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Encyclopedia of Canine Clinical Nutrition
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Royal Canin Nutritional Information

Author(s):
Elliott D.A. and
Lefebvre H.
In: Encyclopedia of Canine Clinical Nutrition by Pibot P. et al.
Updated:
JUN 03, 2008
Languages:
  • DE
  • EN
  • ES
  • FR
  • IT
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    Royal Canin Nutritional Information

    An adapted diet helps triple the median survival time of dogs with chronic renal disease
    An adapted diet helps triple the median survival time of dogs with chronic renal disease. (© Lanceau).

    Key Points to Remember:

    The Role of Nutrition in the Management and Prevention of Chronic Renal Disease

    Chronic renal disease (CRD) in dogs is often associated with a waxing and waning appetite. Therefore the palatability of the food is a key criterion in the management of CRD.

    When the kidney loses its functional capacity, phosphorus is no longer adequately excreted and the concentration increases in plasma. Ultimately, hyperphosphatemia causes hyperparathyroidism that aggravates CRD. One of the goals of treatment is to normalize the blood phosphate concentration. It has been clearly shown that the dietary restriction of phosphorus slows the progression of renal disease in dogs.

    Supplementation with alkalizing agents such as sodium bicarbonate, calcium carbonate or potassium citrate can prove necessary to combat metabolic acidosis.

    Contrary to a common misconception, the protein content of the food does not have any impact on the progression of renal disease. It is therefore useless to systematically reduce the protein in the diet of an aging dog. Conversely, in dogs with CRD the goal of protein reduction is to reduce the magnitude of uremia. To prevent protein malnutrition, moderate restriction of the order of 35 - 40 g protein/1000 kcal is preferable. Too severe protein reduction could actually have negative effects, by forcing the dog to catabolize its body proteins to meet its needs.

    Energy intake must be sufficient to prevent endogenous protein cata-bolism that leads to malnutrition and aggravated azotemia.

    An increased intake of omega 3 fatty acids (EPA and DHA) helps limit the reduction in glomerular filtration rate.

    Hypokalemia is commonly observed in dogs with renal disease, except in the terminal stage, when hyperkalemia may be observed. Reestablishing a normal serum potassium concentration is essential to the dog's quality of life.

    It has long been recommended to reduce the sodium content in the diets of patients with CRD. However, recent work (see Chapter 7) would appear to show that too low of a sodium content (0.4 - 0.5 mg/1000 kcal) could have a deleterious effect on renal function. Low sodium intake could contribute to glomerular hypertension by increasing the secretion of aldosterone and activating the renin-angiotensin system. These results are yet to be confirmed but they caution against too severe sodium restriction in the diet of patients with CRD.

    Aging dogs generally suffer from renal disease hence it is necessary to enrich the food with antioxidants to help combat free radical production.

    Focus On: Phosphorus

    Etymologically speaking, the word phosphorus means "light-bringing". It was discovered in 1669 by a German alchemist, Hennig Brandt. By evaporating urine and calcifying the residue, he obtained phosphorus in gas form that shone in the dark.

    In the form of phosphates, phosphorus enters into the composition of bone. Eighty-six percent of the phosphorus in the organism is stored in the structure of the skeleton.

    Phosphorus is also incorporated into large molecules such as DNA, RNA and membrane phospholipids. In addition, it is an active constituent of the adenosine tri-phosphate molecule (ATP), which stores the energy living organisms need to function properly.

    The reasons why phosphorus leads to progression of CRD have yet to be determined with certainty. Following the reduction of the renal function, phosphorus accumulates in the blood. The organism responds physiologically by increasing the secretion of parathyroid hormone (PTH). This reponse initially helps maintain the phosphorus within normal thresholds, but also leads to the release of phosphate and calcium from bone reserves.

    In time, even this compensatory response is not enough to reestablish homeostasis. Phosphorus and calcium accumulate, leading to the mineralization of soft tissue. In the kidney, this phenomenon accelerates the loss of functional nephrons. In addition, PTH may act as an uremic toxin, which also aggravates the clinical symptoms and progression of CRD.

    Main biological roles of phosphorus
    Figure 16. Main biological roles of phosphorus.  

    In CRD patients, the goal is therefore to limit the phosphorus content of the food to 0.40 - 0.80 g/1000 kcal. At the same time, the increase in the calcium content also helps reduce the digestive absorption of phosphorus. If such a level does not help normalize the serum phosphate concentration, the use of phosphate binding agents (aluminum hydroxide, calcium carbonate etc.) should be considered.

    While it is vital to limit the phosphorus content in the food, the difficulty lies in the necessity of finding raw ingredients that are low in phosphorus. Animal protein sources traditionally used in dog food are fairly high in phosphorus. For example, there is 1.6 - 2.5% phosphorus on a DMB in dehydrated poultry proteins. This level is dependent on the overall content of remaining mineral matter after sieving. Vegetable protein sources that are lower in phosphate concentration (wheat or corn gluten, soy protein isolate hydrolysate) are an interesting alternative.

    Phosphorus content of several protein sources used in dog food
    Figure 17. Phosphorus content of several protein sources used in dog food.

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    References

    1. Adan Y, Shibata K, Sato M et al. Effects of docosahexaenoic and eicosapentaenoic acid on lipid metabolism, eicosanoid production, platelet aggregation and atherosclerosis in hypercholesterolemic rats. Biosci Biotechnol Biochem 1999; 63(1):111-9.

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    About

    How to reference this publication (Harvard system)?

    Elliott, D. A. and Lefebvre, H. (2008) “Royal Canin Nutritional Information”, Encyclopedia of Canine Clinical Nutrition. Available at: https://www.ivis.org/library/encyclopedia-of-canine-clinical-nutrition/royal-canin-nutritional-information-6 (Accessed: 09 February 2023).

    Affiliation of the authors at the time of publication

    1Royal Canin USA, MO, USA. 2Experimental Physiopathology and Toxicology, National Veterinary School of Toulouse, Toulouse, France.

    Author(s)

    • Denise Elliott

      Elliott D.A.

      BVSc (Hons) PhD Dipl ACVIM Dipl ACVN
      Royal Canin USA, 500 Fountain Lakes Boulevard, Suite 100
      Read more about this author
    • Lefebvre H.

      DMV, PhD, Dipl ECVPT
      Experimental Physiopathology and Toxicology, National Veterinary School of Toulouse, 23 Chemin des Capelles
      Read more about this author

    Copyright Statement

    © All text and images in this publication are copyright protected and cannot be reproduced or copied in any way.
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