Abstract
Introduction and Aims: Chronic kidney disease (CKD) is a major risk factor of cardiovascular disease and mortality in both the general population and post-myocardial patients. Kidney function gradually decreases with age (±1 ml/min/y), but in patients with a myocardial infarction (MI) this deterioration is accelerated (±2 ml/min/y). Epidemiological and experimental studies suggest that n-3 fatty acids supplementation may prevent or slow the decline of kidney function. We examined the effect of the marine n-3 fatty acids eicosapentaenoic acid (EPA) and docosahexaenoic (DHA) and of the plant-derived alpha-linolenic acid (ALA) on the decline of kidney function among patients who have had a first myocardial infaction.
Methods: In a secondary analysis of the randomized, double blind, placebo-controlled Alpha Omega Trial, 2426 of 4937 (49%) patients (aged 60-80y; 79% men) were included of whom kidney function was measured both at baseline and at 41 months of follow-up. Margarine spreads were used to deliver 400 mg EPA-DHA/d, 2g ALA/d, both EPA-DHA and ALA, or a placebo for 40 months. We measured at baseline and end of follow-up both serum creatinine and Cystatin-C and calculated the estimated GFR (eGFR) from the CKD Epidemiology Collaboration (CKD-EPI) equations. Baseline characteristics were compared among the four treatment groups using ANOVA. The decline of kidney function in the three treatment groups ALA, EPA-DHA and EPA-DHA plus ALA were compared to the placebo group.
Results: The 4 randomly assigned groups did not differ in baseline characteristics. Supplementation of ALA, EPA-DHA, EPA and DHA increased plasma cholesteryl ester concentrations of ALA, EPA, and DHA. At baseline kidney function did not differ between the four groups, mean (SD) creatinine and cystatin-C based eGFR were 76 (20) ml/min/1.73m2 and 80 (19) ml/min/1.73m2, respectively. During 41 months of follow-up the yearly decline of creatinine and cystatin-C based eGFR (SE) were in the placebo group (background): -2.28 (SE 0.20) and -1.31 (SE 0.12) ml/min/1.73m2/y, respectively. In comparison to the placebo group the mean difference (SE) of the yearly decline of creatinine and cystatine-C based eGFR (SE) were in the ALA supplementation group 0.05 (SE 0.28, P=0.86) and 0.23 (SE 0.18, P=0.20), in the EPA-DHA group 0.56 (SE 0.29, P=0.058) and 0.33 (SE 0.18, P=0.060) and in the EPA-DHA plus ALA group 0.24 (SE 0.29, P=0.40) and 0.28 (SE 0.18, P=0.10; Figure 1). Decline of kidney function (with error bars indicating SE) after 41 months, according to study group. P-value by three independent samples t-tests compared to the placebo group.
Conclusions: In patients who had experienced a MI, low-dose supplementation with n-3 fatty acids did not statistically significantly reduce the decline in kidney function. However, there was a trend for EPA-DHA supplementation to slow down the decline of kidney function. These results should be confirmed in a study supplementing with higher doses of n-3 fatty acids.
Methods: In a secondary analysis of the randomized, double blind, placebo-controlled Alpha Omega Trial, 2426 of 4937 (49%) patients (aged 60-80y; 79% men) were included of whom kidney function was measured both at baseline and at 41 months of follow-up. Margarine spreads were used to deliver 400 mg EPA-DHA/d, 2g ALA/d, both EPA-DHA and ALA, or a placebo for 40 months. We measured at baseline and end of follow-up both serum creatinine and Cystatin-C and calculated the estimated GFR (eGFR) from the CKD Epidemiology Collaboration (CKD-EPI) equations. Baseline characteristics were compared among the four treatment groups using ANOVA. The decline of kidney function in the three treatment groups ALA, EPA-DHA and EPA-DHA plus ALA were compared to the placebo group.
Results: The 4 randomly assigned groups did not differ in baseline characteristics. Supplementation of ALA, EPA-DHA, EPA and DHA increased plasma cholesteryl ester concentrations of ALA, EPA, and DHA. At baseline kidney function did not differ between the four groups, mean (SD) creatinine and cystatin-C based eGFR were 76 (20) ml/min/1.73m2 and 80 (19) ml/min/1.73m2, respectively. During 41 months of follow-up the yearly decline of creatinine and cystatin-C based eGFR (SE) were in the placebo group (background): -2.28 (SE 0.20) and -1.31 (SE 0.12) ml/min/1.73m2/y, respectively. In comparison to the placebo group the mean difference (SE) of the yearly decline of creatinine and cystatine-C based eGFR (SE) were in the ALA supplementation group 0.05 (SE 0.28, P=0.86) and 0.23 (SE 0.18, P=0.20), in the EPA-DHA group 0.56 (SE 0.29, P=0.058) and 0.33 (SE 0.18, P=0.060) and in the EPA-DHA plus ALA group 0.24 (SE 0.29, P=0.40) and 0.28 (SE 0.18, P=0.10; Figure 1). Decline of kidney function (with error bars indicating SE) after 41 months, according to study group. P-value by three independent samples t-tests compared to the placebo group.
Conclusions: In patients who had experienced a MI, low-dose supplementation with n-3 fatty acids did not statistically significantly reduce the decline in kidney function. However, there was a trend for EPA-DHA supplementation to slow down the decline of kidney function. These results should be confirmed in a study supplementing with higher doses of n-3 fatty acids.
| Original language | English |
|---|---|
| Pages (from-to) | ii64-ii64 |
| Journal | Nephrology Dialysis Transplantation |
| Volume | 27 |
| Issue number | Suppl. 2 |
| DOIs | |
| Publication status | Published - May 2012 |
