Chronic kidney disease (CKD) is a common disease both in dogs and cats. The prevalence of this condition has been reported to be 0.5-7% in dogs and 1.6-20% in cats¹, with a marked increase in prevalence with age. There are multiple etiologies for chronic kidney disease (both familial and acquired), but in the majority of cases the etiology is unknown. The International Renal Interest Society (IRIS, www.iris-kidney.com) has developed a staging method of the disease (from stage I to stage IV). The staging of the disease facilitates communications and treatment. Staging is based initially on fasting plasma creatinine, assessed on at least two occasions in the stable patient. The patient is then substaged based on proteinuria and systemic blood pressure.

Dietary Management

Nutrition is a very important treatment tool in animals with CKD. There are studies showing that commercial diets formulated for kidney disease prolong survival time and improve laboratory values in both dogs^2,3 and cats^4,5.

The main goal of nutritional management in any patient is to provide enough energy and nutrients. Additional goals in these patients are to minimize electrolyte and acid-base imbalances, improve quality of life by reducing clinical signs (especially in stages III-IV) and slow down progression of the disease (in particular in stage I and stage II). The main strategies to achieve these goals are summarized below.

1. Energy

Animals with kidney disease (especially in IRIS stage III and IV) classically show a waxing and waning appetite. Inadequate energy intake will result in muscle wasting, malnutrition, and increase in azotemia. Diets formulated for CKD are high in energy density and are usually high in fat (>30% fat on a metabolizable energy (ME) basis or > 3.5 g per 100 kcal). Fat not only provides energy density, it also provides palatability.

If the patient will not eat any of the many commercial diets for CKD, a veterinary nutritionist can formulate a home cooked diet. However, in some cases, assisted feeding may be necessary. The use of esophageal and gastrostomy feeding tubes allows feeding appropriate amounts of the appropriate diet. A feeding tube is very well tolerated, and is also an easy route to provide water and medications.

2. Phosphorus

Phosphorus excretion is impaired in CKD, resulting in increased serum phosphorus concentrations and renal secondary hyperparathyroidism, which has a number of negative effects, including soft tissue mineralization of the kidneys. There is evidence that dietary phosphorus restriction slows down progression of the disease in both cats⁶ and dogs⁷, and it should be instituted as soon as CKD is diagnosed. The IRIS society gives guidelines regarding the desired range of serum phosphorus concentration in each stage. As the disease progresses towards stage IV it becomes harder to control serum phosphorus with only diet and phosphate binders will be necessary. Therapeutic diets for CKD in the US provide approximately 0.4-1.1 g/1000 kcal (in dogs) and 0.8-1.2 g/1000 kcal in cats. The minimum requirement according to AAFCO (Association of American Feed Control Officials) is 1.4 g phosphorus/1000 kcal for dogs and 1.2 g/1000 for cats.

3. Protein

Protein should be restricted to minimize azotemia and decrease clinical signs, especially in later stages of CKD. Excessive restriction can result in protein malnutrition and muscle wasting. For this reason, high quality protein sources are used in therapeutic diets for CKD. Different therapeutic diets have different degrees of protein restriction, and the choice of diet should be made for the individual patient. There is not a consensus on when to institute protein restriction.

The effect of protein restriction in progression of CKD is still very controversial.^8,9 In proteinuric animals, protein loss through the glomeruli is considered to be damaging to the tubules (and result in progression of the disease), and protein restriction may help prevent further damage.^10,11

4. Sodium

Therapeutic diets have a decreased concentration of sodium to help prevent systemic and glomerular hypertension due to volume expansion, although clinical evidence of its usefulness is lacking. Sodium restriction can also have downfalls such as loss of palatability, dehydration, and activation of the rennin-angiotensin-aldosterone system.¹² Renal diets provide less sodium than maintenance diets (<1 g/1000 kcal), but are still above minimum requirements.¹³

5. Potassium

It is common to see hypokalemia in CKD, especially in cats, which can result from increased renal losses, acidosis, and decreased food intake.¹² However, hyperkalemia can also be seen.¹⁴ Some medications, like enalapril (commonly used in proteinuric kidney disease), are potassium sparing and can contribute to hyperkalemia.

The potassium status should be assessed individually in each patient. If potassium restriction is needed, clinicians should compare the potassium levels of the therapeutic diets available and choose the lowest potassium diet. If hyperkalemia is still present, a home cooked diet formulated by a veterinary nutritionist will be necessary.

6. B Vitamins

Animals with CKD are polyuric and their B vitamin losses are thus increased. Therapeutic diets have added levels of these vitamins to avoid deficiencies.

7. Acid-Base

Due to the important role of the kidney in controlling acid-base balance, these patients are prone to acidosis. Acidosis promotes hypokalemia, bone pathology, and muscle mass loss.¹² Commercial therapeutic diets for kidney disease are alkalinizing to reduce the acid load of the body. This is difficult to replicate with home cooked diets, since the alkalinizing potential of a complex recipe cannot be known beforehand.

8. Omega 3

Long chain omega 3 polyunsaturated fatty acids (PUFA) from marine fish oil (rich in the fatty acids EPA and DHA) have been shown to slow down progression in experimental kidney disease in dogs, which is attributed to their anti-inflammatory effects.^15,16 Similar evidence is still lacking in feline CKD. The efficacy of the vegetable omega 3 PUFA precursor, alpha-linolenic acid (ALA, abundant in flaxseed oil), has not been demonstrated. Conversion of ALA to EPA and DHA is not very good in cats and dogs (17), so an equally beneficial effect cannot be attributed to ALA. Not all commercial therapeutic diets have fish oil in their formula.

In summary, there is evidence that dietary modification can slow down progression of CKD and help manage clinical signs. There are a number of commercial therapeutic diets formulated with most of the strategies described above, and they all differ in their level of protein, phosphorus, potassium, sodium, and omega 3 fatty acids. These differences will help choose the diet most appropriate for the individual patient. Home cooked diets can be formulated mimicking these strategies, and can be useful in animals that do not find commercial diets palatable, in hyperkalemic patients, and in patients with comorbidities that necessitate fat restriction (such as pancreatitis).

References

1.  Polzin et al. Chronic kidney disease. In: Textbook of Veterinary Internal Medicine. Ettinger SJ and Feldman EC (eds), 2005; 1756-1785.

2.  Leibetseder JL, Neufeld KW. J Nutr. 1991;121:S145-9.

3.  Jacob F, et al. J Am Vet Med Assoc. 2002; 220:1163-70.

4.  Elliott J, et al. J Small Anim Pract. 2000; 41:235-42.

5.  Ross SJ, et al. J Am Vet Med Assoc 2006; 229:949-957.

6.  Ross LA, et al. Am J Vet Res 1982; 43:1023-1026.

7.  Brown SA, et al. J Am Soc Nephrol. 1991 1:1169-79.

8.  Adams LG, et al. Am J Vet Res 1993; 54:1653-1662.

9.  Finco DR, et al. Am J Vet Res 1998; 59:575-582.

10. Adams LG, et al. J Vet Intern Med 1990; 4:125 (abstract).

11. Burkholder WJ, et al. J Vet Intern Med. 2004;18(2):165-75.

12. Elliott DA. Vet Clin North Am Small Anim Pract. 2006; 36:1377-84.

13. National Research Council. Nutrient Requirements of Dogs and Cats. Washington, D.C.: National Academy Press, 2006.14. Cowgill

14. Brown SA, et al. J Lab Clin Med. 1998 May;131(5):447-55.

15. Brown SA, et al. J Lab Clin Med. 2000 Mar;135(3):275-86.

16. Bauer JE. J Am Vet Med Assoc. 2007; 231:1657-61.