Conservative medical management of chronic renal failure in the cat (Proceedings)


Conservative medical management of chronic renal failure in the cat (Proceedings)

Nov 01, 2010

Despite recent technological advances in dialysis and transplantation, conservative medical management remains the most practical and accessible approach to the treatment of chronic renal failure (CRF) for most cat owners and veterinarians. When initially presented, many cats with CRF are moderately to severely dehydrated and require rehydration over 24-96 hours to resolve pre-renal azotemia and correct existing acid-base and electrolyte disturbances. Medical management is begun only after rehydration has been completed.


Owners must understand the importance of providing the cat access to fresh water at all times. Cats with CRF cannot concentrate their urine and rapidly become dehydrated without ready access to water. Fresh water should always be available and consumption of liquids should be encouraged. Cats should consume a minimum of 20% of their daily calories (approximately 4 g/kg/day when consuming 70 kcal/kg/day) as high quality protein. These guidelines represent absolute minimum values and do not allow for maintenance of body nitrogen reserves. Most commercially available cat foods modified for renal failure provide additional protein, and such diets also are phosphorus and sodium restricted. Protein restriction should be considered when moderate azotemia persists in the wellhydrated state. The clinician should strike a balance between reducing protein intake and the cat's willingness to eat. In one study of cats with experimental CRF, progressive renal lesions developed in cats fed 6.8 g/kg/day protein and 75 kcal/kg/day as compared to cats fed 2.7 g/kg/day protein and 56 kcal/kg/day, but these findings were not confirmed in another study. Maintenance of stable body weight and serum albumin concentration suggests adequate intake of calories and protein whereas progressive declines in body weight and serum albumin concentration suggest malnutrition or progression of disease and are indications to increase the amount of protein fed. If possible, the cat should be acclimated to the new diet while its appetite is still reasonably good. Recent studies have shown a beneficial survival effect of feeding commercially-available modified renal diets to cats with CRF. Cats with CRF fed a protein-restricted, phosphorus-restricted veterinary diet survived a median of 633 days compared to 264 days for cats fed a conventional diet. In a retrospective study of cats with CRF fed several different commercially available modified diets, median survival time was 16 months in cats fed the modified diets compared to 7 months in cats fed conventional diets, and the diet associated with the longest survival time (23 months) had a relatively high content of eicosapentaneoic acid. Cats with CRF are less flexible in adjusting to changes in dietary sodium load, and many commercial pet foods provide more sodium than needed (often about 1%). Commercial products marketed for cats with CRF provide about 0.2-0.3% sodium. Gradually switching an animal to a renal diet will result in gradual sodium restriction. Excessive sodium restriction in cats with reduced renal mass may result in reduced glomerular filtration rate, inappropriate kaliuresis, and activation of the renin-angiotensin-aldosterone system without beneficial effect on systemic blood pressure, and the use of sodium-restricted diets may warrant reconsideration. Water soluble vitamins should be supplied in the diet of cats with CRF because the ability of the diseased kidney to conserve these vitamins is not known.


Early phosphorus restriction in CRF has been shown in dogs and cats to blunt or reverse renal secondary hyperparathyroidism. When CRF is diagnosed, phosphorus restriction is initiated by feeding a low-phosphorus, low-protein diet. If necessary, oral phosphorusbinding agents can be added to the treatment regimen for additional control of hyperparathyroidism. In a study of cats with naturally-occurring CRF, renal secondary hyperparathyroidism was successfully managed by dietary restriction of phosphorus, and only one-third of the cats also required treatment with phosphorus binders. Phosphorusbinding agents should be given with meals or within 2 hours of feeding to maximize their binding of dietary phosphorus. Commonly employed oral phosphorus binders include aluminum hydroxide, calcium carbonate, and calcium acetate. The starting dosage of these phosphorus binders is approximately 90 mg/kg/day and the dosage should be adjusted by periodic evaluation of the serum phosphorus concentration in a blood sample obtained after a 12-hour fast. Animals should be monitored for development of hypercalcemia whenever phosphorus binders containing calcium are used, especially if calcitriol is being administered concurrently. Sevelamer HCl is a phosphorus binder that does not contain aluminum or calcium. Due to its potential for binding vitamins in the gastrointestinal tract, vitamin supplementation is recommended during treatment with sevelamer. Lanthanum carbonate is another phosphorus binder that does not contain calcium or aluminum. It is similar in its effects to calcium carbonate, but clinical reports of its use in cats are not yet available. A nutritional supplement called Epakitin® contains chitosan and calcium carbonate and has been recommended for use as a phosphorus binder in cats. At the recommended dosage (1 g per 5 kg body weight q12h) this product supplies 20 mg/kg of calcium carbonate q12h. Thus, in addition to the potential adsorbent effect of chitosan on urea and ammonia, the calcium carbonate contributes a phosphorus-binding effect.