As I said elsewhere, I am concerned about phosphorus levels. And
Science Diet is the only company that will publish in the public
domain, www.hillspet.com, the phosphorus levels on a dry matter basis,
in addition to the other as fed and so on.

That makes me feel they actually test their foods.

Yes I dropped Science Diet for other foods that look better. But when I
find out they don't control the phosphorus levels as low as I like,
0.70% dry matter basis, I go back to Science Diet.

Now I can be critical of Science Diet. My cat on a 100% dry SD Light
diet did not do as well on a 50% dry and 50% wet or something like
that. Her hair or fur was dry and not at all satisfactory. I feed her a
variety of wet foods but I try to feed only those wet foods with 0.70%
phosphorus. This leaves out most, not all, but almost all of
Purina/Nestle Fancy Feast and Friskies.

I do buy 2 or 3 types of Friskies or Fancy Feast when I find them
because they are extremely low in phosphorus compared to all the other
types of Fancy Feast and Friskies. Like Fancy Feast Marinated Chicken
or Salmon in Gravy is quite good in
this regard.

Here are some Friskies that I consider acceptable for my favorite
feline:

The percentages are phosphorus on a Dry Matter Basis:

Friskies Fine Cuts With Real Chicken in
Gravy...............................0.68% (DMB)
Friskies Seared Filets With Turkey &
Giblets..................................0.68% (DMB)
Friskies Special Diet Sliced Chicken In
Gravy................................0.77% (DMB)
Friskies Prime Filets With Chicken In
Gravy...................................0.77% (DMB)

What someone said about wet food is ignorance of the science. Was this
your vet? I put up a reference here a while ago to a European study
which showed that cats fed 100% wet food had 0% that's right, 0%
crystals in their urine, either fresh urine or urine put away for
sampling and analysis.

But I agree, I think Science Diet does testing and that is why they can
publish a tremendous amount of information on their web site. The
others are reluctant to publish the information because it is probably
extremely difficult and costly to get such consistency. So if Science
Diet trades off filler for consistency, I will go for consistency and
try to get those Science Diet foods with less filler.

For me kilocalories and phosphorus levels and pH are what I look for.
If I cannot find that easily, I am extremely concerned and suspicious.
And for kilocalories, I want a way to know that by grams or ounces, not
just a cup of this or that. That's just too crude. It'll do in a pinch
but it's a sloppy way to deal with details.

pH is important for acidity compared to the age of the feline, for me.
I want a pH of 6.2 to 6.4 for cats that are 7 or younger. A little more
if older, like 6.4 to 6.6 perhaps. This just happens to coincide with
all of SD foods :)

I'll also inspect the protein levels, the fiber levels, the salt
levels.

I am way too fussy.

And nope, I do not work for Science Diet. My cat could. She loves
Science Diet, even when she was a street feral. She really loves
Science Diet, it's weird.

Lots of good information there, but I couldn't get to it through your
link so cut it to http://www.maxshouse.com/feline_nutrition.htm.
Here's some more information on feeding dry food diets:

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The Journal of Nutrition Vol. 128 No. 12 December 1998, pp. 2753S-2757S

The Effect of Diet on Lower Urinary Tract Diseases in Cats1
Peter J. Markwell2, C. Tony Buffington*, and Brigitte H. E. Smith

Waltham Centre for Pet Nutrition, Waltham-on-the-Wolds, Melton Mowbray,
Leicestershire, UK and * College of Veterinary Medicine, The Ohio State
University, Columbus, OH

ABSTRACT
Abstract
Introduction
References

Because dietary ingredients and feeding patterns influence the volume,
pH and solute concentration of urine, diet can contribute to the
etiology, management or prevention of recurrence of some causes of
lower urinary tract disease. Most research assessing the effect of diet
has focused on the latter two aspects, primarily because of interest in
struvite urolithiasis. Manipulation of urine pH through dietary means
has proven an effective tool for the management and prevention of
struvite urolithiasis; acidification of urine, however, may be a risk
factor for calcium oxalate urolithiasis, which now appears to occur
with approximately equal frequency in cats. Prediction of urine pH from
dietary analysis would thus be a valuable tool, but considerable
further research is required before this can be achieved with
commercial canned foods. With the growing importance of urolith types
other than struvite, alternatives to the measurement of urine pH are
required to assess critically the likely beneficial (or detrimental)
effects of manipulation of nutrient profile. Measurement of urinary
saturation may permit the development and fine tuning of nutrient
profiles aimed at controlling lower urinary tract diseases in cats that
are associated with a range of different mineral types. The majority of
cats with signs of lower urinary tract disease do not, however, have
urolithiasis; indeed, no specific cause can be established in most of
these cats. Recent observations suggest that recurrence rates of signs
in cats classified as having idiopathic lower urinary tract disease may
be more than halved if affected animals are maintained on high, rather
than low moisture content diets. J. Nutr. 2753S-2757S, 1998

Clinical disorders of the lower urinary tract of cats are not new
phenomena. Kirk (1925), for example, described "retention of urine" as
a very common condition in cats. He also noted that the most common
cause of the problem was obstruction of the urethra by a sabulous
material; less frequent causes were cystic or urethral calculi. Blount
(1931) noted that seven different types of urinary calculi could occur
in cats, and that "triple phosphates" (presumably magnesium ammonium
phosphate) were present in the majority of calculi deposited in
alkaline urine. Milks (1935) recorded only one urethral calculus from a
cat in his own studies, but suggested that there was evidence
indicating that they were fairly common in cats. This is in contrast to
the observations of Krabbe (1949) who noted no examples of "real stone
formers" in a series of over 1000 cats seen at the Royal Veterinary and
Agricultural College in Copenhagen throughout the 1930s and 1940s.
"Sedimentation" of the urine was reported, however, in ~1% of cases.
These observations demonstrate that uroliths and urethral plugs have
afflicted cats for many years. Although they are difficult to relate to
more recent data, the observation by Krabbe of an ~1% incidence is
strikingly similar to the estimates of 0.64 and 0.85% reported more
recently in Europe and the U.S. (Lawler et al. 1985, Walker et al.
1977).

The term feline urological syndrome (FUS)3 was coined in 1970 to
describe "the feline disease syndrome characterized by dysuria,
urethral obstruction, urolithiasis and hematuria " (Osbaldiston and
Taussig 1970). Interestingly, despite use of the term urolithiasis in
the definition of FUS, no occurrences of urolithiasis appeared among
the cases reported (Osbaldiston and Taussig 1970). A study of 46 cats
with "FUS" led to the conclusion that "FUS may not be a single disease
entity, but rather a group of separate urological problems." Thus the
term FUS describes the presence of signs of lower urinary tract disease
without implying any specific cause. Subsequent epidemiologic studies
identified many risk factors associated with FUS (Willeberg 1984).
Proposed dietary influences, the results of many diet-related studies
and the fact that struvite (the stone most commonly associated with
FUS) is composed of magnesium, ammonium and phosphorus led toward the
conclusion that most cases of FUS were diet induced and away from
investigation of other potential causes. Noting the confusion that
subsequently arose surrounding the term FUS, it has been proposed that
it be used either as a synonym for lower urinary tract disorders in
cats (Osborne et al. 1984) (Osbaldiston and Taussig's original meaning)
or abandoned altogether (Markwell and Buffington 1994). It has been
proposed that signs of lower urinary tract disease in the absence of a
specific diagnosis be simply called idiopathic lower urinary tract
disease; in cases in which a specific cause is identified, the
appropriate descriptive term should be used (Markwell and Buffington
1994).

Fig 1. Effect of changing activity product on saturation and its effect
on crystallization and crystal growth. Modified from Markwell and
Buffington (1994) with permission.

View this table:
[in this window] [in a new window]
Table 1. Results from regression of mean urine pH values on dietary
base excess (BE) in cats fed canned foods1

View larger version (13K):
[in this window]
[in a new window]
Fig 2. Some solutes affecting crystallization in urine. Other factors
affecting crystal formation include time, temperature, and the
presence, absence and effectiveness of endogenous protein
crystallization inhibitors.

WHAT ARE THE MAIN CAUSES OF SIGNS OF LOWER URINARY TRACT DISEASE IN
CATS IN THE 1990S?

Two detailed investigations of specific causes of signs of lower
urinary tract disease in cats have been reported. The first study
described 143 cases of hematuria and dysuria, collected between 1982
and 1985 (Osborne et al. 1989, Kruger et al. 1991). Urethral plugs were
present in 32 cases, urolithiasis without urinary tract infection (UTI)
in 30 cases, UTI alone in two cases and UTI with uroliths in two cases.
Seventy-seven cases were classified as idiopathic. Idiopathic disease
was present in ~69% of the nonobstructed cats.

In a more recent study, 132 cats with signs of lower urinary tract
disease were evaluated by the Ohio State University urology service
(Buffington et al. 1997). Twelve of these cats had urethral obstruction
and a further 11 had concurrent systemic disease. Etiologies were not
reported in the obstructed cats. Specific causes for the signs of lower
urinary tract disease were identified in 29 of the remaining cats.
Urolithiasis (eight struvite, seven calcium oxalate, one unknown) was
present in 16 cats (14.7% of nonobstructed cats without concurrent
systemic disease), anatomic defects in 12 (this included one of the
cats with urolithiasis), neoplasia in 2 (this included one cat with
urolithiasis), and urinary tract infection in 1. Ten cats were
considered to have behavioral abnormalities and 70 had idiopathic
cystitis (64.2% of nonobstructed cats without concurrent systemic
disease). These data stress the importance of idiopathic disease; it is
interesting to note that the proportion of nonobstructed cases with
idiopathic disease was similar in both studies, despite the 10-y gap
between them. The more recent study does show, however, that
urolithiasis remains an important cause of lower urinary tract disease
in cats. It also suggests that two types of urolith predominate
(struvite and calcium oxalate), an observation supported by extensive
data on quantitative analysis of uroliths (Kirk et al. 1995, Osborne et
al. 1995a and 1995b).

DOES DIETARY MODIFICATION HAVE A ROLE IN THE MANAGEMENT OR PREVENTION
OF ANY OF THE LOWER URINARY TRACT DISEASES SEEN IN CATS IN THE 1990S?

Diet can contribute to the etiology, management or prevention of
recurrence of some of these causes of lower urinary tract disease
because dietary ingredients and feeding patterns influence the volume,
pH and solute concentration of urine. Knowledge of these effects of
diet and of the specific cause of signs in individual cases of lower
urinary tract disease enables identification of those cases in which
modification of the diet may truly be of value. Augmenting urine volume
may be a reasonable prophylactic measure for a number of types of lower
urinary tract disease. If the influence of diet on this parameter is
set aside, dietary modifications may be appropriate only in the cases
of lower urinary tract disease in which precipitation of minerals plays
a significant part [based on the data cited above, urethral plugs were
present in~22% and uroliths in ~13-22% of cases of lower urinary tract
disease (Buffington et al. 1997, Kruger et al. 1991, Osborne et al.
1989)]. Furthermore, although dietary recommendations appropriate to
the management of some mineral types are well developed, those for
other types (particularly calcium oxalate) require extensive further
research.

DOES AUGMENTING URINE VOLUME HAVE A ROLE IN MANAGING OR PREVENTING ANY
OF THE LOWER URINARY TRACT DISEASES SEEN IN CATS IN THE 1990S?

Most research relating diet to lower urinary tract disease in cats has
focused on mineral content, or more recently, on the effect of diet on
urinary pH; much less research has been devoted to the effect of diet
on urine volume or specific gravity. It can be predicted from
theoretical considerations that increasing urine volume for a given
solute load has a greater influence on the likelihood of struvite
crystal formation than a reduction in urinary magnesium concentration
(Markwell and Buffington 1994, Marshall and Robertson 1976). This
concept has also been demonstrated experimentally in studies of
struvite activity product in feline urine (Buffington et al. 1990).

In addition, enhancing urine volume may increase the frequency of
urination, which should hasten crystalloid and crystal transit time
through the urinary tract, thus reducing the potential for crystal
growth. Holme demonstrated that hematuria, induced in cats by feeding a
high magnesium, low moisture-containing diet, could be abolished by
feeding the same diet as a slurry containing 80% water (Holme 1977). Of
particular importance, perhaps, are recent observations in cats
classified as having idiopathic lower urinary tract disease. The
proportion of cats showing recurrence of lower urinary tract disease
was significantly less in a group fed a canned, commercial acidifying
diet (11%) than in another group fed the dry formulation of the same
product (39%) (Markwell et al. 1998). The mechanism for this effect was
not determined in the study, but was considered likely to be the result
of changes in the concentration or type of solutes in urine and/or
changes in urine volume.

Epidemiologic studies of signs of lower urinary tract disease conducted
in the 1970s implicated dry cat foods as a risk factor (Reif et al.
1977, Walker et al. 1977, Willeberg 1984); more recently, consumption
of dry foods has been implicated as a risk factor specifically for
idiopathic lower urinary tract disease (Buffington et al. 1997).
Multiple diet-related factors may be involved with this increased risk,
but included within these is the tendency for cats to produce smaller
volumes of more concentrated urine when fed dry foods (Burger et al.
1980, Gaskell 1985). Explanations originally offered for these
observations were that cats might not repair a water deficit as well as
dogs, and that cats fed dry foods take in less water. These
interpretations clearly require further discussion.

In studies of five cats and three dogs, Adolph (1947) found that both
species incurred similar water deficits in 48°C environments when
water was available. After heat exposure without available water, dogs
replaced moderate, but not severe deficits more rapidly than did cats.
Both species, however, drank proportionately more than humans when
dehydration exceeded 5%. These results suggest that differences in
response to dehydration between dogs and cats, if they exist at all,
are relatively small and probably not clinically relevant as a risk
factor for lower urinary tract disease.

It is also doubtful that cats reduce water intake in some unusual way
when fed dry foods. It has been shown that cats fed diets containing
differing amounts of moisture drink quite different amounts of water
(Burger et al. 1980). A large number of these differences may be
accounted for by changes in the potential renal solute load (PRSL) of
the diets fed. The PRSL of a diet is the amount of solute, i.e.,
minerals and nitrogen, that must be excreted in the urine (Kohn and
DiBartola 1992, Ziegler and Fomon 1989). The PRSL has been estimated as
the urea (mg nitrogen/28) plus the sum of the sodium, chloride,
phosphorus and potassium content of the diet (mg N/28 + Na + Cl + K +
P) (O'Connor and Potts 1969). Calculations of PRSL reveal that the
majority of diet-induced changes in water intake (Burger et al. 1980,
Jackson and Tovey 1977, Kane et al. 1981), or urine formation (Sauer et
al. 1985) reported in several studies can be explained by the solute
load of the diet.

Similar data were reported in another study involving cats fed a single
diet to which increasing amounts of water were added (Gaskell 1985).
When the water content of the food was 10 or 45%, total water intake,
urine volume and specific gravity were not different among groups. When
the water content of the food was increased to 75%, however, total
water intake and urine volume increased, and urine specific gravity
decreased. Because the diet was the same in all cases, water intake
(from food) probably increased as a consequence of increased food
intake to meet energy needs from the water-diluted diet. Thus the
differences in urine volumes and specific gravities observed in some of
the studies discussed may be more a reflection of differences in the
PRSL and/or the energy content of dry and wet diets, rather than
moisture content per se. In consequence, if a cat is changed from a dry
to a wet diet as part of a management program for lower urinary tract
disease, it is important to ensure that the intended increases in urine
volume and decreases in specific gravity actually occur.

DOES MANIPULATING URINE PH HAVE A ROLE IN MANAGING OR PREVENTING ANY OF
THE LOWER URINARY TRACT DISEASES SEEN IN CATS IN THE 1990S?

Dietary manipulation has been a mainstay of the management and
prevention of struvite urolithiasis in cats for some years, primarily
because of the influence of dietary ingredients on urine pH. Urine pH
is a much more important determinant of struvite formation than is the
magnesium content of the diet (Buffington et al. 1985, Buffington 1988,
Marshall and Robertson 1976, Taton et al. 1984). Changing pH has a
proportionately much greater effect on changing struvite activity
product (solute activity is the concentration of crystalloid that is
free to react with other solutes in a solution, and is the ultimate
determinant of crystal formation) than changing the concentration of
one or more of the crystalloid components of struvite. Reduction of
urinary pH through dietary manipulation is thus the most reliable means
of creating urine that is undersaturated with struvite; under these
circumstances, crystallization and crystal growth will not occur, and
preformed material will dissolve (Fig. 1) (Buffington 1988, Markwell
and Buffington 1994). Acidification of the urine may not be
appropriate, however, in the management of other types of urolith. It
has been suggested, for example, from epidemiologic data that
acidifying diets, and in particular those that result in a urine pH
<6.29, may increase the risk of calcium oxalate formation (Kirk et al.
1995, Osborne et al. 1995b). Given this background, the ability to
predict the likely urinary pH resulting from consumption of a
particular diet from its analysis would be of considerable value.

Major dietary contributors of acid include the oxidation of sulfur
amino acids and the balance of metabolizable anions and cations
(Brosnan and Brosnan 1982, Patience and Wolynetz 1990). Oxidation of
organic cations yields hydrogen ions, whereas oxidation of organic
anions consumes them (Lennon et al. 1966). The net concentration of
these organic ions can be measured indirectly by analyzing inorganic
cations and anions in the diet (Austic and Patience 1988). This
approach to predicting the influence of diet on urine pH and acid base
balance has been evaluated in a number of species, including humans
(Lennon et al. 1966), pigs (Patience and Wolynetz 1990) and cats
(Kienzle et al. 1991, Kienzle and Schuknecht 1993, Kienzle and
Wilms-Eilers 1994).

The initial studies reported in cats evaluated whether the dietary
"base excess" [calculated from the sum of "alkalogenic" components
(calcium, magnesium, sodium and potassium) minus the sum of
"acidifying" components (phosphorus, chloride, methionine and
cysteine)] could be used to predict urinary pH (Kienzle et al. 1991,
Kienzle and Schuknecht 1993). These studies suggested that there was a
highly significant correlation between dietary base excess and mean
urine pH. They involved, however, only six wet and four dry commercial
diets. We have conducted studies to determine if the same principle
could be applied across a much wider range of canned commercial foods.
In the course of these studies, 32 canned diets from a range of
manufacturers were evaluated (Smith et al. 1995). These were fed to
groups of four to eight healthy, adult cats for between 10 and 23 d.
The cats were housed individually in purpose-built lodges, and urine pH
was measured continuously using an automated system that has been
described previously (Markwell and Smith 1993). Dietary analyses were
used to calculate the base excess for each food using four different
equations (Table 1). Individual mean urine pH values were then
regressed on individual base excess intakes (calculated for each cat
during each trial using its mean food intake) to investigate the
suitability of a linear relationship. Although all four methods of
calculating dietary base excess provided significant linear
relationships, none of the resultant regression equations explained

A second approach to evaluating the data was to establish whether
various combinations of the individual components used to calculate
dietary base excess could be used to predict urinary pH. When the
individual intakes of each component were regressed against individual
urine pH results, the best linear regression procedure suggested a more
effective relationship to be the following:
(units are g/100 g diet as fed). This relationship accounted for 35.5%
of the variation seen in pH values. The signs of the coefficients were
in agreement with expectations, i.e., increases in pH were positively
correlated with the calcium, sodium and potassium content, and
negatively correlated with the methionine and phosphorus content of the
diet. These data indicate that dietary content may explain a
significant proportion of the variation seen in the urine pH of
meal-fed cats. More research is required, however, before dietary
analysis can be used to yield an accurate prediction of the urine pH of
cats fed commercial canned foods.

DIET AND URINARY SATURATION

The primary goal of dietary manipulation to alter urinary pH and solute
concentration is to achieve urine that is undersaturated with
calculogenic crystalloids, although as described above, enhancement of
urine volume may have the added benefit of increasing the frequency of
urination, and hence reducing retention time. Undersaturation of urine
is a prerequisite for urolith dissolution, and supersaturation with
calculogenic crystalloids is an essential requirement for formation of
a crystal nucleus, the initial step in development of a urine crystal
(Fig. 1) (Buffington 1988, Markwell and Buffington 1994, Osborne et al.
1995a).

The study of the effects of diet on urinary saturation requires
determination of solute activity. Although the concentration of ions in
a solution, e.g., a urine sample, can be measured relatively easily,
this is not a measure of activity because an individual ion may form a
complex with many other ions; magnesium, for example, may form
complexes with phosphate, citrate, oxalate and sulfate (Fig. 2). The
extent to which these complexes form can be predicted from known
dissociation constants, allowing free ion concentrations to be
predicted. Noncomplexed ions are further restricted in their movement
by the nonspecific effect of other ions in solution, an effect that
varies with the electrical field strength of the solution. This effect
is represented by the term "activity coefficient" (Senior and Finlayson
1986). Computer programs are available to calculate urinary saturations
(Werness et al. 1985), although a series of complex analyses are
required after collection. One further limitation is that the
calculations do not account for some additional factors such as urine
proteins which may influence crystal formation. Despite these
difficulties, measurement of activity products provides a more critical
appraisal of the likely beneficial, or detrimental effects of
manipulation of nutrient profile than, for example, assessment of urine
pH. These techniques may permit the development and fine tuning of
nutrient profiles in cats with the aim of controlling lower urinary
tract diseases associated with a range of different mineral types.

FOOTNOTES
1 Presented as part of the Waltham International Symposium on Pet
Nutrition and Health in the 21st Century, Orlando, FL, May 26-29, 1997.
Guest editors for the symposium publication were Ivan Burger, Waltham
Centre for Pet Nutrition, Leicestershire, UK and D'Ann Finley,
University of California, Davis.
2 To whom correspondence should be addressed.
3 Abbreviations used: RUS, feline urological syndrome; PRSL, potential
renal solute load; UTI, urinary tract infection.

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Abstract
Introduction
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