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Downloaded from http://inpractice.bmj.com/ on April 30, 2017 - Published by group.bmj.com
MANAGEMENT AND TREATMENT
Management and treatment of
chronic kidney disease in cats
Sarah Caney
Making a diagnosis of chronic kidney disease (CKD) in cats marks the start
of a new and complex journey to provide optimal treatment for the patient.
A successful outcome depends on attention to detail and a good working
relationship with the carer and patient. If it is possible to institute good
treatment measures, many patients with CKD survive for several years
following diagnosis, with an excellent quality of life.
AFTER a diagnosis of chronic kidney disease
(CKD) attention moves to treating and managing
the disease. Treatment should include
addressing any underlying disease which is
contributing to ongoing renal damage, strategies
aimed at reducing progression of disease and
symptomatic support of complications of CKD,
such as poor appetite and dehydration. CKD is
a progressive condition and, ultimately, despite
its chronicity, is likely to be responsible for the
patient’s death. Phosphate-restriction, ideally
through feeding a specially formulated renal
diet, has been shown to be the most effective
management option. Cats with CKD that will eat
a renal diet live on average two to three times
longer than those fed a standard commercial cat
food, so all efforts should be put into supporting
transition to a renal diet. Further treatments,
tailored to the individual’s needs, can make a big
difference to quality of life.
What aspects of management
should be considered in all
patients?
Management of CKD should aim to:
■■
■■
■■
Identify and treat any underlying disease.
Where possible, use strategies that are
known or thought to slow the progression
of renal disease.
Provide supportive and symptomatic
treatments to improve quality of life.
Identifying underlying disease
Diagnosing underlying disease is important to
halt ongoing renal damage and slow progression
of CKD. Investigations such as ultrasonography,
radiography, urine culture, renal biopsy and
Sarah Caney,
Cat Professional, Midlothian Innovation
Centre, Roslin, Midlothian EH25 9RE, UK
e-mail: [email protected]
10
other tests, according to the individual’s needs,
may be required to identify underlying disease.
Examples of conditions where diagnosis makes
a difference to the treatment recommendations
for CKD would include renal lymphoma
and bacterial pyelonephritis where specific
treatment can improve the patient outcome. In
many CKD patients, the underlying cause of the
disease cannot be identified.
Strategies aimed at slowing the
progression of renal disease
Phosphate restriction
The most proven general treatment for CKD
is feeding a specially designed renal diet. A
number of studies have shown that feeding one
of these diets improves quality and length of
life of affected cats. Renal diets are modified
in a number of ways to support cats with
CKD, including being protein and phosphaterestricted, supplemented in potassium and
B vitamins, higher in fat and calories, highly
palatable and non-acidifying. The greatest
benefit of feeding a renal diet is thought to be
the phosphate-restriction.
In normal cats, excess phosphorus
consumed in the diet is excreted by the kidneys
and renal excretion of phosphate is dependent
on glomerular filtration. Therefore, cats with
CKD are vulnerable to phosphate retention and
hyperphosphataemia. Regulation of phosphate
excretion is under the control of parathyroid
hormone (PTH) which has a phosphaturic effect.
PTH increases renal reabsorption of filtered
calcium while increasing renal excretion of
phosphate. PTH has other effects including
mobilisation of calcium (and phosphate) from
bone, and increasing calcitriol production,
which facilitates calcium absorption from the
intestine. Hyperphosphataemia and reduced
renal production of calcitriol contribute
to the development of renal secondary
hyperparathyroidism (R2HPTH); a condition
which more recently has been referred to as
feline mineral and bone disorder. In a healthy
cat, increased amounts of PTH would help to
correct hyperphosphataemia by increasing
renal elimination of this substance. However,
this strategy is only effective when there are
sufficient functioning nephrons available
to respond. Once the renal mass is below a
critical level, increases in PTH are counterproductive and merely result in mobilisation
of calcium and phosphate from the bone.
Calcium and phosphate mobilisation may
lead to renal osteodystrophy and clinical
consequences including ‘rubber jaw’. Release
of calcium and phosphate also leads to
soft tissue mineralisation. Where present,
nephrocalcinosis is especially damaging to
renal function.
Unless treated, R2HPTH progressively
worsens. High levels of PTH are thought to
contribute to the uraemic state through acting as
one of the uraemic toxins. High levels of PTH also
contribute to ongoing renal damage by causing
calcium influx into renal tubular cells and
precipitation of calcium phosphate in the lumen
of the tubules. R2HPTH is seen in most – if not
all - cats with CKD and may precede azotaemia.
Hyperphosphataemia is used as a marker of
R2HPTH; if phosphate levels are raised in a cat
with CKD they can be assumed to be suffering
from R2HPTH. If phosphate levels are normal
unfortunately this does not rule out R2HPTH.
The International Renal Interest Society (www.
iris-kidney.com)
recommend
phosphate
restriction for all cats with azotaemic CKD
(IRIS stages 2, 3, 4) irrespective of their
blood phosphate levels and have guidelines
regarding ideal (target) blood phosphate levels
(Table 1). The aim of phosphate restriction is to
prevent and reverse development of R2HPTH
and hence slow progression of renal disease.
Use of a renal diet and/or phosphate binder
is effective in achieving phosphate restriction.
Acceptance of a renal diet can take several weeks
or months to achieve and success depends on
Table 1: International Renal Interest
Society (IRIS) guidelines for target
phosphate levels in cats with CKD
IRIS
stage
Blood creatinine
Target phosphate
level
1
<140 µmol/l
n/a
2
140-249 µmol/l
0.9-1.5 mmol/l
3
250-439 µmol/l
0.9-1.6 mmol/l
4
≥440 µmol/l
0.9-1.9 mmol/l
CKD Chronic kidney disease, n/a Not applicable
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Hydration support
Fig 1: Owners can be
taught to administer
subcutaneous fluids
to their cat at home
and this can be
helpful in maintaining
optimal hydration
in some patients.
A typical regime
involves giving 50 to
100 ml Hartmann‘s
solution once daily,
administered via a
giving set and 21 G
needle using gravity to
aid the flow of the fluid
supporting carers through this period. Cats with
CKD can be challenging to transition to a new diet
and often require treatment for complications
that have a negative impact on appetite. If feeding
a renal diet is not possible then senior cat food
is preferable to standard commercial cat food. If
blood phosphate levels remain above IRIS target
levels (Table 1) in spite of phosphate restriction,
a combination of renal diet and one or more
phosphate binders may be required.
A number of phosphate binders are available.
Used alone with a standard commercial cat
food, phosphate binders may provide sufficient
phosphate-restriction for a cat in IRIS stage 2
CKD, but those in more advanced stages are
likely to need a phosphate-restricted diet to
maintain normophosphataemia. ‘Veterinary’
formulated options include calcium carbonate
(eg, Pronefra, Virbac; Ipakitine, Vétoquinol,
Easypill Cat Kidney Support, Vetinnov); other
options include human formulations such
as aluminium hydroxide (eg, Alu-cap, Meda
Pharmaceuticals) and lanthanum carbonate
(Fosrenol, Shire Pharmaceuticals Contracts).
Phosphate binders should be mixed with food
and included with every meal that the cat eats.
They work by binding to phosphate present in
the food, retaining this in the bowel and hence
limiting the amount of phosphate that can be
absorbed by the body. Calcium-containing
binders should be avoided in hypercalcaemic
patients and in those receiving calcitriol.
RAAS suppression
Loss of nephrons leads to activation of the
renin angiotensin aldosterone system (RAAS),
which results in hypertrophy of residual
nephrons with reduced arteriolar resistance
and increased glomerular blood flow. As renal
disease progresses, the afferent arteriolar
tone decreases more than the efferent arteriole
tone, resulting in glomerular hypertension
and hyperfiltration. Although this increase
helps support glomerular filtration rate and
excretory function, ultimately RAAS activation
has
negative
consequences
including
proteinuria, renal damage, fibrosis and further
progression of renal disease. Angiotensin II is
responsible for many of the damaging effects
of RAAS activation.
Two veterinary-licensed options exist for
suppression of the RAAS in cats with CKD:
■■
The angiotensin receptor blocker (ARB)
telmisartan works by preventing angiotensin
II from binding to one of its receptors,
the angiotensin receptor-1 (AT-1). The
AT-1 receptor mediates the most harmful
consequences of angiotensin II, whereas the
AT-2 receptor is thought to result in some
beneficial effects in cats with CKD.
■■
Angiotensin converting enzyme inhibitors
(ACEI) such as benazepril work by blocking
the production of angiotensin II.
IRIS currently recommend that CKD patients
are treated with medications that suppress
the RAAS if suffering from a persistent renal
proteinuria. Patients are classed as proteinuric
if their urine protein to creatinine ratio (UPC) is
over 0.4 and borderline proteinuric if their UPC
is between 0.2 and 04. RAAS suppression using
telmisartan or benazepril has been shown to
be effective in reducing proteinuria although as
yet a survival benefit has not been shown.
Some clinicians advocate treating borderline
proteinuric cats (UPC 0.2 to 0.4) on the basis
that survival times in these cats are reduced
compared to non-proteinuric CKD cats (UPC
<0.2) and this is considered logical by the
panel responsible for the recently published
International Society of Feline Medicine
(ISFM) consensus guidelines on diagnosis and
management of CKD (Sparkes and others 2016).
ACEI and ARBs should only be used in clinically
stable, normally hydrated cats. There may
be some benefits in treating non-proteinuric
CKD patients with an ARB or ACEI since some
studies have shown improved quality of life and a
tendency for the renal disease to progress more
slowly in these cats.
Telmisartan has a potential advantage
over an ACEI by not being susceptible to ‘ACE
escape’ – the phenomenon whereby alternative
pathways allow angiotensin II to continue to
be produced despite administration of an
ACEI. Telmisartan also offers a more targeted
mode of action, sparing the AT-2 receptor
which may mediate some beneficial effects.
A recent field study of cats with CKD showed
that telmisartan was effective in significantly
reducing proteinuria at all assessment points
in the 180 day study, whereas benazepril was
not (Sent and others 2015).
Patients with CKD are vulnerable to dehydration.
Dehydration worsens renal perfusion and
therefore renal function leading to exacerbation
of complications associated with CKD such as
metabolic acidosis and poor appetite. Dehydrated
patients should be rehydrated and all patients
should be encouraged to maintain normal
hydration through tactics including feeding a
moist diet and ensuring that access to water is
easy and plentiful. Detailed guidelines on tactics
that can encourage increased water intake are
available in the ‘free downloads’ section of my
website (Caney 2011). Subcutaneous fluids (eg,
50 to 100 ml Hartmann’s solution once daily) can
be helpful in cats struggling to maintain normal
hydration (Fig 1).
Prevention/treatment of
hyperphosphataemia
Around two-thirds of CKD patients are
hyperphosphataemic as a result of their
renal disease. This should be addressed as
discussed earlier.
Prevention/treatment of metabolic
acidosis
Metabolic acidosis (blood bicarbonate or total
CO2 <14 mmol/l) is a common complication
of CKD, especially in those patients that are
suffering from dehydration, and is estimated to
affect more than 60 per cent of patients at some
point in the course of their illness. In many
patients, where present, the metabolic acidosis
resolves on correction of dehydration with only
a small number of patients requiring more
aggressive management such as intravenous
sodium bicarbonate* and/or oral potassium
citrate* (40 to 75 mg/kg twice daily as a
starting dose) Maintaining optimal hydration
(as discussed above) and feeding a renal diet
minimise the incidence of metabolic acidosis.
Support of poor appetite
Variable to poor appetite is common in cats with
CKD, estimated to affect more than 30 per cent
of patients. Where documented, it is important
to look for and address treatable causes of poor
appetite such as dehydration, hypokalaemia,
nausea and anaemia. General nursing support,
such as sitting with the cat, gently warming the
food and offering the food by hand can help.
Appetite stimulants such as mirtazapine* (1 to 2
mg per cat every 48 hours, as needed), which also
has some antiemetic effects, can be useful. In
cats that are bright and relatively well but where
appetite remains poor, one long-term possibility
includes placing a feeding tube such as an
oesophagostomy or gastrostomy tube (Fig 2).
Support of anaemia
Supportive and symptomatic
treatments
Anaemia is a potential complication of CKD,
estimated to affect around a third of patients, and
may lead to poor appetite, lethargy and weakness.
Anaemia develops due to a lack of production of
erythropoietin by the diseased kidneys, reduced
survival of red blood cells and potentially blood
A variety of supportive and symptomatic
treatments may be helpful in the individual
patient. These should be chosen according to
the individual patient’s needs and include:
* Used for products which do not have a
veterinary license for use in cats
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Fig 2: Placing a feeding tube for nutritional support can be helpful in some cases. Fig 3: Clinical evidence of severe muscle weakness, including ventroflexion
A large bore tube is preferable so that liquidised renal food can be administered of the neck, may be seen in cats suffering from severe hypokalaemia
loss from gastric ulcers and excessive blood
sampling. Patients may suffer from a relative or
absolute iron deficiency, which can contribute to
anaemia development. Iron deficiency should be
differentiated from chronic disease by assessing
iron status (iron saturation, total iron binding
capacity [TIBC] and iron levels) and looking for
features consistent with iron deficiency, such
as microcytic and hypochromic red cells. Low/
normal serum iron and saturation with a low
TIBC is generally considered compatible with
an anaemia of chronic disease; in a patient with
iron deficiency, iron levels and saturation are low
while TIBC is normal. Treatment of anaemia is
generally recommended once the packed-cell
volume (PCV) falls to around 20 per cent and most
successful is a combination of an erythrocyte
stimulating agent, such as darbepoetin*
(induction dose 1 µg/kg subcutaneously once
a week) combined with intramuscular iron
dextran (50 mg per cat, can be repeated monthly
if needed). Once the PCV reaches the reference
range, the dose and/or frequency of darbepoetin
can be reduced (eg, 1 µg/kg subcutaneously
every two to three weeks) to maintain red blood
cell parameters within the reference range.
Management of anaemia associated with CKD is
reviewed in detail by Chalhoub and others (2011).
Treatment of systemic hypertension
Systemic hypertension is estimated to be
present in around 20 to 30 per cent of patients
with CKD and has potentially life-threatening
consequences. IRIS recommends that systolic
blood pressure (SBP) is assessed in all patients
and treated if persistently elevated (SBP >160
mmHg on two to three occasions) or if high on
a single occasion in a patient also found to have
evidence of target organ damage such as retinal
haemorrhage, oedema or detachment. Systemic
hypertension can be treated with amlodipine
(Amodip, Ceva Animal Health) at a dose of 0.625
or 1.25 mg per cat once daily. Mild hypertension
(SBP 160 to 180 mmHg) may respond adequately
to an ACEI (eg, benazepril 0.5 to 1.0 mg/kg once
daily) or ARB (eg, telmisartan 1 to 3 mg/kg once
daily). Refractory cases of systemic hypertension
can respond to a combination of amlodipine with
either an ACEI or ARB at the above doses.
Treatment and prevention of
hypokalaemia
Up to a quarter of CKD patients suffer from
hypokalaemia as a result of inappropriate
12
kaliuresis and inadequate intake through diet
related to poor appetite. Typically, the resulting
hypokalaemia is mild (potassium 3.0 to 3.5
mmol/l) and can be difficult to identify clinically.
Cats with more severe hypokalaemia may show
evidence of muscle weakness with ventroflexion
of the neck (Fig 3), evident in the most severe
of cases. Hypokalaemia can be corrected
using potassium chloride in intravenous or
subcutaneous fluids and/or oral potassium
gluconate (1 to 2 mmol per cat once or twice
daily). Hypokalaemia can be prevented by
feeding a renal diet since this is supplemented
in potassium. Acidifying diets, high protein
diets and potassium deficient diets should be
avoided. In cats receiving subcutaneous fluids,
potassium chloride can be added to the bag
before administering to the patient, for example,
10 mmol potassium chloride per 500 ml fluids.
Management of nausea and vomiting
Uraemia associated with CKD commonly
causes nausea and vomiting which can have
a significant negative impact on quality of life
and contribute to weight loss. Symptomatic
treatment options include mirtazapine* (also
an appetite stimulant) (1 to 2 mg per cat every
48 hours), maropitant (1 to 2 mg/kg once daily),
H2 blockers such as famotidine* (0.5 to 1 mg/kg
once daily) and proton pump blockers such as
omeprazole* (0.5 to 1 mg/kg once or twice daily).
Bacterial urinary tract infections
Patients with CKD are vulnerable to bacterial
lower urinary tract infections with up to a
quarter of patients suffering from this at
some point in the course of their illness.
Current recommendations are that these
should be treated if the patient shows clinical
signs (systemic and/or lower urinary),
if pyuria is present, where ultrasound
evidence of pyelonephritis is present and/or
if renal function has recently deteriorated. An
appropriate antibiotic should be chosen on the
basis of culture and sensitivity testing. Typically
a prolonged course of treatment (eg, four to six
weeks) is needed to eliminate the infection.
Repeat urine culture is recommended during
the treatment period and seven to 10 days after
treatment has concluded to confirm treatment
success. If recurrent or refractory infections
are encountered, ultrasound of the kidneys and
bladder is indicated to look for evidence of a
nidus or other explanation.
Renal proteinuria
Proteinuria is an acknowledged complication
of feline CKD through activation of the RAAS.
Treatment of proteinuria should be considered
as discussed earlier.
Compliance and owner support
A successful outcome depends on an
individualised approach that is developed
with involvement of the cat’s owner. CKD is a
complex disease and many owners appreciate
support and education in how best to care for
their cat. A recent survey of owners of cats
receiving long-term medical management for
their hyperthyroidism reported that 47 per cent
of owners requested more leaflets and printed
information to help them learn more about their
cat’s condition, and it is likely that owners of
cats with CKD will have similar priorities (Caney
2013). Support and tuition in how to administer
medications is also important. Owners should
be encouraged to be open about any difficulties
they are having so that these can be supported as
best as possible. Tips for supporting medication
are presented in Table 2.
Managing patients with additional
medical needs
Since CKD is common in older cats it is not
unusual for these patients to have additional
illnesses. Common examples would include
hyperthyroidism, diabetes mellitus and
osteoarthritis.
Managing cats with concurrent
hyperthyroidism
All treatments for hyperthyroidism have the
potential to worsen renal function since they
cause a reduction in renal blood flow. This
has the potential to ‘unmask’ kidney disease
that was previously unknown and to worsen
pre-existing renal disease. Unfortunately,
there is no way to predict which cats will suffer
renal problems following treatment of their
thyroid disease. Fortunately, most cats with
hyperthyroidism can be optimally treated, even
when CKD is present, and it is only those with
very severe renal disease (IRIS stage 4) where
optimal management of hyperthyroidism may
precipitate a clinical deterioration. Optimal
management of hyperthyroidism is desirable
* Used for products which do not have a
veterinary license for use in cats
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Table 2: Strategies for making medication ‘easy’ for carers
Problem
Possible solution/s
Giving oral
medication is
difficult
Are other formulations available which may be easier for the carer? Some cats and
owners find a liquid preparation easier than a tablet. For example, a recent survey of
owners using Semintra (Boehringer Ingelheim) in their cat with CKD indicated a strong
preference for a liquid formulation compared to their previous experience of administering
tablets (Zimmering and others 2014, 2015)
Are there any palatable formulations available which may prove more popular with the
patient? Look for products with an ISFM ‘Easy to give award’ as this may help identify
palatable products
Is hiding the medication in a small amount of tasty food possible? Popular treats to hide
medication in include butter, cheese, tuna, prawns and cat treats (eg, Greenies, Webbox)
Is parenteral treatment an option? For example, a patient needing extra potassium could
receive this in their subcutaneous fluids (see section on hypokalaemia in the main text)
Separate medication from meal times where possible to avoid induction of a food aversion
(cats associating stressful events with food may stop eating that food)
Consider having a different person responsible for medicating the cat to those responsible
for feeding and other positive interactions
The patient
is receiving
multiple
medications
and this is
difficult for
the carer
As above, plus consider using empty gelatin capsules to contain two or more medications,
if needed (Fig 4). If using gel caps, it is important to be aware of possible drug interactions,
where known. For example, aluminium hydroxide and lanthanum carbonate phosphate
binders may reduce absorption of H2-blockers like famotidine. If using this combination of
medications, they should be administered two hours apart. Use of proton pump blockers
and H2-blockers can make the phosphate binder calcium carbonate less effective, so this
should be considered a possibility, where relevant. Where possible, phosphate binders
should be given mixed with food or close to a meal time
since hyperthyroidism itself can contribute to
the progression of CKD.
Managing cats with concurrent diabetes
mellitus
While a low phosphate and low protein diet
is recommended for cats with CKD, a high
protein and low carbohydrate diet is generally
recommended for cats with diabetes. If both
CKD and diabetes mellitus are present, the
best dietary approach is usually to concentrate
on whichever condition is the biggest concern
for the cat; for example, if the renal disease is
mild, a phosphate binder added to a diabetic diet
might be most appropriate in addition to other
strategies for management of both conditions
(Sparkes and others 2015, 2016).
Managing cats with concurrent
osteoarthritis
Osteoarthritis is a common cause of mobility
problems in older cats. Environmental
modification can help affected cats to cope
more easily; for example, by providing
comfortable beds that are easy for the cat to
step on and off and/or steps to allow cats access
to their favourite sleeping places. In severely
affected cats, non-steroidal anti-inflammatory
drugs (NSAIDs), such as meloxicam, can
be very effective in reducing pain and are
usually very well tolerated. Potential adverse
effects include gastrointestinal signs (eg,
vomiting, loss of appetite) and renal damage.
Renal damage is most likely in cats that are
dehydrated or hypotensive when dosed. Several
published studies have shown that most cats
with concurrent osteoarthritis and CKD can
safely receive a low daily dose of meloxicam
(eg, 0.01 to 0.03 mg/kg once daily), should
they need it, without adversely affecting their
renal function. For cats with CKD receiving an
NSAID for osteoarthritis, the following general
guidelines exist for owners:
■■
■■
■■
■■
Do what you can to encourage maintenance
of normal hydration: feed a moist diet,
encourage drinking by using water
fountains, and so on (Caney 2011).
Do not administer the NSAID if your cat
appears unwell (eg, not eating, vomiting).
Mix the NSAID with food: if your cat is unwell
and does not eat, it will not receive the
medication.
Use at the lowest effective dose.
For those cats that cannot tolerate an NSAID,
other painkiller options that might be helpful
would include opiates like buprenorphine.
Where anaesthesia is needed in CKD
patients, for example for dental treatment, the
patients should be stabilised preoperatively
so that their hydration is optimal, electrolytes
are normal and they are in as good a state as
possible to cope with anaesthesia. Anaesthetic
regimes which may result in hypotension
should be avoided and blood pressure should
be monitored and supported, as necessary,
throughout the procedure.
Check-ups for cats with CKD
Monitoring visits are very important to ensure
that owners are supported and that clinical
problems are identified and treated promptly.
Compliance to medication and diet is enhanced
by veterinary support; a recent study showed
improved compliance to a renal diet in those
cats whose owners had received a veterinary
recommendation to feed this diet (Caney
2016). The required frequency of check-ups
varies according to the patient’s needs but
should initially be at least once a month. All
check-ups should include weighing the patient
and assessing for clinical problems (such as
dehydration). Blood pressure and laboratory
monitoring should be checked according to the
patient’s needs and owner’s concerns; I measure
Fig 4: Empty gelatin capsules can be used to
combine several medications into one ‘dose’.
The photo shows my thumb next to several
size 4 empty gel caps
blood pressure every three to six months and
reassess blood and urine parameters every
six to 12 months, depending on the individual
patient’s needs. Check-ups can be performed
by a veterinary nurse/technician working under
direction of a veterinary surgeon.
Summary
CKD is often a challenging condition to manage
but treatment is extremely successful in most
patients where optimal treatment is possible.
Attention to detail and providing an individualised
plan leads to the best treatment outcome.
References
CANEY, S. M. A. (2011) Encouraging your cat to drink
– a guide for cat owners. www.vetprofessionals.com/
catprofessional/free_downloads.html. Accessed
July 27, 2016
CANEY, S. M. A. (2013) An online survey to determine
owner experiences and opinions on the management
of their hyperthyroid cats using oral anti-thyroid
medications. Journal of Feline Medicine and Surgery
15, 494-502
CANEY, S. M. A. (2016) An online survey of dietary
and phosphate binder practices of owners of cats
with chronic kidney disease. Journal of Feline
Medicine and Surgery (In press)
CHALHOUB, S., LANGSTON, C. & EATROFF, A.
(2011) Anemia of renal disease: what it is, what to
do and what’s new. Journal of Feline Medicine and
Surgery 13, 629-640
SENT, U., GÖSSL, R., ELLIOTT, J., SYME, H. M. &
ZIMMERING, T. (2015) Comparison of efficacy of longterm oral treatment with telmisartan and benazepril
in cats with chronic kidney disease. Journal of
Veterinary Internal Medicine 29, 1479-1487
SPARKES, A. H., CANNON, M., CHURCH, D.,
FLEEMAN, L., HARVEY, A., HOENIG, M. & OTHERS
(2015) ISFM consensus guidelines on the practical
management of diabetes mellitus in cats. Journal of
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SPARKES, A. H., CANEY, S., CHALHOUB, S.,
ELLIOTT, J., FINCH, N., GAJANAYAKE, I. & OTHERS
(2016) ISFM consensus guidelines on the diagnosis
and management of feline chronic kidney disease.
Journal of Feline Medicine and Surgery 18, 219-239
ZIMMERING, T. M., HECK, E. V., ADAMS, J. &
RAMBAGS, B. (2014) Ease of use of Semintra – cat
owner feedback under European field conditions
(‘Easy Programme’). Abstract. Journal of Feline
Medicine and Surgery 16, 764-765
ZIMMERING, T. M. (2015) Ease of use of Semintra®
and its effects on quality of life. Abstract. SEVC.
Barcelona,October 15 to 17, 2015
Competing interests
No competing interests declared.
doi: 10.1136/inp.i4901
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Management and treatment of chronic kidney
disease in cats
Sarah Caney
In Practice 2016 38: 10-13
doi: 10.1136/inp.i4901
Updated information and services can be found at:
http://inpractice.bmj.com/content/38/Suppl_3/10
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