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  4. Feeding Strategy
Encyclopedia of Canine Clinical Nutrition
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Feeding Strategy

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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    8. Feeding Strategy

    Dietary therapy is only effective in ameliorating the clinical signs of uremia if it is administered appropriately. Patients with chronic renal failure often have reduced appetites. In addition, an altered sense of taste and smell has been reported in people. These factors can be aggravated by the handicap of reduced dietary intake due to reduced palatability of the modified protein diets for dogs with chronic renal failure.

    However, it is not the palatability of the diets per se, but the effect of uremia on the sense of taste and smell and the development of food aversion that contribute to inappetance. In this regard, it is not advisable to institute dietary changes when patients are hospitalized, as there is a high risk that the patient will develop food aversion. Rather, the renal support diet should be instituted in the home environment when the pet is stable.

    Reduced food intake leads to malnutrition and wasting, which contribute to many aspects of uremia including impaired immune function, delayed wound healing, decreased strength and vigor, and increased morbidity and mortality. Indeed, malnutrition has been implicated as a factor influencing outcome in humans with renal failure. Therefore, prevention of malnutrition by ensuring adequate nutrient intake is crucial in the management of renal failure.

    Enteral feeding tubes should be instituted for nutritional support upon documentation of a 1015% loss of BW in conjunction with a declining body condition score and a history of poor dietary intake. Enteral feeding tubes are also advantageous as they circumvent the need for subcutaneous fluid therapy and ease the administration of oral medications.

    (For more details concerning enteral tube feeding, see Chapter 14: Critical Care Nutrition).

    Clinical Studies of the Influence of the Diet on Naturally Occurring Chronic Renal Failure

    The effects of feeding diets with a low phosphorus and moderately restricted protein content have been investigated in dogs with mild to moderate chronic renal failure (Leibetseder & Neufeld, 1991). Thirty-two dogs with early chronic renal failure were fed a low phosphorus medium protein commercial diet for 28 weeks, and an additional 28 dogs were fed a home-made diet formulated to mimic the commercial diet. Fourteen dogs were euthanized throughout the course of the study due to progression of renal failure. Within four weeks of feeding either the commercial or the home made diet, the concentrations of blood urea nitrogen and phosphorus had almost normalized. Both diets were found to be palatable, body weights and serum albumin concentrations remained stable, and the physical condition of the dogs was considered improved. The results of this study suggest that dogs with mild to moderate chronic renal failure benefit from early management with a phosphate and protein restricted diet.

    The effect of a modified protein, low phosphate diet on the outcome of dogs with stable, naturally occurring CRF has recently been reported (Jacob et al, 2002). Dogs with mild to moderate CRF that were fed a renal diet had a 70% reduction in the relative risk of developing a uremic crisis, remained free of uremic signs almost 2.5 times longer and had a median survival that was three times longer than dogs with CRF that were fed a maintenance diet. Renal function declined more slowly in the dogs that were fed the renal diet. The primary cause of death in dogs fed the maintenance diet was renal-related.

    Monitoring

    Regular monitoring to ensure that dietary and medical management remains optimal for the needs of the patient is crucial for the well being and long term successful treatment of the chronic renal failure patient. Owner compliance may also be improved by frequent patient evaluation. Patients should be reevaluated within 2 weeks of initiating therapy and then 3 to 4 times per year. Recheck examinations should always be made 2 weeks following medication or dietary change. Erythropoietin and antihypertensive therapy will initially require weekly evaluation until the appropriate maintenance dosage is achieved.

    A complete history, physical examination, body weight, body condition score and laboratory evaluation including CBC, biochemical panel, urine analysis, urine culture and blood pressure evaluation is indicated. Urine culture should become a routine part of follow up studies as chronic renal failure patients are predisposed to urinary tract infection, which are often clinically "silent".

    A complete list of all medications and doses that the client is currently administering to the pet should be obtained to verify compliance. In addition, some owners will self-adjust medications or simply may be confused by previous instructions.

    A complete dietary history including the type of diet (dry versus wet), the amount eaten each day (eaten is more important than amount offered), the method of feeding, and all treats, snacks and supplements should also be obtained. This information is invaluable for monitoring the response to dietary therapy.

    Practical measures to improve intake include the use of highly odorous foods, warming the foods prior to feeding and stimulating eating by positive reinforcement with petting and stroking behavior.

    When oral ulcerations are present, application of local xylocaine gel about 10 minutes before the meal may decrease the pain associated with food intake.

    Appetite stimulants such as the benzodiazepam derivatives or serotonin antagonists may be judiciously administered, however, in these cases, more aggressive therapy such as esophagostomy or gastrotomy tube feeding is often more effective (Elliott et al, 2000).

    Expected Outcome and Prognosis

    CRF is a progressive disease that ultimately results in death. The goal of medical and nutritional management is to ensure the highest quality of life for the patient, for the longest period of time. Success depends on owner acceptance and compliance and a coordinated medical approach.

    Despite appropriate tailoring of the therapy to the patient's condition, chronic renal failure is typically dynamic and progressive and eventually leads to end-stage renal failure. The severity of the clinical signs and uremic complications and the probability of improving renal function (by removing pre-renal contributions, controlling infection etc.) will aid in determination of the prognosis. The severity of the renal function and long term prognosis is best determined by the serum creatinine concentration. Prognosis and outcome will be heavily influenced by the response to conservative medical therapy and the rate of progression of the renal dysfunction.

    Dietary and conventional medical therapy generally become poorly accepted or ineffective at stage IV of CRF as defined by IRIS (when plasma creatinine exceeds 5 mg/dL or 400 μmol/L). At this point owners are frustrated with the poor quality of life of their pet and euthanasia is often the ultimate outcome. Renal transplantation or chronic intermittent hemodialysis (two or three times per week) are then the only viable options.

    Conclusion

    Chronic renal failure is the clinical syndrome resulting from irreversible loss of the metabolic, endocrine and excretory capacities of the kidney. CRF is the third leading cause of death in dogs. Nutrition has been the cornerstone of management for decades. The goals of dietary modification are to meet the patient's nutrient and energy requirements, alleviate clinical signs and consequences of uremia, minimize disturbances in fluid, electrolyte, vitamin, mineral, and acid base balance and to slow progression of renal failure. Regular monitoring to ensure that dietary and medical management remains optimal for the needs of the patient is crucial for the well being and long term successful treatment of the chronic renal failure patient.

    Definition

    Azotemia:
    Increased concentrations of blood urea nitrogen and/or creatinine and other nitrogenous waste products in the blood

    Renal Azotemia:
    Denotes azotemia caused by renal parenchymal lesion

    Renal Disease:
    Implies renal lesions are present, however, does not qualify the etiology, severity or distribution

    Renal Failure:
    State of decreased renal function that allows persistent abnormalities (azotemia, inability to concentrate urine) to exist

    Renal Insufficiency:
    Begins when renal reserve is lost. Animals appear outwardly normal, but have a reduced capacity to compensate for stresses such as infection or dehydration

    Renal Reserve:
    The percentage of nephrons not necessary to maintain normal renal function. The renal reserve is generally greater than 50%

    Uremic Syndrome:
    Constellation of clinical signs including anemia, gastroenteritis, acidosis which occur at the ultimate stage of renal failure

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    References

    1. Adams LG. Phosphorus, protein and kidney disease. Proceeding of the Petfood Forum 1995 (13-26).

    2. Bauer JE, Markwell PJ, Rawlings JM et al. Effects of dietary fat and polyunsaturated fatty acids in dogs with naturally developing chronic renal failure. J Am Vet Med Assoc 1999; 215: 1588-1591.

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    About

    How to reference this publication (Harvard system)?

    Elliott, D. A. and Lefebvre, H. (2008) “Feeding Strategy”, Encyclopedia of Canine Clinical Nutrition. Available at: https://www.ivis.org/library/encyclopedia-of-canine-clinical-nutrition/feeding-strategy (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

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