Diet and Renal Disease: Myths and Realities
World Small Animal Veterinary Association World Congress Proceedings, 2003
Scott A. Brown, VMD, PhD, DACVIM (Internal Medicine)
College of Veterinary Medicine, University of Georgia
Athens, GA, USA

Nutrition plays a central role in the management of renal diseases in veterinary medicine. Most of the clinically observable abnormalities produced by the disruption of renal function are influenced by dietary intake of calories, phosphorus, sodium, potassium, protein, or acid load. Further, the kidney is susceptible to self-perpetuating injury, an inherent property of this organ, and the extent of this injury may be modified by adjustments in dietary intake of phosphorus and polyunsaturated fatty acids. The response of each animal with renal insufficiency to the disease and to nutritional intervention will vary dramatically and individualized therapy is required; the only constant nutritional characteristic of renal insufficiency is inappetance and loss of body weight. Successful interventional nutrition must take all of these principles into account.

For animals with chronic renal insufficiency, the ideal goals of interventional nutritional management are to maximize the quality and longevity of life by ensuring adequate intake of energy, limiting the extent of the clinical manifestations of the disease, and slowing the rate of progression of renal disease. Although our understanding of dietary considerations for dogs and cats with diseases of the kidney is limited, general recommendations can be made for dietary intervention in chronic and acute renal insufficiency. There are three guiding principles of nutritional intervention in renal disease:

Principle 1: Abnormalities produced by disruption of renal function are influenced by dietary intake. The kidney is an organ of homeostasis. Many important abnormalities may occur as a result of failure of renal homeostatic mechanisms. If these derangements in body homeostasis are severe enough to produce clinical signs, the condition is referred to as uremia. However, some abnormalities are observed during early renal disease, even though clinical signs may not be initially apparent. Dietary intake affects the magnitude of the complications of renal disease. For example, ingestion of a diet with a moderate phosphorus content (0.9% phosphorus on a dry weight basis) will have few, if any, consequences in a normal animal; in contrast, in animals with chronic renal insufficiency this level of dietary phosphorus intake worsens hyperphosphatemia and hyperparathyroidism and leads to progressive declines in renal function.3

Principle 2: The kidney is susceptible to self-perpetuating injury and the extent of this injury may be modified by adjustments in dietary intake. In animals with chronic renal disease, the kidney is susceptible to injury from two general mechanisms of renotoxicity caused by (i) maladaptations and (ii) the complications of renal disease. Maladaptations occur because of the nature of the organ's response to disease. For example, in chronic kidney disease there are adaptive changes are an increase in the glomerular filtration rate of the single nephron, an increase in hydrostatic pressure within the glomerular capillaries, and an increase in glomerular size. These changes are referred to as glomerular hyperfiltration, hypertension, and hypertrophy, respectively.

These glomerular functional and structural changes appear to be maladaptive, leading to further renal injury.

Some of the abnormalities attributable to a disruption of renal homeostatic mechanisms in animals with renal disease--such as systemic hypertension and hyperphosphatemia--may also damage the kidney, further contributing to a vicious cycle of inherent, progressive renal injury.

Principle 3: The responses of animals with renal insufficiency to the disease and to interventional nutrition will vary dramatically and individualized therapy is required; the only constant feature of nutrition in renal disease is inappetance and loss of body weight. The dietary composition appropriate for one animal with renal insufficiency may prove intolerable to another.

Thus, dietary modifications must be made on the basis of objective clinical data and the response of the animal must be evaluated. It is particularly inappropriate to rely solely upon a diet that the animal finds unpalatable.

Role of dietary lipids in progression: Dietary polyunsaturated fatty acids (PUFA) may alter the long-term course of renal injury. Dogs with spontaneous renal diseases exhibit alterations in vasoactive urinary eicosanoid excretion; these changes were interpreted to support a role for glomerular hyperfiltration in progressive canine renal injury. Interestingly, short-term studies in dogs with naturally occurring renal disease indicate that supplementation with omega-6 PUFA led to increased glomerular filtration rate. However, in studies of induced renal disease, the long-term effects of similar supplementation (15% safflower oil; providing approximately 12% omega-6 PUFA on a dry matter basis) were deleterious: elevated intraglomerular pressure, increased renal eicosanoid series-2 excretion, and hastened progression of renal failure. It appears that the increase in glomerular pressure caused by omega-6 PUFA supplementation may be of short-term benefit as a GFR-enhancing response in dogs with spontaneous renal disease.

However, on the basis of studies in induced renal insufficiency, glomerular hypertension caused by omega-6 PUFA is detrimental in the long run.

In contrast, dietary supplementation with 15% menhaden oil (providing approximately 4% omega-3 PUFA on a dry matter basis) lowered glomerular pressure, decreased renal eicosanoid series-2 excretion, and provided renoprotection. Dietary supplementation with lesser amounts of menhaden fish oil (providing approximately 0.6% omega-3 PUFA on a dry weight basis) reduced the dietary omega-6:omega-3 PUFA ratio from 50:1 to 5:1 and lowered glomerular pressure and altered urinary excretion of eicosanoids. This latter dietary maneuver is likely to be of long-term benefit to delay progression of renal injury, though it remains to be established in dogs with spontaneous renal insufficiency.

Recommendations for dietary lipid intake: In dog with chronic renal disease, dietary supplementation with omega-6 PUFA may increase GFR in the short-term and dietary supplementation with omega-3 PUFA may offer renoprotection in the long-term. Since these PUFA act competitively, it is not possible to achieve both affects simultaneously in the same animal. At present, there is no clear rationale for which PUFA to utilize in chronic renal disease. One alternative is to ignore the contribution of PUFA to GFR and renal disease in dogs. Alternatively, until further information is available, another approach would be to utilize omega-3 PUFA supplementation for dogs with mild azotemia (serum creatinine elevated but < 4.0 mg/dl). In more severe canine renal failure (serum creatinine > 4 mg/dl), the GFR-enhancing effects of omega-6 PUFA may be preferred. Safflower or corn oil are rich in n-6 PUFA and are generally readily available; omega-3 supplements may be procured from health food stores in the USA. On the basis of studies in induced renal insufficiency, dietary supplementation with approximately 0.5-1.0 gm of omega-3 PUFA/100 kcal of diet or 0.5-1.0 ml of safflower oil (omega-6 source)/100 kcal of diet might provide a reasonable starting dose for commercially available preparations. Some commercially available preparations are supplemented with PUFA and further supplementation should be done with caution. Supplementation with PUFA alters a variety of nonrenal tissues, including immunologic and hemostatic functions. Since PUFA within cell membranes are subject to oxidative damage, the addition of PUFA to the diet increases an animal's antioxidant (vitamin E) requirements; supplementation with vitamin E should be considered (minimum of 1.1 units of supplemental vitamin E/gm of added oil). The PUFA within a diet may also be oxidized. Although petfood manufacturers generally add antioxidants to diets, oils intended for addition to canine diets should be stored in the refrigerator and used in a timely manner.

Caution is urged, as the role of dietary PUFA supplementation in dogs with spontaneous renal insufficiency remains to be clearly defined. No information is available on PUFA supplementation in cats with renal insufficiency.


1.  Polzin D, Osborne C, Adams L, et al: Medical management of feline chronic renal insufficiency, in Bonagura JD, Kirk RW (eds): Current Veterinary Therapy XI. Philadelphia, PA, Saunders, 1992, pp 848-853

2.  Hostetter TH, Olson JL, Rennke HG, et al: Hyperfiltration in remnant nephrons: A potentially adverse response to renal ablation. Am J Physiol 241:F85-F92, 1981

3.  Brown SA, Finco DR, Brown CA, et al. Beneficial effects of dietary supplementation with omega-3 polyunsaturated fatty acids in dogs with chronic renal insufficiency. J Lab Clin Med (in press)

4.  Finco DR, Brown SA, Crowell WA, et al: Effects of dietary phosphorus and protein in dogs with chronic renal failure. Am J Vet Res 53:2264-2271,

5.  Ross LA, Finco DR, Crowell WA. Effect of dietary phosphorus restriction of the kidneys of cats with reduced renal mass. Am J Vet Res 43:1023-1026, 1982

6.  Adams L, Polzin DJ, Osborne CA, et al.: Influence of dietary protein/calorie intake on renal morphology and function in cats with 5/6 nephrectomy. Lab Invest 70:347-357, 1994

7.  Finco DR, Brown SA, Brown CA, et al: Protein and calorie effects on progression of induced chronic renal failure in cats. Am J Vet Res 59:575-582, 1998

8.  Bauer J, Crocker R, Markwell P, et al: Dietary N-6 fatty acid supplementation improves ultrafiltration in spontaneous canine chronic renal failure. J Vet Int Med, 11:126, 1997 (abstr)

9.  Brown SA, Brown C, Crowell W, Barsanti J, Finco DR: Effects of dietary fatty acid composition on the course of chronic renal disease in dogs. J Lab Clin Med 131:447-455, 1998.

10. Brown SA, Brown C, Crowell W, Barsanti J, Finco DR: Effect of dietary fatty acid supplementation in early renal insufficiency in dogs. J Lab Clin Med 135:275-286, 2000.

Speaker Information
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Scott A. Brown, VMD, PhD, DACVIM (Internal Medicine)
College of Veterinary Medicine, University of Georgia
Athens, GA, USA

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