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Nutritional management of the dog and cat with chronic renal failure

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Category: Schede
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  • Disciplina: Alimentazione
  • Specie: Cane e Gatto

Thenutritional management of chronic renal failure (CRF) plays a key role in supporting medical treatment and has four main objectives:

A-meet the nutritional and energy requirements of the patient;
B- relieve the clinical signs and the consequences of uraemia;
C- minimize alterations in fluid, electrolyte and acid-base balance;
D- slowing of the rate of progression of kidney disease.

 

ENERGY

The diet shouldprovide an adequate energy intake to prevent protein catabolism, which can worsen the state of malnutrition and of hyperazotaemia. The daily energy requirement of renal patients is similar to that of healthy animals and must be carefully calculated, i.e. 110 kcal x (kg of live weight)0.75 for the dog and 50-70 kcal x kg of live weight for the cat. These requirements must then be adjusted based on the animal’s body condition and level of activity. The non-protein energy source of the diet should be made up of carbohydrates and fats. The fat content in renal diets is usually high, as fat provides approximately twice the energy per gram compared to carbohydrates, whilelimiting food volume (Elliot, 2012).

 

WATER

Polydipsia is the body’s compensatory mechanism to contrast the excessiveloss of fluids, which is caused bythe osmotic polyuria that develops in patients with renal failure. Several strategies may be used to increase water intake: use of a diet with a moisture content of about 70-85%, increased number of meals per day, supplementation of water to the meal and making available multiple easily-accessible sources of fresh water in different places of the house (Dumon etal., 1999; Kirschvink et al., 2005).

 

PROTEINS

Hyperazotaemia and uraemia are caused by an accumulation of protein metabolites resulting from an excess of protein in the diet and from the degradation of endogenous proteins. The use of reduced amounts of protein of high biological value allows to meet the requirements of essential amino acids with the least possible overloading of kidney function. This said, before opting for protein restriction it is first necessary to make a distinction between two possible conditions, based on the clinical data:

A) IRIS CKD Stages I/II: in these stages of renal failure the glomerular filtration of functioning nephrons is increased and the selective capacity of the glomerular barrier is impaired, causing an increased passage of proteins into the glomerular filtrate. In addition, the tubular reabsorption process is impaired due to the presence of fibrosis and interstitial inflammation.

In rats and in humans, protein restriction has been shown to reduce the degree of glomerular filtration and proteinuria, while in dogs and cats dissenting views are still present. Some authors have reported that protein restriction does not reduce hypertension, hypertrophy and glomerular hyperfiltration, and is therefore ineffective in limiting the progression of the disease (Brown et al., 1990, Brown et al., 1991).

Other studies in the dog have shown the existence of a positive correlation between protein intake level and the degree of proteinuria (Polzin et Osborne, 1988); in the dog, proteinuria (UPC) has been shown to be correlated with increased uraemic morbidity and mortality (Jacob et al., 2005). In view of the above, it would be important for us to fully understand the association existing between dietary protein restriction, proteinuria and the progression of chronic renal failure.

B) IRIS CKD Stages III/IV: excess protein in the diet can exacerbate azotaemia. Several studies have shown that by modifying the protein content in the diet of dogs with kidney disease the level of blood urea nitrogen may be reduced, avoiding protein malnutrition and thus improving overall clinical conditions (Polzin et al., 1983; Finco et al., 1985; Polzin et Osborne, 1988; Jacob, 2002). IRIS III/IV animals may therefore benefit from protein-restricted diets. To date, the minimum protein requirements of dogs and cats with chronic renal failure are not known, but they can be assumed to be close to 2-2.2 g/kg of live weight/day in the dog and 3.3-3.5 g/kg of live weight/day in the cat (NRC, 2006).

 

MINERALS

Phosphate

Phosphate retention is one of the most common disorders that occurs in the presence of chronic renal failure, due to the retention of phosphorus in the glomerulus. Dietary phosphate restriction has been associated with decreased hyperphosphoraemia, decreased soft tissue mineralization and the prevention of hyperparathyroidism. By reducing blood phosphorus to a minimum it is in fact possible to prevent secondary hyperparathyroidism and its sequelae, thus slowing down the progression of chronic renal failure (Lopez-Hilker et al., 1990; Brown et al., 1991b; Finco et al., 1992). In a study on cats, for each unit (mg/kg) of increased blood phosphorus the risk of mortality increased by 11.8% (Boyd et al., 2008). If dietary phosphate restriction alone is not sufficient to reach a normal blood concentration of phosphorus within 2 weeks, phosphate binders must be added to phosphate restriction (Elliott, 2012). Phosphorus kelating agents bind to phosphates at intestinal level (Fig. 1), preventing their absorption, but require an initial monitoring of blood phosphorus every 2-4 weeks, until the recommended concentration has been reached (IRIS reference).

Sodium

Sodium restriction to control systemic hypertension has extensively been considered in the past. Systemic hypertension is a frequent finding in the clinical course of chronic renal failure and has been indicated as a factor that can contribute to disease progression. Some studies favour the dietary restriction of sodium so as to reduce the systemic hypertension associated with the inability of the kidneys to successfully excrete this element. Other authors argue that a sudden decrease in sodium intake could be contraindicated, as it could result in dehydration and fluid volume contraction, with a  worsening of the renal status. To date, no study exists showing that dietary sodium restriction is able to reduce systemic hypertension or decrease the rate of progression of kidney disease. The current recommendation is to use diets with normal or slightly reduced sodium levels.

Potassium

The supplementationof potassium is necessary to counteract hypokalemia, a metabolic condition which manifests itself in the course of chronic renal failure following a reduction of dietary potassium intake and the increased loss of this electrolyte in the urine. This loss is due to the reduced glomerular filtration rate that occurs in about 20% of cats and 14% of dogs with CKD (Theisen etal., 1997; Segev etal., 2010). Potassium can be supplemented orally in the form of gluconate or citrate, when its blood concentration is lower than 4mEq/L. When supplemented, the blood concentration of potassium must be monitored constantly and the dose must be continually adjusted.

 

OMEGA-3 FATTY ACIDS

Omega-3 polyunsaturated fatty acids (PUFA), derived from fish oil, have been shown to be very useful as a dietary supplement in the course of chronic renal failure. Several studies have in fact shown that dogs and cats suffering from this condition and fed with omega-3 fatty acids showed an improved renal function and an increased mean survival time. In fact, omega-3 fatty acids have a nephroprotective effect, achieved through several mechanisms: control of systemic hypertension and of glomerular hyperfiltration; reduction of inflammation, oxidative stress (Fig. 2) and cholesterolaemia (Brown et al.,1998).

 

Suggested reading

  1. Brown, S.A., W.A. Crowell, J.A. Barsanti et al. 1991. “Beneficial effects of dietary mineral restriction in dogs with marked reduction of funtional renal mass.” Journal of the American Society of Nephrology 1(10): 1169-1179.
  2. Brown, S.A., D.R. Finco, W.A. Crowell et al. 1990 “Single-nephron adaptations to partial renal ablation in the dog.” American Journal of Physiology 258(3 Pt 2): F495-503
  3. Brown, S.A., Brown, C.A., W.A. Crowell et all. 1998. “Beneficial effects of chronic administration of dietary omega-3 polynsaturated fatty acids in dogs with renal insufficiency.” Journal of Laboratory Clinical Medicine 131(5): 447-455
  4. Dumon, H., P. Nguyen, L. Martin et al. 1999. “Influence of wet vs. dry food on cat urinary pH: Preliminary study.” Journal of Veterinary Internal Medicine 13:726.
  5. Elliott D.A. Nutrition Management of Kidney Disease. In: Fascetti A. J. S and Delaney S.J. eds: Applied Veterinary Clinical Nutrition. Pubblished 2012 by John Wiley & Sons.
  6. Finco, D.R., W.A. Crowell, and J.A. Barsanti. 1985. “Effects of three diets on dogs with induced chronic renal failure.” American Journal of Veterinary Research 46(3): 646.653.
  7. Finco, D.R., S.A. Brown, W.A. Crowell et al. 1992a “Effects of dietary phosphorus and protein in dogs with chronic renal failure.” American Journal of Veterinary Research 53(12): 2264-2271.
  8. Finco, D.R., S.A. Brown, W.A. Crowell et al. 1992b. “Effects of phosphorus/calcium-restricted and phosphorus/calcium-replete 32% protein diets in dogs with chronic renal failure.” American Journal of Veterinary Research 53(1): 157-163.
  9. Jacob, F., D.J. Polzin, C.A. Osborne et al. 2002. “Clnical evaluation of dietary modification for treatment of spontaneous chronic renal failure in dogs.” Journal of the American Veterinary Medical Association 220(8): 1163-1170.
  10. Jacob, F., D.J. Polzin, C.A. Osborne et al. 2005. “Evaluation of the association between initial proteinuria and morbidity rate or death in dogs with naturally occurring chronic renal failure.” Journal of the American Veterinary Medical Association 226(3): 393-400.
  11. Lopez-Hilker S, Dusso AS, Rapp NS, Martin KJ, Slatopolsky et al. “Phosphorus restriction reverses hyperparathyroidism in uremia independent of changes in calcium and calcitriol.” American Journal of Physiology 259(3 pt 2): F432-7.
  12. National Research Council (NRC). 2006. “Nutrient Requirements of Dogs and Cats”. Washington DC: National Academies Press.
  13. Polzin, D.J., J.R. Leininger, C.A. Osborne et al. 1988 “Development of renal lesions in dogs after 11/12 reduction of renal mass. Influences of dietary protein intake.” Laboratory investigation 58(2): 172-183
  14. Polzin, D.J., and C.A. Osborne 1988. “The importance of egg protein in reduced protein diets designed for dogs with renal failure.” Journal of Veterinary Internal Medicine 2(1): 15-21
  15. Polzin, D.J., C.A. Osborne, J.B. Stevens et al. 1983. “Influence of modified protein diets on the nutritional status of dogs with induced chronic renal failure.” American Journal of Veterinary Research 44(9): 1694-1702.
  16. Segev, G., A. Fascetti, L. Weeth et al. 2010. “Correction of hyperkaliemia in dogs with chronic kidney disease consuming commercial renal therapeutic diets by a potassium reduced home prepared diet.” Journal of the American Veterinary Medical Association 24(3): 546-550.
  17. Theisen, S.K., S.P. Dibartola, M.J. Radin et al. 1997. “Muscle potassium content and potassium gluconate supplementation in normokaliemic cats with naturally occurring chronic renal failure.” Journal of Veterinary Internal Medicine 11(4): 212-217.