Dietary fish oil after renal transplantation
ACP J Club. 1994 Mar-April;120:41. doi:10.7326/ACPJC-1994-120-2-041
van der Heide JJ, Bilo HJ, Donker JM, Wilmink JM, Tegzess JM. Effect of dietary fish oil on renal function and rejection in cyclosporine-treated recipients of renal transplants. N Engl J Med. 1993 Sep 9;329:769-73.
To study the effect of dietary fish oil on renal function, blood pressure (BP), and incidence of acute rejection episodes in patients who had received a first cadaveric kidney transplant.
Randomized controlled trial with 1-year follow-up. The study was blinded for the first 3 months only.
4 university hospitals in the Netherlands.
66 adults (mean age, 45 y; 62% men) who had received a first cadaveric renal transplant. Patients taking nonsteroidal anti-inflammatory drugs, including aspirin, were excluded. Follow-up was 88%.
Patients took cyclosporine and prednisolone. Hypertension was treated with β-blockers and, if necessary, calcium channel blockers. 3 days after receiving their transplant, patients started taking 4 oil capsules, 3 times daily. 33 patients were allocated to receive 6 g of fish oil (30% eicosapentaenoic acid and 20% docosahexaenoic acid with 1 IU of vitamin E per gram as an antioxidant). 33 control patients were assigned to receive 6 grams of coconut oil with vitamin E and fish-oil odor. After 3 months, placebo was stopped but fish oil was continued.
Main Outcome Measures
Biopsy-proven episodes of rejection based on clinical and ultrasound criteria, renal function (glomerular filtration rate and effective renal plasma flow), and mean arterial BP.
At 1 year, compared with patients taking placebo, patients taking fish oil had fewer acute rejection episodes (8 vs. 20; P = 0.029), higher median glomerular filtration rates (53 vs. 40 mL/min per 1.73 m2, P = 0.038), higher effective renal plasma flow (214 vs. 178 mL/min per 1.73 m2, P = 0.023), lower urinary protein excretion (0.2 vs. 2.0 g/24 h; P = 0.008), lower mean number of hospital readmissions (0.4 vs. 1.1; P = 0.023), and lower mean arterial BP (103 vs. 118 mm Hg; P = 0.001), and they required less antihypertensive medication. The groups did not differ for 1-year graft survival, length of hospitalization,cyclosporine dose, postoperative hemorrhage, or other adverse effects.
Patients with renal transplants receiving cyclosporine who took fish oil for 1 year had a lower incidence of acute rejection episodes, better renal function, and lower mean arterial blood pressure than control patients.
Source of funding: Dutch Kidney Foundation.
For article reprint: Dr. H. van der Heide, Renal Transplant Division, Department of Internal Medicine, University Hospital Groningen, Oostersingel 59, 9713 EZ Groningen, the Netherlands. FAX 31-50-6134-74.
Dietary manipulations can alter the composition of cell membrane fatty acids and their attendant metabolites, prostaglandins and other eicosanoids. Mammals cannot desaturate double bonds on fatty acid chains proximal to the ninth carbon from the methyl (omega-9) terminus, creating an essential dietary requirement for these compounds as precursors of cell membrane lipids. Fish oils contain omega-3 fatty acids, and the eicosanoids derived from them tend to be anti-inflammatory, antithrombotic, and vasodilatory (1). Patients prone to acute immunologic rejection take cyclosporine, which causes hypertension and renal vasoconstriction.
Van der Heide and colleagues studied the benefits of fish oil supplementation in the first year after renal transplant, extending earlier research on the effect of omega-3 fatty acids on renal dysfunction, done principally in animal models of immune nephritis and chronic renal failure. Overall graft survival was not improved at 1 year, a result not surprising in the era of potent and directed immunosuppression. Clinicians interested in fish oil supplementation will be heartened by the lack of hemostatic complications reported (2).
The mechanism of the salutary effects reported is not clear. Prostaglandin, leukotriene, and thromboxane levels were not directly measured nor were other factors, such as interleukin-1, tumor necrosis factor, or serum lipids, that have been altered by manipulation of cellular fatty acids in other studies (3). These same elements are speculated to contribute to glomerular hyperfiltration and eventual sclerosis during the final common pathway of renal failure from all causes. Interestingly, protein restriction alone has improved the profile of cell membrane lipids (3), and this along with good BP control, particularly using angiotensin-converting enzyme inhibitors, remains the main intervention in the treatment of chronic renal failure.
Charles T. Lynch, MD
California Pacific Medical Center San Francisco, California, USA