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Abstract

Calcium, phosphorus, and vitamin D are nutrients that play a key role in maintaining normal organ, cell, and tissue function. Much is known about their role in bone metabolism, but these nutrients are also important in renal health, urinary tract disease, and multiple other organ systems. It is nutritionally important to meet the physiologic requirements for each of these nutrients, but the interplay between them should also be considered.
Calcium, Phosphorus, and
Vitamin D in Dogs and Cats
Beyond the Bones
Jonathan Stockman, DVM
a
, Cecilia Villaverde, BVSc, PhD
b
,
Ronald Jan Corbee, DVM, PhD
c,
*
INTRODUCTION
Calcium, phosphorus, and vitamin D are important essential nutrients in the dog and
the cat. As such, these nutrients are required as a part of a complete and balanced
diet. Most commercial diets for dogs and cats provide sufficient amounts of calcium,
phosphorus, and vitamin D,
1–3
but homemade diets may be deficient or unbalanced in
J. Stockman is a consultant for Petco Animal Supplies, Inc. C. Villaverde has received honoraria
for consulting and speaking engagements from pet food manufacturers. R.J. Corbee declares
no conflict of interest regarding this article.
a
Department of Clinical Veterinary Sciences, LIU College of Veterinary Medicine, Long Island
University, 720 Northern Boulevard, Brookville, NY 11548, USA;
b
Expert Pet Nutrition, Fermoy,
Cork P61KX38, Ireland;
c
Department of Clinical Sciences, Faculty of Veterinary Medicine,
Utrecht University, Yalelaan 108, Utrecht 3584 CM, The Netherlands
* Corresponding author.
E-mail address: R.J.Corbee@uu.nl
KEYWORDS
Metabolism Renal Urinary tract Gastrointestinal Cancer
KEY POINTS
Calcium, phosphorus, and vitamin D have a key role in skeletal development and health as
well as other important metabolic functions.
Insufficient or unbalanced dietary provision of these nutrients can have multiple negative
health impacts.
Excess vitamin D intake may cause hypercalcemia and negative health effects in dogs and
cats, and the health-related effects of high calcium and phosphorus intake are being
studied.
The dietary provision of calcium, phosphorus, and vitamin D and their interactions must be
considered in patients with renal-urinary diseases.
The role of vitamin D in chronic conditions, such as enteropathies and neoplasia, is
receiving considerable attention, but research is still inconclusive, and no clinical recom-
mendations can be made at this time.
Vet Clin Small Anim -(2021) --
https://doi.org/10.1016/j.cvsm.2021.01.003 vetsmall.theclinics.com
0195-5616/21/ª2021 The Author(s). Published by Elsevier Inc. This is an open access article under
the CC BY license (http://creativecommons.org/licenses/by/4.0/).
these nutrients, which may lead to negative outcomes.
4
Calcium and phosphorus are
stored mostly in skeletal tissue, although they are present throughout the body. Bone
metabolism and calcium and phosphorus absorption and retention are influenced by
vitamin D as well as the relative dietary concentrations of these and other minerals.
Although bone health is closely impacted by the nutrition and metabolism of these nu-
trients, these nutrients also impact animal physiology in many additional ways and
have health impacts that transcend skeletal health alone. The following summary is
aimed to explore and explain the various ways calcium, phosphorus, and vitamin D
all play complex roles in canine and feline health.
The Nutritional Requirements for Calcium, Phosphorus, and Vitamin D in Dogs and
Cats
Calcium and phosphorus are essential nutrients in dogs and cats, and therefore, they
need to be provided in the diet in adequate amounts and in bioavailable forms. Cal-
cium and phosphorus are the first and second most abundant minerals in the body,
respectively, where they play both structural (such as of bone and teeth) and functional
roles. For example, calcium is involved in blood coagulation and nerve impulse trans-
mission, and phosphorus has a major role in energy metabolism as a component of
adenosine triphosphate. The National Research Council gives a recommended allow-
ance for calcium and phosphorus for different life stages (Table 1).
5
It also defines a
safe upper limit for calcium of 4.5 g/1000 kcal of metabolizable energy for puppies,
specifically those of large and giant breeds, where excess can result in skeletal abnor-
malities.
6,7
Adult dogs seem able to adequately handle high dietary calcium intakes.
8
Vitamin D is also an essential nutrient in dogs and cats, because synthesis from sun-
light exposure seems to be limited.
9,10
Therefore, it must be included in complete and
balanced diets for dogs and cats in all life stages. Vitamin D plays an important role in
calcium and phosphorus homeostasis and, consequently, its deficiency is associated
with skeletal abnormalities. There is a lack of research on vitamin D requirements,
especially in adult animals,
11
and the dietary recommendations
5,12,13
are educated es-
timates based on intakes that appear to support skeletal health. There is a growing
body of research that supports the importance of vitamin D in other areas, as the
vitamin D receptor is present in multiple tissues, which could result in changes in di-
etary recommendations in the future.
14–17
Dietary Sources of Calcium, Phosphorus, and Vitamin D and Their Absorption and
Bioavailability
Calcium and phosphorus in pet food can be provided by bony raw materials (from
meat and fish). Phosphorus is also provided by meat and vegetable ingredients,
such as cereals, although phosphorus in grains can be present as phytate, which
has a reduced bioavailability compared with other forms in monogastric animals.
18
Table 1
Recommended allowances (grams per 1000 kcal of metabolizable energy) for calcium and
phosphorus for growth, maintenance, and reproduction in dogs and cats
5
Growth Maintenance Reproduction
Calcium Dog 3 1 1.9
Cat 2 0.72 2.7
Phosphorus Dog 2.5 0.75 1.2
Cat 1.8 0.64 1.9
Stockman et al
2
Both minerals can also be provided as purified salts, together (as calcium phosphate
salts) or separately.
Calcium and phosphorus availability is affected by several dietary factors, such as
total amount and relative proportion to each other. Because of the close relationship of
calcium and phosphorus, the Association of American Feed Control Officials (AAFCO)
guidelines
12
recommend that commercial dog food not only meets the individual re-
quirements but also provides a minimum calcium-to-phosphorus ratio of 1:1 and a
maximum ratio of 2:1. Bioavailability is also affected by form and source. Data in
cats have shown that highly soluble phosphate salts can result in increased absorption
and postprandial serum levels compared with diets whereby it is provided by the bony
raw materials,
19
which could affect phosphorus homeostasis negatively and
contribute to renal damage.
20,21
Dietary vitamin D is provided as cholecalciferol (vitamin D3) and ergocalciferol
(vitamin D2), from animal and vegetable ingredients, respectively; it can also be added
as a purified additive. Cats discriminate between vitamin D forms and use cholecalcif-
erol more efficiently than ergocalciferol.
22
There is a lack of controlled, well-powered
studies in dogs,
5,11
but vitamins D2 and D3 appear to have a similar potency in this
species.
23
Skeletal Development and Skeletal Health
Because the bone is the major reservoir of calcium and phosphorus, its metabolism is
impacted by their relative homeostasis. During growth, imbalances of these nutrients
have the most detrimental consequences, resulting in factures and limb deformities,
such as valgus or varus stance, and incongruence of the elbow joint.
24–28
Vitamin D
plays a key role in bone remodeling and bone growth by activating osteoblasts and
osteoclasts. It is important for clinicians to distinguish between causes of limb defor-
mities by nutritional evaluation, orthopedic examination, evaluation of radiographs,
and determining plasma levels of calcium, phosphorus, parathyroid hormone (PTH),
calcitonin (CT), and vitamin D metabolites.
29
A common pitfall is to rule out insufficient calcium intake when plasma calcium
levels are within the normal range. Even in cases of dietary calcium insufficiency,
plasma calcium levels are usually kept within normal limits, unless the regulatory
compensatory mechanisms fall short. Plasma calcium levels are strongly regulated
because low calcium has immediate detrimental effects, such as cardiac arrhythmias,
that can be fatal. Typically, with a low dietary calcium intake, radiographs will show
decreased mineralization of bone, enlarged medullar areas, and thinner cortices
that easily break (eg, green stick fractures). PTH levels will be increased as well as
active vitamin D levels. Sometimes, deficient intake in both calcium and vitamin D oc-
curs, which is often referred to as “all-meat syndrome.” These cases may show signs
of low vitamin D, such as enlarged growth plates and decreased mineralization of
bone and cartilage. In adult animals, the bone will be gradually demineralized and
replaced by connective tissue under the influence of fibroblast growth factor-23
(FGF-23).
30
Many times, these diets also lead to a high phosphorus intake, which ex-
acerbates the pathologic condition by increasing PTH activity, resulting in more oste-
oclastic activity. In contrast, low phosphorus intake results in decreased levels of
PTH.
31
In cases of adequate calcium and phosphorus but deficient vitamin D intake,
enlarged growth plates can be seen radiographically as well as decreased mineraliza-
tion of bone. PTH levels are expected to be high, and active vitamin D levels will be
low. To prevent hypercalcemia, CT levels will be increased. In growing animals, this
will result in decreased osteoclastic activity, as osteoclasts can no longer make con-
tact to the matrix with their ruffled borders. Prolonged decrease of osteoclastic activity
Calcium, Phosphorus, Vitamin D in Dogs and Cats 3
may result in enostosis, which can be visible on radiographs as an opaque cloud within
the medullar area, and by painful reaction on deep palpation of the long bones during
orthopedic examination. Treatment of these dietary imbalances is largely dependent
on normalizing dietary intake, combined with pain medication and exercise
instructions.
32
The Importance of These Nutrients for Urinary Health
Urolithiasis is among the most common urinary diseases in companion animals. Uro-
liths and urinary crystals may occur as a result of multiple causes, including hereditary
disease, infections, toxicity, and nutritional deficiency or excess. There are multiple
uroliths and urinary crystals of varying compositions in dogs and cats, including
organic and inorganic compounds. Some of the most common compounds are min-
eral salts, which include calcium and phosphorus. In fact, it is estimated that at least
90% of the uroliths in dogs and cats are composed of either calcium oxalate monohy-
drate or dehydrate compounds or struvite (magnesium-ammonium-phosphate hexa-
hydrate).
33
Although crystalluria can be benign (with the exception of urethral plugs in
male cats), crystal aggregation and nucleation may lead to the formation of uroliths.
The risk for urolith formation depends on the urinary saturation with minerals or
organic compounds that precipitate into crystals
34
; however, this process also de-
pends on the involvement of inhibitors of urolithiasis, including urinary proteins (neph-
rocalcin, uropontin, Tamm-Horsfall mucoprotein), urinary pH, and the presence and
saturation of ions in the solution.
35,36
Calcium oxalate urolithiasis
Hypercalcemia (of any cause) is a risk factor for the formation of calcium oxalate uro-
liths in both dogs and cats, as it may result in hypercalciuria.
37,38
Dietary phosphorus
restriction below the established requirements may increase the risk for hypercalce-
mia, as a high calcium-to-phosphorus ratio may result in increased calcium absorp-
tion. When phosphorus intake is low, a decrease in FGF-23, which is a regulator of
calcium and phosphorus excretion, results in increased activity of 1-alpha hydroxy-
lase,
39
resulting in more active vitamin D, which increases intestinal calcium absorp-
tion and exacerbates hypercalciuria.
Normally, dogs and cats do not excrete much calcium in the urine even when the
calcium intake is increased, as calcium homeostasis is regulated primarily via fecal
excretion, presumably because dietary calcium absorption is reduced.
8,21
Increased
dietary calcium was also found not to significantly change the urinary relative super-
saturation for calcium oxalate.
8
However, in cases of hypercalcemia, the fractional
excretion of calcium is increased, resulting in hypercalciuria.
33,40
Although hypercal-
ciuria may not be a finding in all cases of canine and feline calcium oxalate urolithia-
sis,
41
it is a prominent risk factor.
Dogs with a medical history of calcium oxalate urolithiasis from highly predisposed
breeds (miniature schnauzers, bichon frise, and shih tzu) were found to have greater
urinary calcium excretion than control dogs of the same breed but not increased uri-
nary oxalate excretion or overt hypercalcemia (although the ionized calcium was
higher in case dogs).
42
The same researchers also found no increase in bone turnover
markers in these dogs, possibly suggesting that the observed hypercalciuria is the
result of increased intestinal calcium absorption or renal calcium leakage.
43
Diets that are formulated to promote urine acidity may contain acidifiers, such as
ammonium chloride, that have been shown to increase urinary calcium excretion.
44
Acidic urine may negatively impact urolith inhibitors, such as citrate or urinary muco-
proteins, that prevent the formation of calcium oxalate crystals. It is thought that
Stockman et al
4
metabolic acidosis promotes osteoclast activity and inhibits osteoblasts for a net bone
resorption and release of a strong calcium-containing alkaline buffer, hydroxyapa-
tite.
45
The increase in bone turnover and the release of calcium increase the ionized
calcium concentrations and can result in hypercalciuria and possibly increased risk
for calcium oxalate urolithiasis.
Feeding a high-fiber diet has been suggested as a nutritional strategy for the man-
agement of hypercalcemia in both dogs and cats; however, conflicting evidence indi-
cates that further research is needed as far as the clinical benefit of this approach,
particularly because evidence suggests that soluble fiber may increase intestinal cal-
cium absorption.
32,40,46–48
Because some fiber sources are high in oxalates, this
should also be taken into account when formulating a diet plan.
Struvite urolithiasis
Urinary phosphorus excretion is influenced by its intake (amount and bioavailability) as
well as the intake of sodium, calcium, and magnesium.
21,49
Increased dietary phos-
phorus is not sufficient to increase the relative supersaturation for struvite in cats or
dogs to values that are considered supportive of crystallization.
8,21
As a result of
hyperphosphatemia, increased PTH promotes urinary phosphorous excretion in the
kidneys by reducing expression of sodium phosphate cotransporter on the apical
membrane of the proximal tubule. The active form of vitamin D, calcitriol, increases uri-
nary phosphorus excretion indirectly as it increases the sodium phosphorus trans-
porters (NaPi-2b transporters) in the intestines.
50
There are no reports to the
authors’ knowledge of a higher incidence of struvite urolithiasis in dogs or cats with
hyperphosphatemia, presumably because hyperphosphatemia most often occurs in
cats who suffer from renal disease and may have other related metabolic complica-
tions, such as dilute urine and metabolic acidosis.
Sterile struvite urinary calculi in cats and dogs may be dissolved with a diet that is
reduced in phosphorous, magnesium, and protein, which contribute the components
of struvite urolithiasis, and with an acidic urinary pH (6.0 or lower).
51–53
Nonsterile stru-
vite uroliths may be dissolved with use of targeted antimicrobial treatment primarily
and complementary nutritional therapy.
52
Urine pH may be influenced by the dietary
anion-to-cation balance. Therefore, a diet that is aiming to reduce urine pH may be
lower in cations, such as calcium, sodium, or potassium, and higher in phosphate, sul-
fate, and chloride.
5
There are also acidifying compounds that may be added to the diet
to achieve low urine pH, including phosphoric acid, methionine, and ammonium chlo-
ride. Base excess and urine pH appear to be more important than the relative mineral
intake for struvite prevention.
54
Dietary prevention of recurrence of sterile struvite uro-
lithiasis is possible with a diet that promotes urine dilution, targets an acidic pH, and
provides reduced amounts of phosphorus and magnesium, although recurrence rates
are unknown.
33
Addressing predisposing factors for infection, such as anatomic fea-
tures and obesity, can help prevent the recurrence of nonsterile struvite.
Calcium phosphate and calcium carbonate urolithiasis
Calcium phosphate and calcium carbonate are often a small component of complex
uroliths precipitated with struvite or calcium oxalate. Pure calcium phosphate or car-
bonate uroliths are uncommon in dogs and cats. Several calcium phosphate com-
pounds include hydroxyapatite, brushite, whitlockite, and octacalcium phosphate,
of which hydroxyapatite and calcium carbonate compounds are most common.
55
In
dogs, many times these result from bacterial cystitis, as is struvite, and are formed un-
der alkaline conditions.
33
Other conditions, such as hyperparathyroidism, that lead to
hypercalciuria and hyperphosphaturia are also possible risk factors. Physical removal
Calcium, Phosphorus, Vitamin D in Dogs and Cats 5
of these uroliths is usually necessary, although they may dissolve when the primary
cause is addressed (for example, hyperparathyroidism).
56
Nutritionally, high dietary
phosphorus in a bioavailable form may increase the relative supersaturation for brush-
ite in cats.
21
Otherwise, there are no nutritional prevention strategies for these uroliths
aside from addressing the primary cause (ie, bacterial cystitis) if possible.
In summary, calcium and phosphorus compounds are most common among those
that are involved in precipitation in the canine and feline urinary system; however, the
pathogenesis for these urinary calculi is complex, and simple dietary excess of these
minerals is not the sole cause. As more data regarding the physiology and nutritional
requirements and tolerance for calcium and phosphorus are accumulated, there will
be a greater understanding of how best to nutritionally prevent and manage these in
dogs and cats.
The Importance of These Nutrients for Renal Health
Calcium and phosphorus metabolism is commonly dysregulated in dogs and cats with
chronic kidney disease (CKD), which has a major impact on the progression of disease
and the associated clinical signs.
As discussed above, hypercalcemia may increase the risk of calcium oxalate uro-
lithiasis as well as lead to soft tissue mineralization and possibly to kidney injury
and impaired function. Hypercalcemia can be the result of dietary, metabolic,
neoplastic, renal, and idiopathic causes in dogs and cats. The degree of hypercalce-
mia and its chronicity impacts prognosis. In cats, clinical signs of hypercalcemia are
usually most severe when the increase in calcium is rapid.
40
Most often, clinical signs
are noted when serum total calcium is higher than 14.0 mg/dL and ionized calcium is
greater than 6.5 mg/dL (1.6 mmol/L). If serum total calcium increases to 16.0 mg/dL or
if ionized calcium increases to above 7.5 mg/dL (1.9 mmol/L), clinical signs are severe
and require hospitalization and immediate care.
40
A reduction in dietary vitamin D,
which is one of the most important regulators of calcium absorption, is recommended
when the cause of hypercalcemia is vitamin D toxicity. Some anecdotally recommend
feeding a diet with moderately reduced calcium and vitamin D in addition to added
insoluble fiber for all-cause hypercalcemia.
40
High dietary calcium on its own does
not appear to be a cause of hypercalcemia or renal disease in dogs, such as Labrador
retrievers and beagles.
8
It is unknown if dietary calcium reduction would benefit dogs
with existing hypercalcemia.
Although regulatory mechanisms are aimed to maintain serum ionized calcium and
inorganic phosphorus, shifts may occur and worsen with CKD progression and are
associated with increased mortality.
57–59
A reduction of functioning nephrons, as oc-
curs in advanced CKD, leads to lower glomerular filtration rate and a reduced phos-
phorus excretion, ultimately resulting in increased serum inorganic phosphorus. The
result of this would be a compensatory increase in filtration, but with a gradual in-
crease in the serum inorganic phosphorus set point, as compensation fails to keep
up unless phosphorus intake is reduced. The retention of phosphorus can lead to
soft tissue mineralization, which may further damage the renal tissue and lead to
reduced renal function.
60
The function of 1-a-hydroxylase enzyme is necessary to form calcitriol from calci-
diol; this is reduced in CKD patients because of the decrease in renal mass and as
a result of the activity of secreted FGF-23. Decreased calcitriol results in reduces cal-
cium absorption from the intestines, decreased ionized calcium, and an increase in
PTH.
39
PTH increase may lead to additional negative health implications, including
osteodystrophy, pathologic fractures, and “rubber jaw.”
60
Stockman et al
6
Serum phosphorus may remain in normal reference ranges thanks to compensatory
mechanisms despite pathologic shifts in renal glomerular filtration, urine concentra-
tion, creatinine, PTH, and FGF-23.
39
Therefore, relying on increased serum phos-
phorus as a marker of CKD or as a primary indication to limit dietary phosphorus
has important limitations. PTH and FGF-23 are not typically included in routine
biochemistry panels; therefore, clinicians may not be aware of early dysregulation
that occurs in CKD patients. Increases in FGF-23 and symmetric dimethylarginine, a
biomarker for decreased glomerular filtration in early CKD, are intercorrelated in geri-
atric preazotemic cats.
61
The timing of these increases indicates that alterations in
normal phosphorus metabolism occur in early CKD or even before CKD in cats.
62,63
Evidence regarding the potential benefits of early phosphorous intake reduction is
lacking; however, the shifts in normal phosphorous metabolism may be nutritionally
managed with dietary phosphorus restriction in advanced CKD (approximating or un-
der the minimum accepted dietary requirements), as this may slow CKD progression
and reduce related health complications.
60,64–67
Recent data suggest that dietary phosphorus greater than 3.0 or 3.6 g/1000 kcal
may lead to kidney damage and CKD in healthy cats when it is provided in a highly
available form of soluble inorganic salts and when the ratio between calcium and
phosphorus is low.
20,21
The relevance of this is highlighted by recent surveys that eval-
uated the total calcium and phosphorus in feline diets and found that approximately
33% of the tested products had a higher total phosphorus than 3.6 g/1000 kcal and
highly variable calcium-to-phosphorus ratio (0.5–1.7).
2
Although the ratio between
organic and inorganic phosphorus in those diets was not evaluated, several diets
had a low calcium-to-phosphorus ratio in addition to high total phosphorus. However,
there is no evidence that commercial cat foods indeed cause renal disease in healthy
cats, as the aforementioned studies included experimental diets with a high proportion
of soluble phosphorus salts possibly exceeding that of most commercial diets. There
is no current maximum for dietary phosphorus for adult cats in the guidelines by
AAFCO, nor is there a guidance regarding calcium-to-phosphorus ratio or the use
of inorganic phosphorus salt additives.
12
Although more research is required to estab-
lish safety maximums, the authors believe that interim limits should be considered as
well as a recommended calcium-to-phosphorous ratio greater than 1. In dogs, there is
currently no evidence that high dietary phosphorus (up to 4.0 g/1000 kcal) in organic or
inorganic form leads to renal injury when the calcium-to-phosphorus ratio is greater
than 1
8
; however, further research to determine the tolerability of high dietary phos-
phorus in dogs is needed.
Vitamin D and Its Importance for Other Conditions Such as Gastrointestinal
Disease and Cancer
The vitamin D receptor is present in multiple organs, such as the small intestine and
colon. Apart from the traditional role of increasing calcium absorption by active trans-
cellular transportation in the small intestine in the case of low plasma calcium levels,
68
calcitriol (active vitamin D) has additional important functions within the gastrointes-
tinal tract. Calcitriol is needed to maintain the gastrointestinal barrier function by upre-
gulation of tight junction protein expression,
69
the production of brush border
enzymes,
70
as well as the formation of microvilli.
71
An intact gastrointestinal barrier
prevents pathogen invasion and bacterial translocation; therefore, vitamin D is
regarded as protective for chronic gastrointestinal diseases. Calcitriol further protects
against damage to the gastrointestinal tract by suppressing tumor necrosis factor-
alpha and nuclear factor kappa-beta pathways. These proinflammatory pathways
play a key role in the first line of defense against pathogens; however, when
Calcium, Phosphorus, Vitamin D in Dogs and Cats 7
overexpression occurs, this can contribute to chronic gastrointestinal diseases. The
inhibition of these proinflammatory pathways makes calcitriol an interesting therapeu-
tic option for multiple chronic inflammatory conditions (eg, osteoarthritis, atopic
dermatitis), but so far, clinical studies in dogs and cats are lacking.
Vitamin D has several immune-modulating effects, demonstrated by in vitro studies,
whereas the clinical effects are largely not yet elucidated.
72
Vitamin D–deficient mice
are more prone to infection and support overgrowth by pathogenic bacteria because
of inadequate response of the immune system.
71
Supplementation of vitamin D me-
tabolites as a possible effective treatment or prevention of chronic gastrointestinal dis-
eases in dogs and cats requires further investigation. Vitamin D also affects tissue
fibrosis by suppressing the transforming growth factor-beta pathway, as was demon-
strated in colon cell lines from people,
73
in gastrointestinal cells of mice,
74
and in the
feline liver (hepatic stellate cells).
75
These studies suggest a possible preventative role
for vitamin D in the progression of chronic inflammatory diseases to cancer (which has
high relevance for prevention of colorectal cancer in people).
Together with the antifibrotic effects, vitamin D has antiproliferative effects. Calci-
triol inhibits cyclins and enhances expression of inhibitors of cyclin-dependent ki-
nases; however, clinical studies are scarce. Currently, the strongest clinical
evidence is based on epidemiologic studies in people demonstrating lower odds ratios
for colorectal cancer (0.88) and breast cancer (0.72) associated with increased vitamin
D intake compared with a typical Western-type diet.
73
In people, deficient intake of
vitamin D, combined with insufficient exposure to sunlight, is common, whereas
most dogs and cats consume sufficient dietary vitamin D thanks to complete and
balanced diets. Clinical studies in dogs and cats on the effects of vitamin D on different
types of cancer have not been conducted thus far to the authors’ knowledge.
CLINICS CARE POINTS
Vitamin D might be protective for several inflammatory and proliferative diseases,
like gastrointestinal disease and cancer, which are subjects for future research.
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... Free FA are long chain saturated if released; they form acid-calcium soaps that are insoluble in aqueous media at the pH of the intestine, which causes impaired absorption of both SFA and calcium [17,18]. Calcium loss can affect Ca:P ratio in the diet, which can be associated with kidney damage in cats [19,20]. ...
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... Phosphorus (P) is the main factor that causes eutrophication; thus, P must be removed from water to avoid algal bloom [1]. P is also considered an indispensable element for living [2]. With sharp the decrease in the world's P resource reserves, the demand for phosphate fertilizer is increasing for food production in agriculture [3]. ...
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... However, studies have established that high levels of dietary Ca for puppies and growing dogs can result in adverse growth and health effects, with certain breeds and dog size categories being most susceptible [3][4][5][6]. Cofactors such as health status [7,8] or synergistic or inhibitory interactions of Ca with other minerals [9][10][11][12][13], particularly P and vitamins [14,15], are also thought to be influential in modifying its potential effect on health. ...
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This study sought to establish a baseline understanding of immune function and its association with serum vitamin D in shelter dogs. Ten apparently healthy shelter dogs housed in the Arizona Humane Society for ≥7 days and 10 apparently healthy, age, breed, and sex-matched control dogs were included. Serum 25-hydroxyvitamin D (25[OH]D), the major circulating vitamin D metabolite, was measured using high performance liquid chromatography. Whole blood samples were stimulated with lipopolysaccharide (LPS), lipoteichoic acid, or phosphate buffer solution, and tumor necrosis factor (TNF)-ɑ, interleukin (IL)-6, and IL-10 were measured using a canine-specific multiplex bead-based assay. Phagocytosis of opsonized-Escherichia coli and E. coli-induced oxidative burst were evaluated with flow cytometry. Shelter dogs had decreased percentages of granulocytes and monocytes (GM) that had phagocytized opsonized-E coli (P = 0.019) and performed E. coli-induced oxidative burst (P = 0.011). There were no significant differences in TNF-α, IL-6, IL-10, or 25(OH)D concentrations between shelter and control dogs. Serum 25(OH)D concentrations had a weak positive association with the intensity of GM E. coli-induced oxidative burst (r² = 0.23, P = 0.03). There was a moderate inverse association between serum 25(OH)D concentration and LPS-stimulated TNF-ɑ production in shelter dogs (r² = 0.40, P = 0.04). These results demonstrate immune dysregulation in vitro in shelter dogs housed for ≥7 days when compared to age, breed, and sex-matched control dogs. While serum 25(OH)D concentrations did not differ between shelter and control dogs, significant associations between 25(OH)D concentration and immune function parameters in vitro were identified.
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People with calcium oxalate (CaOx) urolithiasis and idiopathic hypercalciuria (IH) often have evidence of increased bone resorption, but bone turnover has not previously been investigated in dogs with these conditions. The aim of this study was to determine whether a marker of bone resorption, β-crosslaps, differs between dogs with CaOx urolithiasis and IH compared to controls. This retrospective, cross-sectional study used a canine specific ELISA to measure β-crosslaps concentrations in stored frozen serum samples from 20 dogs with CaOx urolithiasis and IH and 20 breed-, sex-, and age-matched stone-free controls (18 Miniature Schnauzers, 14 Bichons Frise, and 8 Shih Tzus). Dogs with CaOx urolithiasis and IH had lower β-crosslaps concentrations relative to controls (P =.0043), and β-crosslaps had a moderate negative correlation with urinary calcium-to-creatinine ratios (r = −0.44, P =.0044). Miniature Schnauzers had lower β-crosslaps concentrations than the other two breeds (P =.0035). The ELISA had acceptable intra-assay precision, but concentrations decreased when samples were repeatedly assayed over time. Assay recovery rates were also below acceptance criteria. In conclusion, Miniature Schnauzers, Bichons Frise, and Shih Tzus with CaOx urolithiasis and IH have evidence of decreased bone resorption compared to stone-free controls. This suggests that other causes of IH, such as intestinal hyperabsorption of calcium, underlie risk for CaOx urolithiasis in these breeds. Results should be confirmed in larger populations and with other β-crosslaps assays and additional biomarkers of bone turnover. The stability of canine serum β-crosslaps after freeze-thaw cycles and storage at various temperatures requires investigation.