil supplementation is equally effective in slowing the progression of IgA nephropathy.
Donadio, JV, et al. A randomized trial of high-dose compared with low-dose omega-3 fatty acids in severe IgA nephropathy. Journal of the American Society of Nephrology, Vol. 12, 2001, pp. 791-99



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