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Home » Uncategorized » How Important is a low protein diet for pets with Kidney disease.

How Important is a low protein diet for pets with Kidney disease.

Turns out to be much less important than we once thought.

Science and medicine change over time as we acquire more precise methods of measuring the effect of disease and the benefits of treatments.

The tried and true recommendation of giving pets a low protein diet, when their Kidneys begin to fail, started before the 1970’s, Based on two observations. 1. Modified low protein diets improved symptoms and increased survival in humans. 2. Research in dogs, who had lost 75% of their kidneys, revealed that their kidneys enzymes (BUN and creatinine) came down and the dogs acted and ate better, when fed a low protein diet.

One common problem with Kidney diets is that pet won’t eat the food (K/D). Mainly because it tastes bland and they often have a little nausea when first diagnosed.

So how important is a low protein diet? First, not very important in cats. Cats will metabolize their body tissues if dietary protein is too low, so diet can only do so much. More important in cats, is that the proteins be all from meat, fish or eggs so that all the essential amino acids are included in easily digestible forms. Excess animal source proteins are readily converted into blood glucose in cats. Excess plant source protein are not converted into usable amino acids and instead just raise the BUN & creatinine.

This recent study shows that normal levels of protein in the diet does not cause kidney damage as once believed in dogs. Further, low protein diets did not increase life span in dogs. In my veterinary practice of dogs or cats with kidney disease, I find it is the quality of the protein in the diet that impacts the pet the most.

We know that dogs digest and metabolize, at most only 30% of plant source protein, and fats. So diets should first be low in plant proteins.  Second go to low protein diets to further lower the BUN.

So, even though lower protein diets don’t change the future of the kidney lifespan, these diets do reduce the elevated BUN which is the cause of nausea. Dogs and cats, eat better when on high quality, animal source protein only diet. I start by mixing their regular diet with a kidney diet until they are eating well. Or a homemade kidney diet is the answer for many animals because it tastes much better than commercial K/D.  Easy, balanced, kidney diets are listed on this site under nutrition/diets.

Here is the science for the interested, vets and nutritionists:

Supplement to Compendium on Continuing Education for the Practicing Veterinarian Vol. 21, No. 11(K), Nov. 1999 15

Dietary protein restriction has been widely accepted as a
form of nutritional management
for animals with reduced renal function for over
four decades. While scientific evidence has not been presented
to justify this practice, it is particularly used in
dogs. Advertising claims suggest that dogs with a list of
urinary problems could benefit from protein restriction
including those with renal insufficiency, progressive renal
failure, acute renal failure, normal aging, polydipsia/
polyuria, glomerulonephritis, urinary tract infection,
urolithiasis, and prostatitis. The most widely accepted of
these is the notion that dogs with reduced renal function
or advanced age will benefit from reduced
dietary protein intake.
In recent years, 10 experimental studies using dogs have
been published that clarify the controversy of protein restriction.
A multicenter study conducted in human medicine
is also noteworthy to review.
A number of false assumptions about the need for reduced
protein intake in regard to renal disease have been
perpetuated in the literature for many years, including:
n Increased urea load causes increased workload for the
n High dietary protein intake injures kidneys.
n High dietary protein intake causes hyperkalemia.
n High dietary protein intake causes acidosis.
n Protein intake results in uremic toxins
n Reduced protein intake slows the progression of renal
Recent evidence in dogs challenges
the validity of the above
assumptions and redirects the
questions about factors that lead to the progression of renal
failure. The beliefs about protein restriction will be discussed
as a medical myth. The question of why the practice
of reduced protein intake persists despite the lack of supportive
scientific evidence is explored.
History of Protein Restriction
Two general reasons are most commonly given to support
the reduction of dietary protein in animals with renal
disease. First, reduced protein may result in reduced
azotemia, which limits the nausea of renal failure and allows
animals to continue eating. While this premise is widely
accepted, its clinical importance has not been quantified.
Second, reduced protein intake may influence the course of
renal failure. The origin of these notions provides some insight
into their appeal and durability.
The first suggestion in the literature that ingestion of
protein aggravates the clinical condition of human patients
with renal insufficiency dates back to 1920. Ambard reported
that uremic patients were often wasted and did
poorly when they ingested meat.1 This clinical description
led to efforts to alleviate the so-called “toxins of uremia” by
reducing dietary protein. Newburgh and Curtis in 1928 reported
the development of renal lesions in rats fed varying
quantities of protein and suggested that rats fed high quantities
of protein containing 75% dry liver developed renal
lesions more quickly than those fed moderate protein or casein
diets.2 Rodents have been widely used to study possi-
Mythology of Protein Restriction
for Dogs with Reduced Renal Function
Kenneth C. Bovée, DVM, MMedSc
Department of Clinical Studies
School of Veterinary Medicine
University of Pennsylvania
Philadelphia, Pennsylvania
Protein in Life Stage Nutrition
16 Proceedings, 1998 Purina Nutrition Forum
Mythology of Protein Restriction for Dogs with Reduced Renal Function
They were unaware of the extrarenal and renal factors separate
from GFR that might influence BUN and reported
that serum creatinine concentration was not a reliable indicator
of kidney damage.22 Morris subsequently developed,
produced, and sold a reduced-protein diet, KD, for dogs
with renal failure. He and others were influenced
by the erroneous work hypertrophy
concept for urea excretion advanced by Addis.
20 While experimental or clinical data
were never published to support the value of
this or other diets, the concept was broadly
accepted without challenge in the veterinary
literature.23 Diets were promoted as lowering
BUN and reducing urine volume.
The notion that high protein feeding to
dogs may be harmful was even adopted by
the National Research Council (NRC) of
the National Academy of Sciences in 1972.24
It was stated that high protein found in some
commercial diets increases the workload of
the liver and kidney and contributes to renal
disease in dogs. There is no evidence to support
this view, and the recommendation has
been dropped. In contrast, there is evidence that high protein
diets enhance renal function in normal dogs. This has
led to confusion among veterinarians who have been told
for decades that low protein diets may be beneficial for kidney
function and therefore high protein diets may be deleterious
to normal dogs.
While the Addis hypothesis of work hypertrophy to excrete
urea is erroneous, a more modern concept associated
with glomerular hyperfiltration was proposed in the 1980s
by Brenner.25 This hypothesis states that after any significant
loss of renal function, surviving nephrons subsequently
undergo functional and structural changes including increases
in single nephron GFR and glomerular capillary
pressure increases. These changes are referred to as
glomerular hyperfiltration and glomerular hypertension.
Micropuncture studies in rats indicate that a progressive
decline in renal function is observed as a consequence of
these adaptations. In addition, glomerular enlargement, hypertrophy,
and glomerular mesangial deposits lead to a progressive
glomerulosclerosis and eventual nephron loss. Surviving
nephrons undergo further increases in filtration rate,
capillary pressure, and size, setting up a vicious cycle of
pathogenic renal injury. A reduction in dietary protein
ble causative factors of progression of renal failure. Some
strains of rats have a high incidence of spontaneous
glomerular and tubular lesions associated with age alone.3–8
The progression and severity can be enhanced by increased
dietary protein,2,9,10 sodium,4 and phosphate.11 Surgical ablation
of renal mass hastens glomerular lesions
as does diabetes in these rats.12–14 While
these observations are limited to certain
strains of rats, they have influenced many investigators
by establishing the possibility of a
dietary protein-induced nephropathy in other
The first published data in the dog linking
dietary protein to renal function appeared in
the 1930s. It was reported that in normal
dogs glomerular filtration rate (GFR), renal
blood flow (RBF), and urea clearance could
be acutely increased by high protein
feeding.15–17 Subsequent studies by Pitts indicated
that intravenous infusion of amino
acids dramatically increased renal hemodynamics.
It should be remembered that during the
1930s and 1940s the basic parameters of kidney function
were first being studied. For example, blood urea concentration
as an accurate measure of kidney function and the
concept of extrarenal azotemia were first reported at that
time.19 It was then believed that the kidney expended considerable
energy to excrete urea into the urine and that
moderate restriction of protein was beneficial to human patients
as contended by Addis.20 This concept fell out of favor
in human medicine when it was realized that renal
work is tied closely to active sodium reabsorption and that
urea is passively handled. Special dietary restrictions were
not thought to be needed in human patients with chronic
renal failure because of the lack of evidence that a normal
protein intake had a deleterious effect on the kidney. Addis
reported that urea production, urea excretion, and blood
urea nitrogen (BUN) increased in normal subjects when
dietary protein was increased. The uselessness of urea
clearance and the limitations of creatinine clearance were
not appreciated at that time.21
In 1941, Allison et al. reported on 10 dogs with kidney
disease as measured by increased BUN and decreased
urine specific gravity, which they felt correlated well and
were of clinical significance in determining kidney damage.
Evidence that high
protein diets enhance
renal function in
normal dogs has led
to confusion among
veterinarians who
have been told for
decades that low
protein diets may be
beneficial for kidney
Supplement to Compendium on Continuing Education for the Practicing Veterinarian Vol. 21, No. 11(K), Nov. 1999 17
and/or calories has been shown to limit this process in some
strains of rats.26 If this mechanism were operative in the
dog, there would be good rationale to limit dietary protein.
Experimental Studies in Dogs
Because of the confusion in the veterinary literature and
the lack of evidence to support the use of reduced protein
diets, a number of experimental studies have been performed
in recent years. These studies have utilized the
standard experimental model of reduced renal function and
have addressed many questions when dogs received varied
forms and quantities of protein at different levels of renal
function. These studies represent a major quantity of work
that required the sacrifice of hundreds of dogs to deliver in
the aggregate a clarification of the possible role of dietary
protein in the initiation, maintenance, and progression of
renal dysfunction.
The measurement of progression of renal failure requires
specific definition. In these studies the use of clinical signs,
reduced urinary concentration capacity, elevated BUN, and
elevated plasma creatinine have limited ability to detect efficacy
of protein restriction. Likewise, the presence of hyperphosphatemia,
acidosis, and proteinuria may be misleading
depending on the experimental model and diet and may not
represent a precise measure of progression. The sole most
reliable method is the measure of GFR using inulin or labeled
iothalamate. This is considered the gold standard to
indicate progression of disease, and all other
measures are considered secondary.
Progression to failure may also be estimated
on the basis of morphologic measures.
The agreement of morphologic and functional
measures is extremely complex and appears
to vary with the form of renal disease
or experimental model. A synthesis or comparison
of functional and morphologic measures
may be helpful in some cases. However,
results may or may not agree. Although
histologic or electron microscopic alterations
may indicate something about the pathophysiology,
their relationship to progression of
failure may be difficult to quantify. It is commonly difficult
to quantify histologic lesions because they are not uniformly
distributed, there may be confusion due to compensatory
hypertrophy and hyperplasia, and in some forms of disease
fibrosis may obscure histologic architecture.
Results of the 10 experimental studies on dogs have
failed to provide evidence of the benefit of reduced dietary
protein to influence the course of renal failure.27–36 The results
of these studies should allow veterinarians to disabuse
themselves of the six assumptions related to protein intake
set forth at the beginning of this article. It is clear that the
concept of increased workload, protein intake causing injury
to the kidneys, and reduced protein intake slowing the
progression of renal disease are incorrect. The other three
assumptions dealing with hyperkalemia, acidosis, and uremic
toxin require comment. Hyperkalemia was not found
in the above studies related to increased dietary protein.
The ability to excrete potassium and maintain a normal
serum potassium concentration until the very last stages of
chronic renal failure has been studied in detail in dogs.37,38
The secretory mechanism in the distal tubule represents the
major site for enhanced potassium excretion during renal
failure. Potassium balance is maintained in chronically uremic
dogs even in the presence of changing rates of potassium
intake, changing rates of excretion of sodium, phosphorus,
and ammonium. Acidosis is also uncommon due to
altered tubular mechanisms in dogs with reduced renal
function.39–41 The dog is unique in that the fractional reabsorption
of bicarbonate increases after reduced kidney
function. This enhanced ability to reabsorb bicarbonate
prevents acidosis and is present in spite of tubular adjustment
to regulate other electrolytes such as sodium, potassium,
and phosphate. Finally, the concept of
dietary protein being responsible for socalled
“uremic toxin” has not been proven in
any species despite extensive study.42
Dietary Protein and Progression
of Renal Failure in Humans
The controversy of dietary protein restriction
in humans had been perpetuated by
anecdotal reports and uncontrolled clinical
studies since the early 1960s. In view of the
Brenner hypothesis, the National Institutes
of Health funded an extended multicenter
study, which recruited 585 patients with
chronic renal failure. Patients were fed a standard protein
diet and a low-protein diet for 18 to 45 months. Measurement
of GFR and standard chemistry measurements were
used. The mean decline in GFR at 3 years did not significantly
differ between diet groups.43 Among patients with
Protein in Life Stage Nutrition
Results of the 10
experimental studies
on dogs have failed to
provide evidence of the
benefit of reduced
dietary protein to
influence the course
of renal failure.
18 Proceedings, 1998 Purina Nutrition Forum
Mythology of Protein Restriction for Dogs with Reduced Renal Function
not readily apparent. If we are not given myths by society,
we invent them to make sense of our personal experiences.
There are both positive and negative myths. Positive
myths support and validate our self-worth. They provide
guidance and support. These positive myths
are used as important patterns in human
consciousness, which allow us to cope with a
difficult world, as we are reminded by the
psychiatrist Rollo May,44 Carl Jung,45 and
philosophers Mortimer Adler46 and Joseph
Campbell.47 There are many in our contemporary
popular culture, though profoundly
mistaken, who consider all myths as falsehood.
I would consider a truly negative myth
as one that misleads or has destructive effects.
These could be termed pseudomyths or
exaggeration and they appear to be almost
magical. These are associated with beliefs
without benefit or responsibility.
There are many types of myths: personal,
societal, and professional. We use personal
myths to develop our identity, image, and
moral values. We use myths to define ourselves
in a community. Societal myths include
the New World, the Western frontier,
the lone cowboy, national heroes, and the socalled
American Dream. Professional myths
in veterinary medicine include the images associated with
the stories of James Herriott, the gentle doctor as projected
by our organized profession, and the power of healing related
to modern science.
Are there conflicts between science and myth? As it
turns out, many of our scientific theories are a kind of
mythology. Many scientific discoveries begin as myths or
have their original questions in myths. In many ways, science
is the critique of myth (W.B. Yeats).44
Why Relate Protein Restriction to Myth?
I suggest that we have used the myth of dietary protein
restriction because it is psychologically reassuring in the
face of life-threatening illness. Chronic renal failure presents
multiple difficult problems in the absence of adequate
medical treatment despite all efforts to date. In the absence
of dialysis, which is not practical for the vast majority of
animals, and renal transplantation, which is not successful
more severe renal insufficiency, a very low protein diet
compared to a low protein diet did not significantly slow
the progression of renal disease.
Advantages and Disadvantages
of Dietary Protein Restriction
in Dogs
Based on the previous data, the only advantages
appear to be a lowering of BUN
and the possibility of reduced nausea. Quantifying
the value of these effects has not been
reported in dogs. On the contrary, there appear
to be disadvantages to reduced protein
intake. These include reduced kidney function
as measured by GFR and renal plasma
flow, possibility of a negative nitrogen balance,
and the promotion of a catabolic state
in the presence of proteinuria. In practical
application the use of a vague dietary recommendation
appears to lead to complacency
about long-term surveillance of the animal or
the need for individualized specific treatment.
Because some sort of management appears
available, the search for a more specific
etiologic diagnosis is usually not mounted.
Finally, the use of arbitrary diets leads to a
delusion of ourselves and clients about treatment
and increases the cost to owners.
Why Is Dietary Alteration Still Used if
There Is No Proven Benefit?
The continued use of protein restriction in the absence
of scientific evidence deserves thoughtful consideration. I
would suggest that the dogma and mythology of a possible
benefit are so embedded in the thought process of veterinarians
and owners that these cannot be easily dislodged
despite the scientific evidence. I would refer to this as the
myth of dietary protein and characterize it as a negative
What is a myth? A myth is a way of making sense of a
difficult and senseless world. Myths give a society a degree
of relief from neurotic guilt and excessive anxiety. Philosophers,
psychiatrists, and theologians tell us that humans
have always needed myths. Myths are a self-interpretation
of our inner selves in relation to a larger world. All societies
and individuals are built on a series of myths that are
Disadvantages to
reduced protein
intake include
reduced kidney
function as measured
by GFR and renal
plasma flow,
possibility of a
negative nitrogen
balance, and the
promotion of a
catabolic state in the
presence of
Supplement to Compendium on Continuing Education for the Practicing Veterinarian Vol. 21, No. 11(K), Nov. 1999 19
in the dog because of immunologic barriers, medical treatment
has little to offer. Most cases are presented late in
their natural course, are usually irreversible, and are usually
attendant with a uniform pattern of failure and eventual
death over months. Because of these factors, a sense of
frustration, embarrassment, and even guilt arises in the veterinarian
and owner. Veterinarians grasp for something to
offer to maintain our professional position, status, and power
in this dilemma with the owner. Dietary protein restriction
is simple, relatively inexpensive, and usually not harmful
and has the ring of authority. We can offer vague but
firm assurance of its value since it has been on the scene for
so long. Owners sense this dilemma and appreciate our efforts.
This is an ideal circumstance to trap oneself and the
client in a false myth.
Why Have We Chosen to Keep the
Reduced Protein Myth?
The myth has been maintained even in the past decade
despite negative scientific evidence because the dogma has
persisted about its value for the past 40 years. If we as professionals
are uncertain about the facts concerning a controversy,
we are likely to put ourselves in someone else’s
hands who appears to have authority. Power to command
this authority is in the hands of commercial advertisements
that promote these special products with misleading messages.
Marketing is aggressively aimed at veterinarians and
owners alike. There is a profit motive for veterinarians to
sell these diets. The public has a nutritional mania and preoccupation
with diet in our society. Dietary change has assumed
the status of medical treatment using such terms as
intervention, maintenance, and correction. The profession
and the public do not appreciate that advertising claims
come without proof in the case of diets. Owners can easily
be enrolled to accept such diet change because they feel
they are involved in doing something constructive. Professional
responsibility has been lost in this case. The situation
can remind us that we are part of an uncritical profession
with little review or standards. When scientific proof fails
to justify a practice, a false myth may likely live on.
In conclusion, the continued existence of this false myth
about dietary protein is an uncomfortable reminder of the
lack of sophistication, lack of critical thought, and reliance
on oversimplified and attractive dogma that persists in our
profession. This is only one example of many false myths,
misinformation, and partial truths that are repeated from
decade to decade. Until a more critical approach with standards
and oversight are brought to bear in our profession,
we will likely continue to be ensnared in false myths despite
the presence of sound science.
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2. Newburgh LH, Curtis AC: Production of renal injury in the
white rat by the protein of the diet. Dependence of the injury
on the duration of feeding, and on the amount and kind of
protein. Arch Int Med 42:801–821, 1928.
3. Gray JE: Chronic progressive nephrosis in the albino rat.
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4. Elema JD, Arends A: Focal and segmental glomerular hyalinosis
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5. Gary JE, Weaver RN, Purmalis A: Ultrastructural observations
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21. Walser M: Creatinine measurements often yield false esti-
Protein in Life Stage Nutrition
20 Proceedings, 1998 Purina Nutrition Forum
Mythology of Protein Restriction for Dogs with Reduced Renal Function
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22. Allison JB, Morris ML, Green DF, Dreskin HO: The effects
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23. Morris ML, Doering GG: Dietary management of chronic
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26. Gray JE: Chronic progressive nephrosis in the albino rat.
CRC Crit Rev Toxicol 115–144, 1977.
27. Bovée KC, Kronfeld DS: Reduction of renal hemodynamics
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28. Bovée KC: Long-term measurement of renal function in partially
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29. Polzin DJ, Osborne CA, Stevens JB, Hayden DW: Influence
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