Nutritional Management of Dogs and Cats with Chronic Renal Failure
Dr. Tina Kalkstein

Do chronic renal failure (CRF) patients need low protein diets? This
question represents a current hot topic in veterinary nephrology. There is
no evidence to believe that low protein diets are beneficial to all patients
with renal azotemia (increased BUN and creatinine with isosthenuric urine
specific gravity) and in fact this practice may be harmful to some patients.
Higher protein diets may needed in some patients but also be harmful to other
CRF patients. So how do we decide what is the best diet for our CRF
patients? The bottom line is that nutritional therapy should be individually
tailored for each patient's clinical condition (body weight, body condition,
albumin status), degree of azotemia, and dietary preferences.

Rationale for low protein diet: The kidneys are responsible for
eliminating urea and acids from the body, failing kidneys cannot perform this
excretory function. By decreasing protein intake, the amount of urea and
acid that are produced are limited, therefore minimizing the clinical
manifestations of high BUN (e.g. uremic gastroenteritis, stomatitis,
anorexia) and acidosis that cause CRF patients to feel so poor. The benefits
of a low protein diet are only seen with advanced RF (i.e. animals with
moderate to severe azotemia showing clinical signs of uremia such as
anorexia, weight loss, vomiting, diarrhea, constipation) and these benefits
are strictly non-renal. This means that a low protein diet will benefit the
patient's clinical condition (i.e. they will feel better), but does not
prevent the progression of renal lesions or stall progressive decline in
renal function.

Rationale against low protein diets: All body protein is functional protein
(muscle, organs, and cells, circulating proteins such as albumin and
globulins). There are no stores of protein in the body as there are for fat
in obvious places or carbohydrates in the liver or muscles. Therefore any
excess protein during a positive nitrogen balance is eliminated from the
body. Many patients are initially diagnosed with CRF when already in a
protein malnourished state and negative nitrogen balance (significant weight
loss and poor body condition, poor haircoat, hypoalbuminemia). The
clinical signs of protein malnutrition suggest that catabolism has been
chronic, sustained for possibly months before these signs become detectable.
This state develops because protein depletion forces body proteins to be
catabolized to meet regular nutritional needs. Acidosis also causes the
breakdown of body proteins. Catabolism of endogenous proteins for any reason
will increase the level of azotemia (remember: protein is protein no matter
where it comes from-the exogenous food we feed or endogenous body mass that
is catabolized). By forcing all CRF patients to eat a low protein diet,
protein malnutrition may be induced or perpetuated if the diet does not met
the body's nutritional needs and/or the patient finds the diet unpalatable
and chooses not to eat enough or any of the diet. Also remember, limiting
protein intake in CRF is not renoprotective (i.e. this will not prevent
progression of renal damage). It is also worth mentioning that low protein
diets will not delay or prevent the onset of CRF in healthy older animals.
This means that our more senior patients do not need a low protein diet or
one specifically designed for the older pet. A regular maintenance diet is
fine for most older healthy cats and dogs.

The goal of dietary management of CRF patients is to maintain adequate
nutrition while minimizing azotemia and associated clinical signs of uremia.
CRF patients should be fed the maximal amount of protein they can tolerate
until clinical signs of uremia develop. Once this occurs, the protein intake
should be tailored to meet the needs of the patient. If the dog or cat loses
weight, coat condition, or serum proteins on a low protein diet, but feels
otherwise good, consider adding additional protein to their daily meals (egg,
cottage cheese, tofu, etc.) or choosing a different diet that is less
protein restricted until finding the individual's tolerable threshold of
protein intake. Acid-base status should also be monitored and corrected as
needed (adding bicarbonate to the drinking water is a simple way to manage
mild to moderate acidosis). Phosphorus levels are important to monitor and
manage as well.

If a CRF patient is anorexic (complete or partial), appetite stimulants
are fine to try for a day or two. However, anorexia should not be allowed to
persist much longer than that before considering more aggressive nutritional
support via feeding tubes (esophagostomy, pharyngostomy, naso-esophageal,
gastrotomy tubes). Famotidine (Pepcid AC) at 0.5 mg/kg PO or IV q 24 hrs
also helps to improve the appetites of many CRF patients by decreasing uremic
gastritis. I prefer famotidine to cimetidine since it can be given once
daily which improves client and patient compliance.

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