(2023)
2019

All treatments for chronic kidney disease (CKD) need to be tailored to theindividual patient. The following recommendations are useful starting
points for the majority of cats at each stage. Serial monitoring of thesepatients is ideal and treatment should be adapted according to the
response to treatment. Note that staging of disease is undertaken
following diagnosis of CKD – an increased blood creatinine o r
S D M A concentration alone is not diagnostic of CKD.
Treatment recommendations fall into two broad categories, namely:
1. Those that slow progression of CKD and so preserve remaining kidney
function for longer
2. Those that address the quality of life of the cat, addressing the clinicalsigns of CKD
In general, at the early stages of CKD (stages 1 and 2), there are few clinicalextra-renal signs of the disease and the therapeutic emphasis is on slowing
progression. From stage 3 onwards, extra-renal signs become morecommon and more severe. The importance of administering treatments
which address the clinical signs of CKD and improve the cat’s quality of life
assume greater importance and exceeds the importance of treatments
designed to slow progression by stage 4.
Some of the treatment recommendations are not authorized for use in all
geographical regions and some may not be authorized for use in cats. Such
recommended dose rates are therefore empirical. It is the treating
veterinarian’s duty to make a risk:benefit assessment for each patient priorto administering any treatment.

1© 20232019 International Renal Interest Society (IRIS) Ltd. IRIS Ltd. is an independent non-profit organization limited by guarantee in the UK (Registered Number 10213173).

(2023)Treatment Recommendations for CKD in Cats (2019)

1

Treatment recommendations for Cats with Chronic Kidney Disease

Stage 1 Feline patients:
1. Discontinue all potentially nephrotoxic drugs if possible.
2. Identify and treat any pre-renal or post-renal abnormalities.
3. Rule out any treatable conditions like pyelonephritis and ureteralrenal urolithiasis
withobstruction
withradiographs and/or ultrasonography.
4. Measure blood pressure and urine protein to creatinine ratio (UP/C).
Management of dehydration:
In these patients urine concentrating ability may be somewhat impaired and therefore ensure:

They have fresh water available at all times for drinking

If become ill for any reason that leads to fluid losses, correct clinical dehydration withisotonic polyioinic replacement fluid solutions (e.g. lactated Ringer’s) IV or SQ, promptly
as needed

Systemic hypertension:
The blood pressure above which progressive renal injury may be induced is unknown.
Our goal is to reduce systolic blood pressure to <160 mm Hg and to minimize the riskof extra-renal target organ damage (CNS, retinal, cardiac problems/damage). If there
is no evidence of such damage but systolic blood pressure persistently exceeds 160
mm Hg, increasing the risk of this occurring, treatment should be instituted.
‘Persistence’ of increased systolic blood pressure should be judged on multiple
measurements made over the following time-scales in these blood pressure
substages:• Hypertensive (moderate risk of future target organ damage) – systolic bloodpressure 160 to 179 mm Hg measured over 1 to 2 weeks• Severely hypertensive (high risk of future target organ damage) – systolic bloodpressure  180 mm Hg measured over 1 to 2 weeks.
If evidence of target organ damage exists, cats should be treated without the needto demonstrate persistently increased systolic blood pressure. Reducing bloodpressure is a long term aim in managing the patient with CKD and a gradual andsustained reduction should be the goal, avoiding any sudden or severe decreases
leading to hypotension.
A logical stepwise approach to managing hypertension is as follows:
1. Dietary sodium (Na) reduction - there is no evidence that lowering dietary Na
will reduce blood pressure. If dietary Na reduction is attempted, it should beaccomplished gradually and in combination with pharmacological therapy.
2. Calcium channel blocker (CCB), such as amlodipine (0.125 to 0.25 mg/kg once
daily) or angiotensin receptor blocker (ARB), telmisartan (2 mg/kg once daily).

2© 20192023 International Renal Interest Society (IRIS) Ltd. IRIS Ltd. is an independent non-profit organization limited by guarantee in the UK (Registered Number 10213173).

(2023)Treatment Recommendations for CKD in Cats (2019)1

3. Double the dose of amlodipine (0.25 to 0.5 mg/kg once daily) if this is treatment selected.
Note telmisartan label does not advise a dose increase from 2 mg/kg once daily.
4. Combine amlodipine and telmisartan if either drug alone does not lead toadequate control of blood pressure.
Note: Take care not to introduce CCB/RAAS inhibitor treatment to unstable
dehydrated cats as glomerular filtration rate may drop precipitously if these drugs
are introduced before the patient is adequately hydrated.
Monitoring response to antihypertensive treatment:
Hypertensive cats normally require lifelong therapy and may require treatment
adjustments. Serial monitoring is essential. After stabilization, monitoring should
occur at least every 3 months.
Systolic blood pressure <120 mm Hg and/or clinical signs such as weakness or
tachycardia indicate hypotension, which is to be avoided.
Blood creatinine concentration – reducing blood pressure may lead to small andpersistent increases in creatinine concentration (<45 µmol/l or 0.5 mg/dl increase)or SDMA concentration (<2.0 µg/dl), but a marked increase suggests an adverse
drug effect. Progressively increasing concentrations indicate progressive kidneydamage/disease.
Proteinuria:
Cats in Stage 1 with UP/C >0.4 should be investigated for disease processes leading
to proteinuria (see 1 and 2 below) and treated with anti-proteinuric measures (see 3
and 4 below).
Those with borderline proteinuria (UP/C 0.2 to 0.4) require close monitoring (see 1
and 4 below).
1. Look for any concurrent associated disease process that may be treated/corrected.
2. Consider kidney biopsy as a means of identifying underlying disease (seeAppendix and consult experts if unsure of indications for kidney biopsy).
3. Administer an RAAS inhibitor (ACEI or ARB) and feed a clinical renal diet.
4. Monitor response to treatment / progression of disease:– stable blood creatinine concentration and decreasing UP/C = good response.
– serially increasing blood creatinine concentrations and/or increasing UP/C =disease is progressing.
Ordinarily therapy will be maintained lifelong unless the underlying disease has been
resolved in which case dose reduction whilst monitoring UP/C might be considered.
Note:a. The use of an RAAS inhibitor is contraindicated in any cat that is clinicallydehydrated or is showing signs of hypovolemia. Correct dehydration before
using these drugs otherwise glomerular filtration rate may drop precipitously.
b. Cats with proteinuria and hypoalbuminemia likely share the same thromboembolic

32023 International Renal Interest Society (IRIS) Ltd. IRIS Ltd. is an independent non-profit organization limited by guarantee in the UK (Registered Number 10213173).
© 2019(2023)Treatment Recommendations for CKD in Cats (2019)1

risk as dogs (although evidence is lacking in the published literature), but aspirin isdifficult to use in cats to achieve a selective antiplatelet effect. If thromboembolic therapy
risk as dogs (although evidence is lacking in the published literature), but aspirin is
is deemed necessary, clopidogrel (10 to 18.75 mg/day is the drug of choice. Aspirin (1difficult to use in cats to achieve a selective antiplatelet effect. A suggested dose
mg/kg every 72 h) is an alternative (but see above).
rate if plasma albumin is below 20 g/l (2 g/dl) is 1 mg/kg every 72 hours and anc. Cats withalternative
serum phosphate
withinthe IRIS target
mg/dlmg/day).
or 1.5 mmol/l) may be at
to aspirin
is clopidogrel(10 (4.5
to 18.75
increasedriskofdeveloping
hypercalcemia
when
renal
diets
are
introduced.
c. Cats with serum phosphate within the IRIS target (4.5mg/dl or 1.5 mmol/l) may be
Measurement
of
FGF23
may
help
to
identify
cats
which
would
benefitfrom
dietary
at increased risk of developing hypercalcemia when renal
diets
are introduced.
phosphate restriction where plasma phosphate is in the target range. FGF23 >400 pg/ml
Monitor serum calcium and if total calcium exceeds 12 mg/dl (3 mmol/l) switch thein the absence of hypercalcaemia, anemia or marked inflammatory disease is an
cat to a senior diet or mix renal diet (50:50 by volume) with standard grocery food.
indication to start dietary phosphate restriction. Monitor serum calcium and if total
If borderline
proteinuria
persists,
antiproteinuric
treatment could
be offered,calciumd.exceeds
12 mg/dl(3 mmol/l)switch thecat to a less phosphate
restricted
diet.
because the association between progression of CKD and proteinuria includes
d. If borderline
proteinuriacategory.
persists, antiproteinuric
treatment
couldnobeevidence
offered, because
the borderline
However, there
is at present
that
the association
betweenprogression
of
CKD
and
proteinuria
includestheintervention with anti-proteinuric drugs slows progression. borderline
category. However, there is at present no evidence that intervention with anti-proteinuric
drugs slows progression.

4© 20192023 International Renal Interest Society (IRIS) Ltd. IRIS Ltd. is an independent non-profit organization limited by guarantee in the UK (Registered Number 10213173).

(2023)Treatment Recommendations for CKD in Cats (2019)2

Stage 2 Feline patients:
All of the above listed for Stage 1 (listed here again for convenience) plus any additional
steps indicated.
1. Discontinue all potentially nephrotoxic drugs if possible.
2. Identify and treat any pre-renal or post-renal abnormalities.

obstruction
with
3. Rule out any treatable conditions like pyelonephritis and ureteralrenal urolithiasis
withradiographs and/or ultrasonography.
4. Measure blood pressure and urine protein to creatinine ratio (UP/C).
5. Consider feeding a clinical renal diet: this may be accomplished more easily
early in the course of CKD, before inappetence develops.
Management of dehydration:
These patients often have decreased urine concentrating ability and therefore ensure:•

They have fresh water available at all times for drinking•

If become ill for any reason that leads to fluid losses, correct clinical dehydration withisotonic polyioinic replacement fluid solutions (e.g. lactated Ringer’s) IV or SQ, promptly
as needed

Systemic hypertension:
The blood pressure above which progressive renal injury may be induced is unknown.
Our goal is to reduce systolic blood pressure to <160 mm Hg and to minimize the riskof extra-renal target organ damage (CNS, retinal, cardiac problems/damage). If there
is no evidence of this but systolic blood pressure persistently exceeds 160 mm Hg,
increasing the risk of such damage, treatment should be instituted.
‘Persistence’ of increased systolic blood pressure should be judged on multiple
measurements made over the following time-scales in these blood pressure
substages:• Hypertensive (moderate risk of future target organ damage) – systolic bloodpressure 160 to 179 mm Hg measured over 1 to 2 weeks.
• Severely hypertensive (high risk of future target organ damage) – systolic bloodpressure 180 mm Hg over 1 to 2 weeks.
If evidence of target organ damage exists, cats should be treated without the need todemonstrate persistently4increased systolic blood pressure. Reducing blood pressure
is a long term aim in managing the patient with CKD and a gradual and sustained
reduction should be the goal, avoiding any sudden or severe decreases leading tohypotension.
A logical stepwise approach to managing hypertension is as follows:
1. Dietary sodium (Na) reduction - there is no evidence that lowering dietary Na
will reduce blood pressure. If dietary Na reduction is attempted, it should beaccomplished gradually and in combination with pharmacological therapy.
2. Calcium channel blocker (CCB) such as amlodipine (0.125 to 0.25 mg/kg once daily) or
angiotensin receptor blocker (ARB), telmisartan (2 mg/kg once daily).
5© 20192023 International Renal Interest Society (IRIS) Ltd. IRIS Ltd. is an independent non-profit organization limited by guarantee in the UK (Registered Number 10213173).

(2023)Treatment Recommendations for CKD in Cats (2019)2

3. Double the dose of amlodipine (0.25 to 0.5 mg/kg once daily). if this is treatment selected.
Note telmisartan label does not advise a dose increase from 2 mg/kg once daily.
4. Combine amlodipine and telmisartan if either drug on its own does not lead toadequate control of blood pressure
Take care not to introduce CCB/RAAS inhibitor treatment to unstable dehydrated
cats as glomerular filtration rate may drop precipitously if these drugs are introduced
before the patient is adequately hydrated.
Monitoring response to antihypertensive treatment:
Hypertensive cats normally require lifelong therapy and may require treatment
adjustments. Serial monitoring is essential. After stabilization, monitoring should
occur at least every 3 months.
Systolic blood pressure <120 mm Hg and/or clinical signs such as weakness or
tachycardia indicate hypotension, which is to be avoided.
Blood creatinine concentration – reducing blood pressure may lead to small andpersistent increases in creatinine (<45 µmol/l or 0.5 mg/dl increase) or SDMA
concentration (<2.0 µg/dl), but a marked increase suggests an adverse drug
effect. Progressively increasing creatinine concentrations indicate progressive
kidney damage/disease.
Proteinuria:
Cats in Stage 2 with UP/C >0.4 should be investigated for disease processes
leading to proteinuria (see 1 and 2 below) and treated with anti-proteinuric
measures (see 3 and 4 below).
Those with borderline proteinuria (0.2 to 0.4) require close monitoring (see 1
and 4 below).
1. Look for any concurrent associated disease process that may be treated/corrected.
2. Consider kidney biopsy as a means of identifying underlying disease (seeAppendix and/or consult experts if unsure of indications for kidney biopsy).
3. Administer an RAAS inhibitor (ACEI or ARB) and feed a clinical renal diet.
4. Monitor response to treatment/progression of disease:– stable blood creatinine concentration and decreasing UP/C = good response.
– serially increasing creatinine concentrations and/or increasing UP/C =disease is progressing.
– Ordinarily therapy will be maintained lifelong unless the underlying
disease has been resolved in which case dose reduction while
monitoring UP/C might be considered.
Note:a. Use of an RAAS inhibitor is contraindicated in any animal that is clinicallydehydrated and/or showing signs of hypovolemia. Correct dehydration before
using these drugs otherwise glomerular filtration rate may drop precipitously.
b. Cats with proteinuria and hypoalbuminemia likely share the same thromboembolicrisk as dogs, (although evidence is lacking in the published literature), but aspirin isdifficult to use in cats to achieve a selective antiplatelet effect. A suggested dose rate
if plasma
albumin is
below is20deemedg/l (2 g/dl)
is 1 mg/kg
every 72(10hours
andmg/dayan alternativeIf
thromboembolic
therapynecessary,clopidogrel
to 18.75
istoaspirinisclopidogrel
(10
to
18.75
mg/day).
the drug of choice. Aspirin (1 mg/kg every 72 h) is an alternative (but see above).
6© 20192023 International Renal Interest Society (IRIS) Ltd. IRIS Ltd. is an independent non-profit organization limited by guarantee in the UK (Registered Number 10213173).

(2023)Treatment Recommendations for CKD in Cats (2019)2

c. Cats with serum phosphate within the IRIS target may be at increased risk of developingc. Cats with whenserum
phosphate
within the
IRIS targetofmay
athelpincreased
hypercalcemia
renaldiets are introduced.
Measurement
FGF23bemay
to identifyrisk
catsofwhich
would benefit
from dietary phosphate
restrictionwhereplasma phosphate
is in thecalcium
targetdeveloping
hypercalcemia
when renal
diets areintroduced.
Monitor serum
range.
>400
pg/ml inthe absenceof hypercalcaemia,
anemiamarkedinflammatory
andFGF23
if totalcalcium
exceeds
12 mg/dl(3 mmol/l) switch
theorcat
to a seniordiet or diseasemix
is anrenal
indication
tostart
dietary
phosphate
restriction.
Monitorserum
calcium
and
if
total
calcium
diet (50:50 by volume) with standard grocery food.
exceeds 12mg/dl (3mmol/l) switch the cat to a less phosphate restricted diet.
d. If borderline proteinuria is persistent, antiproteinuric treatment could be offered. The
d. Ifrationale
borderline proteinuria
is ispersistent,
antiproteinuric
treatment
could progression
be offered. The
forfor doing sothat there
is an association
betweenofrationale
CKD anddoing so is that there is an association between progression of CKD and proteinuria which extends into
proteinuria which extends into the borderline category. There is no evidence
the borderline category. There is no evidence that intervention with anti-proteinuric drugs slows
that intervention with anti-proteinuric drugs slows progression, however.
progression, however.
Reduction of phosphate intake:
Many cats in Stage 2 will have normal plasma phosphate concentrations but will have
FGF23concentration.
concentration. Evidence suggests that chronic reduction ofincreased plasma PTH
phosphate intake to maintain a plasma phosphate concentration below 1.5 mmol/l(but not less than 0.9 mmol/l; <4.6 mg/dl but >2.7 mg/dl) is beneficial to patients with
CKD.
The following of
measurescanbe tointroduced
sequentiallyin anattempt
todietary
achieve this:Measurement
FGF23 may
help
identify cats
which would
benefitfromphosphate restriction if plasma phosphate is within the IRIS target range. FGF23 >400
1. Dietary(i.e., clinicalrenal
diet therapy).
pg/ml
in thephosphate
absence ofrestriction
hypercalcaemia,
anemiaor marked
inflammatory disease is anindication
tostart
dietary
phosphate
restriction.
2. If plasma phosphate concentration remains above 1.5 mmol/l (4.6 mg/dl) after
dietary restriction, give enteric phosphate binders (such as aluminum hydroxide,
The following measures can be introduced sequentially in an attempt to achieve this:aluminum carbonate, calcium carbonate, calcium acetate, lanthanum carbonate)
to effect, starting at 30-60 mg/kg/day in divided doses to be mixed with each
1. Dietary phosphate restriction (i.e., clinical renal diet therapy).
meal (mixed with the food). The dose required will vary according to the amount
2. Ifofplasma
phosphateremains
above 1.5mmol/lTreatment(4.6 mg/dl)withafter dietaryphosphatebeingconcentration
fed and the stageof kidneydisease.
restriction,
give
enteric
phosphatebinders(suchasaluminumhydroxide,
aluminum
phosphate binders should be to effect (as outlined above), with signs of toxicity
carbonate,carbonate,calcium
acetate,lanthanum
carbonate)effect,calcium
starting atlimiting calcium
the upper
dose ratepossiblein a given
patient.
Monitor toserum
30-60 mg/kg/day in divided doses to be mixed with each meal (mixed with the food). The
and phosphate concentrations every 4-6 weeks until stable and then every 12
dose required will vary according to the amount of phosphate being fed and the stage ofweeks. Microcytosis and/or generalized muscle weakness and neurologicalkidney disease. Treatment with phosphate binders should be to effect (as outlined above),aluminum
toxicity
usingrate
an possible
aluminumbinder– switchwithsigns
signssuggestof toxicity
limiting theupperif dosein containing
a given patient.
Monitortoanother
formofphosphatebindershouldthisoccur.
It
shouldbenoted,
serum calcium and phosphate concentrations every 4-6 weeks until stable and then every
however,
unlikethephosphatedog, aluminum
toxicity
notforbeenreported
the catorand
12 weeks.
Once
serum
is in thetargethas
range
stage
2 (<1.45inmmol/l
4.5it
is possible
to measure
blood
aluminumlevelsto confirm suspectedcases.
mg/dl)
measurementof serumFGF23
may assist
in determining
whether further
Hypercalcemia
should– combinationsof aluminumand calcium
phosphate
restriction
wouldbebeavoided
beneficial
to the cat. If FGF23
is >700 pg/ml,
furtherphopshate
restriction
shouldbe applied
containing
phosphatebindersmay (e.g. by increasing the dose of phosphate binder)
provided
there is noof hypercalcaemia, marked anemia or severe inflammatory
be necessary
in evidencesome cases.
disease (all of which can increase FGF23 independently of mineral bone disturbance).
Excellent
controlof mineral bone disturbance
be indicated by serum FGF23 of
Additional
recommendationsfor Stagewould
2 patients:<500 pg/ml. Microcytosis and/or generalized muscle weakness and neurological signs
suggestaluminum
toxicity if usingaluminumgluconate
containingorbinder– switch
to another
If the patientis hypokalemic,
thenanpotassium
potassium
citrateshouldform of phosphate binder should this occur. It should be noted, however, unlike the dog,
be supplemented to effect (typically 1-2 mmol/kg/day).
aluminum toxicity has not been reported in the cat and it is possible to measure blood
aluminum levels to confirm suspected cases. Hypercalcemia should be avoided –Where there isdiscrepancy
betweencreatinine
and SDMA:
combinationsof aaluminumand calcium
containing
phosphatebinders may be necessaryinsomecases.
If serum or plasma SDMA is persistently >25 µg/dl in a cat with serum creatinine
between 1.6 and 2.8 mg/dl (IRIS CKD Stage 2 based on creatinine), stage and treat
this cat as and IRIS CKD Stage 3 patient.

7© 20192023 International Renal Interest Society (IRIS) Ltd. IRIS Ltd. is an independent non-profit organization limited by guarantee in the UK (Registered Number 10213173).

(2023)Treatment Recommendations for CKD in Cats (2019)2

c. Cats with serum phosphate within the IRIS target may be at increased risk ofdeveloping hypercalcemia when renal diets are introduced. Monitor serum calcium
and if total calcium exceeds 12 mg/dl (3 mmol/l) switch the cat to a senior diet or mix
renal diet (50:50 by volume) with standard grocery food.
d. If borderline proteinuria is persistent, antiproteinuric treatment could be offered. The
rationale for doing so is that there is an association between progression of CKD and
Treat vomiting / decreased appetite / nausea / weight and/or muscle loss with anproteinuria which extends into the borderline category. There is no evidence
antiemetic /appetite stimulant / antinausea agent (such as maropitant, ondansetron, oralthat intervention with anti-proteinuric drugs slows progression, however.
or transdermal mirtazapine, or capromorelin).
If there is marked muscle loss, measure serum SDMA and base staging and treatment
Reduction of phosphate intake:recommendations on SDMA rather than creatinine as it is not affected by muscle wasting.
Inaddition,
evaluate
concurrent
diseasesleading
to vomiting
and weight loss.
Manycats inStage for2 willhave normal
plasmaphosphateconcentrations
but will haveincreased plasma PTH concentration. Evidence suggests that chronic reduction of
Evidencesuggestsoral
mirtazapine(1.88 mg/cat
every
48 h for 3 weeks)
reduces
phosphateintake tomaintaina plasma
phosphateconcentration
below
1.5 mmol/l
vomiting,
improves
appetite
and
leads
to
weightgain
incats
showing
signs
of(but not less than 0.9 mmol/l; <4.6 mg/dl but >2.7 mg/dl) is beneficial to patientswithinappetence and vomiting in this stage. Maropitant (1 mg/kg daily for 2 weeks) reduced
CKD.
vomiting but did not lead to weight gain/ improved appetite. Further investigations areneededon themeasures
use of theseandbeotherdrugs tosequentiallydetermine whether
they arefor this:
The following
canintroduced
in an attempt
to usefulachievemanaging gastrointestinal disturbances in cats with CKD and uremia when administered
longerterm.phosphate restriction (i.e., clinical renal diet therapy).
1. Dietary
2. If plasma phosphate concentration remains above 1.5 mmol/l (4.6 mg/dl) after
dietary restriction, give enteric phosphate binders (such as aluminum hydroxide,
aluminum carbonate, calcium carbonate, calcium acetate, lanthanum carbonate)
to effect, starting at 30-60 mg/kg/day in divided doses to be mixed with eachmeal (mixed with the food). The dose required will vary according to the amountof phosphate being fed and the stage of kidney disease. Treatment withphosphate binders should be to effect (as outlined above), with signs of toxicity
limiting the upper dose rate possible in a given patient. Monitor serum calcium
and phosphate concentrations every 4-6 weeks until stable and then every 12
weeks. Microcytosis and/or generalized muscle weakness and neurologicalsigns suggest aluminum toxicity if using an aluminum containing binder – switch
to another form of phosphate binder should this occur. It should be noted,
however, unlike the dog, aluminum toxicity has not been reported in the cat and it
is possible to measure blood aluminum levels to confirm suspected cases.
Hypercalcemia should be avoided – combinations of aluminum and calcium
containing phosphate binders may
be necessary in some cases.
Additional recommendations for Stage 2 patients:
If the patient is hypokalemic, then potassium gluconate or potassium citrate should
be supplemented to effect (typically 1-2 mmol/kg/day).
Where there is a discrepancy between creatinine and SDMA:
If serum or plasma SDMA is persistently >25 µg/dl in a cat with serum creatinine
between 1.6 and 2.8 mg/dl (IRIS CKD Stage 2 based on creatinine), stage and treat
this cat as and IRIS CKD Stage 3 patient.

7© 2019 International Renal Interest Society (IRIS) Ltd. IRIS Ltd. is an independent non-profit organization limited by guarantee in the UK (Registered Number 10213173).

(2023)Treatment Recommendations for CKD in Cats (2019)3

Stage 3 Feline patients:
The range of presentations for cats in Stage 3 is likely to be wide, from no clinicalsigns to quite marked extra-renal clinical signs. The main treatments mentioned
so far for stages 1 and 2 are aimed at slowing progression of CKD also apply instage 3 and may be the only therapies needed for cats with no or mild extra-renal
signs. However, treatments designed to improve the quality of life of the cat
become more important, the more extra-renal signs are present. These include
treatments to address dehydration, nausea and vomiting, anemia and acidosis.
Treatments include all of the steps listed for Stage 1 and 2 (listed here again forconvenience) plus any additional steps indicated.
1. Discontinue all potentially nephrotoxic drugs if possible.
2. Identify and treat any pre-renal or post-renal abnormalities.
3. Rule out any treatable conditions like pyelonephritis (any urinary tract infection
should be regarded as a potential pyelonephritis and treated appropriately) andureteralobstruction
withradiographs
and/orultrasonography.
renalurolithiasis
withradiographs
and/orultrasonography.
4. Measure blood pressure and urine protein to creatinine ratio (UP/C).
5. Feed a clinical renal diet.
Management of dehydration:
These patients have decreased urine concentrating ability and therefore• correct clinical dehydration/hypovolemia with isotonic, polyionic replacement fluid
solutions (e.g., lactated Ringer’s) IV or SQ as needed.
• have fresh water available at all times for drinking.
• In addition, some of these cats may require maintenance fluids administered routinely tomaintain hydration (see below)
Systemic hypertension:
The blood pressure above which progressive renal injury may be induced is unknown.
Our goal is to reduce systolic blood pressure to <160 mm Hg and to minimize the riskof extra-renal target organ damage (CNS, retinal, cardiac problems/damage). If there
is no evidence of this but systolic blood pressure persistently exceeds 160 mm Hg
increasing the risk of extra-renal target organ damage, treatment should be instituted.
‘Persistence’ of increase in systolic blood pressure should be judged on multiple
measurements made over the following time-scales in these blood pressure
substages:
Hypertensive (moderate risk of future target organ damage) – systolic bloodpressure 160 to 179 mm Hg measured over 1 to 2 weeks.
• Severely hypertensive (high risk of future target organ damage) – systolic bloodpressure 180 mm Hg measured over 1 to 2 weeks.
If evidence of target organ damage exists, cats should be treated without the need todemonstrate persistently increased systolic blood pressure. Reducing blood pressure
is a long term aim in managing the patient with CKD and a gradual and sustained
reduction should be the goal, avoiding any sudden or severe decreases leading tohypotension.
8© 20192023 International Renal Interest Society (IRIS) Ltd. IRIS Ltd. is an independent non-profit organization limited by guarantee in the UK (Registered Number 10213173).

(2023)Treatment Recommendations for CKD in Cats (2019)

A logical stepwise approach to managing hypertension is as follows:3

1. Dietary sodium (Na) reduction – there is no evidence that lowering dietary Na
will reduce blood pressure. If dietary Na reduction is attempted, it should beaccomplished gradually and in combination with pharmacological therapy.
2. Calcium channel blocker (CCB) such as amlodipine (0.125 to 0.25 mg/kg
once daily) or angiotensin receptor blocker (ARB), telmisartan (2 mg/kg
once daily)
3. Double the dose of amlodipine (0.25 to 0.5 mg/kg once daily) if this is treatment selected.
Note telemisartan label does not advise a dose increase from 2 mg/kg once daily.
4. Combine amlodipine and telmisartan if either drug on its own does not lead toadequate control of blood pressure.
Note: Take care not to introduce CCB/RAAS inhibitor treatment to unstable
dehydrated cats as glomerular filtration rate may drop precipitously if these drugs
are introduced before the patient is adequately hydrated
Monitoring response to antihypertensive treatment:
Hypertensive cats normally require lifelong therapy and may require treatment
adjustments. Serial monitoring is essential. After stabilization, monitoring should
occur at least every 3 months.
Systolic blood pressure <120 mm Hg and/or clinical signs such as weakness or
tachycardia indicate hypotension, which is to be avoided.
Blood creatinine concentration – reducing blood pressure may lead to small andpersistent increases in creatinine concentration (<45 µmol/l or 0.5 mg/dl increase)or SDMA concentration (<2.0 µg/dl), but a marked increase suggests an adverse
drug effect. Progressively increasing concentrations indicate progressive kidneydamage/disease.
Proteinuria:
Cats in Stage 3 with urine protein to creatinine ratio (UP/C) >0.4 should be
investigated for disease processes leading to proteinuria (see 1 and 2 below) andtreated with anti-proteinuric measures (see 3 and 4 below).
Those with borderline proteinuria (0.2 to 0.4) require close monitoring (see 1
and 4 below).
1. Look for any concurrent associated disease process that may be treated/corrected.
2. Consider kidney biopsy as a means of identifying underlying disease (seeAppendix and/or consult experts if unsure of indications for kidney biopsy).
3. Administer an RAAS inhibitor (ACEI or ARB) and feed a clinical renal diet.
4. Monitor response to treatment / progression of disease:– stable blood creatinine concentration and decreasing UP/C = good response.
– serially increasing creatinine concentrations and/or increasing UP/C =disease is progressing.
Ordinarily therapy will be maintained lifelong unless the underlying disease has been
resolved in which case dose reduction whilst monitoring UP/C might be considered.
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(2023)Treatment Recommendations for CKD in Cats (2019)

Note:

3

a. Use of an RAAS inhibitor is contraindicated in any animal that is clinicallydehydrated and/or is showing signs of hypovolemia. Correct dehydration
before using these drugs otherwise glomerular filtration rate may drop
precipitously.

Cats with proteinuria andthesamethromboembolicb. Cats
andhypoalbuminemia
hypoalbuminemialikely
likelyshare
share
the
same
thromboembolicrisk asdogs, (althoughevidenceis lacking
in the publishedrisk as dogs, (althoughevidenceis lacking in
the publishedliterature),
but aspirin is
literature),is achievedifficult atoselective
use in catsto achievea selective
antiplatelet
difficult to but
use aspirinin cats toantiplatelet
effect.
If thromboembolic
effect.
dose rateclopidogrel
if plasma albumin
is below
20 isg/lthe(2drugg/dl)ofischoice.
1therapyA issuggested
deemed necessary,(10 to 18.75
mg/daymg/kg
72 hours
alternative
to (but
aspirinclopidogrel (10 to 18.75
Aspirinevery(1 mg/kg
every and72 h)anis analternative
seeisabove).
mg/day).
c. Cats
serumphosphate
phosphatewithin
withinthe
theIRISIRIS
targetmay
at increased
risk ofCats with serum
targetmay
be be
at increased
risk ofdeveloping hypercalcemia
areareintroduced.
Monitorserum
calcium
developing
hypercalcemiawhen
whenrenal
renaldiets
diets
introduced.
Monitor
serum
and
if
total
calcium
exceeds
12mg/dl(3mmol/l)
switchtoalessphosphate
restrictedcalcium and if total calcium exceeds 12 mg/dl (3 mmol/l) switch to a senior dietdiet.
ormix renal diet (50:50 by volume) with standard grocery food.
d. If borderline proteinuria is persistent, antiproteinuric treatment could beoffered. The rationale for doing so is that there is an association between
progression of CKD and proteinuria which extends into the borderline
category. However, there is at present no evidence that intervention with antiproteinuric drugs slows progression.
Reduction of phosphate intake:Evidence suggests that chronic reduction of phosphate intake to maintain a plasma
phosphate concentration below 1.5 mmol/l (but not less than 0.9 mmol/l; <4.6 mg/dl
but >2.7 mg/dl) is beneficial to patients with CKD.
A more realistic post-treatment target plasma phosphate concentration for cats at
Stage 3 is <1.6 mmol/l (5.0 mg/dl).
The following measures can be introduced sequentially in an attempt to achieve this:restriction(i.e.,(i.e.,
clinicalrenalrenal
diet therapy).
1.1. Dietary
Dietaryphosphate
phosphate
restriction
clinicaldiet therapy).
concentration
remainsabove
1.6 mmol/l(5 mg/dl)
after
dietary
2.2. IfIf plasma
plasmaphosphate
phosphateconcentration
remainsabove
1.6 mmol/l(4.6mg/dl)
after
restriction,
give entericgive
phosphate(such asaluminumhydroxide,
aluminum
carbonate,
dietary restriction,entericbinders
phosphatebinders(such
as aluminumhydroxide,
calciumcarbonate,calciumcalcium
acetate, carbonate,
lanthanum carbonate)
to effect,lanthanum
starting at 30-60
mg/kg/dayaluminum
carbonate,calcium acetate,carbonate)
in divided
doses
to
be
mixed
with
each
meal
(mixedwiththefood).
The
dose
required
willmealvary
to effect, starting at 30-60 mg/kg/day in divided doses to be mixed with eachaccording to the amount of phosphate being fed and the IRIS stage. Treatment with phosphate(mixed with the food). The dose required will vary according to the amount ofbinders should be to effect (as outlined above), with signs of toxicity limiting the upper dose rate
phosphate being fed and the IRIS stage. Treatment with phosphate binders should
possible in a given patient. Monitor serum calcium and phosphate concentrations every 4-6
be toeffect(asandoutlined
above),
with signsof toxicity
limiting
the
upper
weeks
until
stablethen every
12 weeks.
Once serum
phosphateis inthetargetdose
rangeratefor
possiblea givenpatient.
Monitor serum
and may
phosphatestage
3 (<1.6inmmol/l
or 5
mg/dl) measurementof calcium
serum FGF23
assist inconcentrations
determining
phosphate
restriction
be beneficial
to thecat. If FGF23and/oris >700 pg/ml,
3.whetherevery further
4-6 weeks
until stable
and would
then every
12 weeks.
Microcytosis
further phosphate restriction should be applied (e.g. by increasing the dose of phosphate
generalized muscle weakness and neurological signs suggest aluminum toxicity ifbinder) provided there is no evidence of hypercalcaemia, marked anemia or severe inflammatory
using an aluminum containing binder – switch to another form of phosphate binderdisease (all of which can increase FGF23 independently of mineral bone disturbance).
should this occur. It should be noted, however, unlike the dog, aluminum toxicity has
Microcytosis
and/or generalized
weakness
signsaluminumsuggest aluminum
not been reported
in the catmuscle
and it ispossibleandto neurologicalmeasure bloodlevels to
toxicity
if
using
an
aluminumcontaining
binder–switchtoanother
formofphosphate binderconfirm suspected cases. Hypercalcemia should be avoided – combinations
ofshouldthis occur.
should benoted, however,unlikebinders
the dog,mayaluminum
toxicity has
been
aluminumandItcalcium
containing
phosphate
be necessary
in notsomereported
in
the
cat
and
it
is
possibletomeasureblood
aluminumlevelstoconfirm
suspected
cases.
cases. Hypercalcemia should be avoided – combinations of aluminum and calcium containing
phosphate binders may be necessary in some cases.
10© 20192023 International Renal Interest Society (IRIS) Ltd. IRIS Ltd. is an independent non-profit organization limited by guarantee in the UK (Registered Number 10213173).

(2023)Treatment Recommendations for CKD in Cats (2019)3

4. Although there is evidence that judicious use of calcitriol prolongs survival in dogs
at IRIS Stage 3, beneficial effects of ultra-low dose calcitriol have not yet been
established in cats.

Additional recommendations for Stage 2 and 3 patients:
1. If the patient is hypokalemic, then potassium gluconate or potassium citrateshould be supplemented to effect (typically 1-2 mmol/kg/day).
Additional recommendations for stage 3 patients
2. If metabolic acidosis exists (blood bicarbonate or total CO<16 mmol/l) once the2patient is stabilized on the diet of choice, supplement with oral sodium
bicarbonate, (or potassium citrate if hypokalemic) to effect to maintain bloodbicarbonate/ total CO in the range of 16-24 mmol/l.
2
3. Treatvomiting/ decreased
appetite/ nausea
weightmuscle
loss withan an antiemetic
Treat vomiting/ decreased
appetite/ nausea/ weight/ and/or
loss with
antiemetic/appetite
stimulant/
antinausea
agent
(such
as
maropitant,/appetite stimulant / antinausea agent (such as maropitant, ondansetron or oral ortransdermal mirtazapine
or capromorelin).
Evidencesuggests
mirtazapine(1.88mg/cat
mg/cat every
ondansetronor mirtazapine).
Evidencesuggests
mirtazapine
(1.88
48
h
for
3
weeks)
reduces
vomiting,
improves
appetite
and
leads
to
weightgain
inevery 48 h for 3 weeks) reduces vomiting, improves appetite and leadscatstoshowinggain
signsinofcats
inappetence
andvomiting
in this stage. Maropitant(1 mg/kg
daily
for 2
weightshowing
signs
of inappetence
and vomitingin thisstage.
weeks)
reducedvomiting
but
did
not
lead
to
weightgain/
improved
appetite.
FurtherMaropitant (1 mg/kg daily for 2 weeks) reduced vomiting but did not lead toinvestigations are needed on the use of these and other drugs to determine whether they areweightgain/ improved appetite. Further investigations are needed on theuseful for managing gastrointestinal disturbances in cats with CKD and uremia when
use of these and other drugs to determine whether they are useful for
administered longer term. If pharmacological management of appetite is ineffective and/or
managing gastrointestinal disturbances in cats with CKD and uremia when
supplemental hydration is required long-term, enteral feeding tube should be considered.
administered longer term.
4. Give appropriate maintenance fluids parenterally as necessary to maintainhydration (see Footnote).
5. Drugs that rely predominantly on renal function for their clearance fromthe body should be used with caution in patients in Stage 3 CKD. It may
be necessary to adjust the dose of these drugs (depending on their
therapeutic indices) to avoid accumulation.

Where there is a discrepancy between creatinine and SDMA:
If serum or plasma SDMA is persistently >35 µg/dl in a cat with serum
creatinine between 2.8 and 5 mg/dl (IRIS CKD stage 3 based on
creatinine) stage and treat the cat as an IRIS CKD Stage 4 patient.

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(2023)Treatment Recommendations for CKD in Cats (2019)

Stage 4 Feline patients:
4

Most cats with stage 4 CKD have many extra-renal signs present. Although it isstill important to administer treatments which slow progression of CKD, theimportance of improving quality of life for these cats is greater at this stage.
Therapies directly addressing clinical signs and aimed at improving quality of life
include management of dehydration, acidosis, vomiting and nausea and anemia.
Treatments include all of the steps listed for listed for Stages 1, 2 and 3 (listed
again for convenience) plus any additional steps indicated.
1. Discontinue all potentially nephrotoxic drugs if possible.
2. Identify and treat any pre-renal or post-renal abnormalities.
3. Rule out any treatable conditions like pyelonephritis and ureteralrenal urolithiasis
withobstruction
withradiographs and/or ultrasonography.
4. Measure blood pressure and urine protein to creatinine ratio (UP/C).
5. Feed a clinical renal diet.
Management of dehydration:
These patients have decreased urine concentrating ability and therefore ensure:• correct clinical dehydration/hypovolemia with isotonic, polyionic replacement
fluid solutions (e.g., lactated Ringer’s) IV or SQ, promptly as needed.
• have fresh water available at all times for drinking.
• In addition, these cats may require maintenance fluids administered routinely to maintainhydration (see below)
Systemic hypertension:
The blood pressure above which progressive renal injury may be induced is unknown.
Our goal is to reduce systolic blood pressure to <160 mm Hg and to minimize the riskof extra-renal target organ damage (CNS, retinal, cardiac problems/damage). If there
is no evidence of this but systolic blood pressure persistently exceeds 160 mm Hg,
increasing the risk of such damage, treatment should be instituted.
‘Persistence’ of increase in systolic blood pressure should be judged on multiple
measurements made over the following time-scales in these blood pressure
substages:• Hypertensive (moderate risk of future target organ damage) – systolic bloodpressure 160 to 179 mm Hg measured over 1 to 2 weeks.
• Severely hypertensive (high risk of future target organ damage) – systolic bloodpressure 180 mm Hg measured over 1 to 2 weeks
If evidence of target organ damage exists, cats should be treated without the need todemonstrate persistently increased systolic blood pressure. Reducing blood pressure
is a long term aim in managing the patient with CKD and a gradual and sustained
reduction should be the goal, avoiding any sudden or severe decreases leading tohypotension.
A logical stepwise approach to managing hypertension is as follows:
1. Dietary sodium (Na) reduction - there is no evidence that lowering dietary Na
12© 20192023 International Renal Interest Society (IRIS) Ltd. IRIS Ltd. is an independent non-profit organization limited by guarantee in the UK (Registered Number 10213173).

(2023)Treatment Recommendations for CKD in Cats (2019)4will reduce blood pressure. If dietary Na reduction is attempted, it should beaccomplished gradually and in combination with pharmacological therapy.
2. Calcium channel blocker (CCB) such as amlodipine (0.125 to 0.25 mg/kg once daily) or
angiotensin receptor blocker (ARB), telmisartan (2 mg/kg once daily)..
3. Double the dose of amlodipine (0.25 to 0.5 mg/kg once daily) if this is treatment selected.
Note telemisartan label does not advise a dose increase from 2 mg/kg once daily.
4. Combine amlodipine and telmisartan if either drug on its own does not lead toadequate control of blood pressure.
Note: Take care not to introduce CCB/RAAS inhibitor treatment to unstable
dehydrated cats as glomerular filtration rate may drop precipitously if these drugs
are introduced before the patient is adequately hydrated. The benefit ofcombining drugs to try to reduce blood pressure to below the target should beweighed against the high risk in a stage 4 cat of precipitating an azotemic crisis
should be carefully considered.
Monitoring response to antihypertensive treatment:
Hypertensive cats normally require lifelong therapy and may require treatment
adjustments. Serial monitoring is essential. After stabilization, monitoring should
occur at least every 3 months.
Systolic blood pressure <120 mm Hg and/or clinical signs such as weakness or
tachycardia indicate hypotension, which is to be avoided.
Blood creatinine concentration – reducing blood pressure may lead to small andpersistent increases in creatinine (<45 µmol/l or 0.5 mg/dl increase) or SDMA
concentration (<2.0 µg/dl), but a marked increase suggests an adverse drug effect.
Progressively increasing concentrations indicate progressive kidneydamage/disease.
Proteinuria:
Cats in Stage 4 with urine protein to creatinine ratio (UP/C) >0.4 should be
investigated for disease processes leading to proteinuria (see 1 and 2 below) andtreated with anti-proteinuric measures (see 3 and 4 below).
Those with borderline proteinuria (0.2 to 0.4) require close monitoring (see 1
and 4 below).
1. Look for any concurrent associated disease process that may be treated/corrected.
2. Administer an RAAS inhibitor (ACEI or ARB) and feed a clinical renal diet.
3. Monitor response to treatment / progression of disease:– stable blood creatinine concentration and decreasing UP/C = good response.
– serially increasing creatinine concentrations and/or increasing UP/C =disease is progressing.
Ordinarily therapy will be maintained lifelong unless the underlying disease has been
resolved, in which case dose reduction whilst monitoring UP/C might be considered.

13© 20192023 International Renal Interest Society (IRIS) Ltd. IRIS Ltd. is an independent non-profit organization limited by guarantee in the UK (Registered Number 10213173).

(2023)Treatment Recommendations for CKD in Cats (2019)

Note:

4

a. Use of an RAAS inhibitor is contraindicated in any animal that is clinicallydehydrated and/or is showing signs of hypovolemia. Correct dehydration
before using these drugs otherwise glomerular filtration rate may drop
precipitously.

Cats withthesamethromboembolicb. Cats
with proteinuria
proteinuria andandhypoalbuminemia
hypoalbuminemialikely
likelyshare
share
the
same
thromboembolic
risk
as
dogs,
(althoughevidenceislackinginthepublished
literature),
aspirinisrisk as dogs, (although evidence is lacking in the published literature), butbut
aspirinis difficult
difficult
to
use
in
cats
to
achieveaselective
antiplatelet
effect.
If
thromboembolic
to use in cats to achieve a selective antiplatelet effect. A suggested dose rate if plasma
therapyisisbelow
deemednecessary,clopidogrel(10 tois the drugtoofaspirin
choice.
albumin20 g/l(2 g/dl) is
1 mg/kg every
7218.75
hoursmg/day
and an alternativeisAspirin (1 mg/kg
everymg/day).
72 h) is an alternative (but see above).
clopidogrel(10 to 18.75
Cats withtargetmay
be be
at increased
risk ofc. Cats
with serum
serumphosphate
phosphatewithin
withinthe
theIRISIRIS
targetmay
at increased
risk ofdeveloping hypercalcemia
hypercalcemia whenintroduced.
Monitorserum
calcium
developing
whenrenal
renaldiets
dietsareare
introduced.
Monitor
serum
and
if
total
calcium
exceeds
12mg/dl(3mmol/l)
switchtoalessphosphate
restrictedcalcium and if total calcium exceeds 12 mg/dl (3 mmol/l) switch to a senior dietdiet.
ormix renal diet (50:50 by volume) with standard grocery food.
d. If borderline proteinuria is persistent, antiproteinuric treatment could be offered.
The rationale for doing so is that there is an association between progression of
CKD and proteinuria which extends into the borderline category. However,there is at present no evidence that intervention with anti-proteinuric drugs
slows progression.
Reduction of phosphate intake:Evidence suggests that chronic reduction of phosphate intake to maintain aplasmaphosphate concentration below 1.5 mmol/l (but not less than 0.9 mmol/l;<4.6 mg/dl but >2.7 mg/dl) is beneficial to patients with CKD.
A more realistic post-treatment target plasma phosphate concentration for cats at
Stage 4 is <1.9 mmol/l (6.0 mg/dl).
The following measures can be introduced sequentially in an attempt to achieve this:
Dietary phosphate(i.e.,
clinicalrenalrenal
diet therapy).
1.1. Dietaryphosphaterestriction
restriction(i.e.,
clinicaldiet therapy).
If plasmaconcentration
remainsabove
1.9 mmol/l(6.0 mg/dl)
after dietary
2.2. If
plasmaphosphate
phosphateconcentration
remainsabove
1.9 mmol/l(6.0 mg/dl)
after
restriction,
give entericgive
phosphate(such binders
as aluminumhydroxide,
aluminum
dietary restriction,entericbinders
phosphate(such
as aluminumhydroxide,
carbonate,calciumcarbonate,calcium
acetate, lanthanum
carbonate)
to effect,carbonate)starting ataluminum
carbonate,calciumcarbonate,calcium acetate,lanthanum
30-60
mg/kg/dayindivided
doses
to
be
mixed
with
each
meal
(mixedwiththefood).
to effect, starting at 30-60 mg/kg/day in divided doses to be mixed with eachThe
dose
requiredwill
varytheaccordingto theamountof phosphate
fed andtothe
meal(mixedwithfood). The
dose
required
will varybeing
accordingthestage of CKD.
Treatment
withphosphatebindersshouldbetoeffect(asoutlined
above),
withofamount of phosphate being fed and the stage of CKD. Treatment with signs
phosphate
toxicity
limiting
the
upper
dose
rate
possibleinagiven
patient.
Monitorserum
calcium
binders should be to effect (as outlined above), with signs of toxicity limiting andphosphate concentrations every 4-6 weeks until stable and then every 12 weeks. Once serum
the upper dose rate possible in a given patient. Monitor serum calcium andphosphate is in the target range for stage 4 (<1.9 mmol/l or 6 mg/dl) measurement of serum
phosphate concentrations every 4-6 weeks until stable and then every 12 weeks.
FGF23 may assist in determining whether further phosphate restriction would be beneficial to
Microcytosis and/or generalized muscle weakness and neurological signs
the cat. If FGF23 is >700 pg/ml, further phosphate restriction should be applied (e.g. bysuggest aluminum toxicity if using an aluminum containing binder – switch toincreasing the dose of phosphate binder) provided there is no evidence of hypercalcaemia,
another form of phosphate binder should this occur. It should be noted, however,marked anemia or severe inflammatory disease (all of which can increase FGF23
unlike the dog,
aluminum
toxicity has not been reported in the cat and it isindependentlyof mineralbone disturbance).
possible to measure blood aluminum levels to confirm suspected cases.
Microcytosis
and/orshould
generalizedmuscle weakness
and neurological signs suggest aluminum
Hypercalcemia
be avoided– combinations
toxicity
if using an
aluminum– switchbinders
to anotherof phosphateof aluminumandcalciumcontaining
containingbinder
phosphatemayform
be necessary
inbindershouldoccur. It should be noted, however, unlike the dog, aluminum toxicity has not beensomethiscases.
reported in the cat and it is possible to measure blood aluminum levels to confirm suspected3.cases.
Althoughthere is evidence
that judicious
use of calcitriol
prolongs
survivalcontaining
in dogs
Hypercalcemia
should be avoided– combinationsof aluminumand calcium
at
IRIS
Stage
4,
beneficial
effectsofultra-lowdose
calcitriol
have
not
yet
been
phosphate binders may be necessary in some cases.
established in cats.

14© 20192023 International Renal Interest Society (IRIS) Ltd. IRIS Ltd. is an independent non-profit organization limited by guarantee in the UK (Registered Number 10213173).

(2023)Treatment Recommendations for CKD in Cats (2019)

Additional recommendations for Stage 2, 3 and 4 patients:

4

1. If the patient is hypokalemic, then potassium gluconate or potassium citrateshould be supplemented to effect (typically 1-2 mmol/kg/day).
Additional recommendations for Stage 3 and 4 patients
2. If metabolic acidosis exists (blood bicarbonate or total CO2 <16 mmol/l) once thepatient is stabilized on the diet of choice, supplement with oral sodium bicarbonate
2(orpotassium citrate if hypokalemic) to effect to maintain blood bicarbonate / total
CO in the range of 16-24 mmol/l.
3. Consider treatment for anemia if it is affecting the patient’s quality of life: typicallythis occurs when the PCV is <0.20 l/l (20%). Human recombinant erythropoietin is
the most effective treatment but is not approved for veterinary use: darbepoetin
is preferable as it is less antigenic than epoetin alfa. Anabolic steroids are of no
proven benefit and may be detrimental.
Treat vomiting
appetite/ nausea/ weight
and/or muscle
lossanwithan antiemetic/ appetite
4. Treatvomiting/ decreased/ decreased
appetite/ nausea/ weight
loss with
antiemetic//appetite
stimulant/
antinausea
agent
(such
as
maropitant,
ondansetron
or
'oral
or
transdermal
mirtazapineorstimulant / antinausea agent (such as maropitant, ondansetron or mirtazapine).
capromorelin).
Evidencesuggestsoral
mirtazapine(1.88
mg/cat
every
48
h
for
3
weeks)
reduces
vomiting,
Evidence suggests mirtazapine (1.88 mg/cat every 48 h for 3 weeks) reduces vomiting,
improves appetite
and
leads
to weight
gain incatsinshowing
signs of inappetence
and vomitingin thisimproves
appetiteandleads
to weight
gaincats showing
signs of inappetence
andstage. Maropitant (1 mg/kg daily for2 weeks) reduced vomiting but did not lead to weight gain/ improved
vomiting in this stage. Maropitant (1 mg/kg daily for2 weeks) reduced vomiting but did notappetite. Further investigations are needed on the use of these and other drugs to determine whether
lead to weight gain/ improved appetite. Further investigations are needed on the use of
they are useful for managing gastrointestinal disturbances in cats with CKD and uremia whenthese and other drugs to determine whether they are useful for managing gastrointestinaladministered longer term. If pharmacological management of appetite is ineffective and/or supplemental
disturbances
in cats with CKD and uremia when administered longer term.
hydration is required long-term, enteral feeding tube should be considered.

5. Give appropriate maintenance fluids parenterally as necessary tomaintain hydration (see Footnote).
Additional recommendations for Stage 4 patients
6. Intensify efforts to prevent protein / calorie malnutrition. Consider feedingtube intervention (e.g., percutaneous gastrostomy tube).
7. Intensify efforts to prevent dehydration. Feeding tubes can be used toadminister fluids as well as food.
8. Consider dialysis and/or renal transplantation.
8. Consider omeprazole in cats in the uncommon situation where GI bleeding is
Drugs
that rely
predominantly
on renal function for their clearance from thesuspected(e.g.
melena, iron deficiency).
body should be used with caution in patients in Stage 4 CKD. It may be necessary
9. adjust the dose of these drugs (depending on their therapeutic indices) to avoid
toaccumulation.

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(2023)Treatment Recommendations for CKD in Cats (2019)

Appendix
Reasons for Undertaking Renal Biopsy
1. Renomegaly
2. CKD in a young patient
3. Persistent and severe proteinuria (UP/C>2.0) in a non-azotemic patient
4. Worsening proteinuria in a CKD patient
5. Acute kidney injury, where renal biopsy may provide a prognostic indicator

Footnote
Maintenance fluids to maintain hydration status are low in sodium (30-40 mmol/l) andideally have added potassium (about 13 mmol/l) to ensure daily requirements for
fluid and electrolytes are met (e.g. Normosol-M® or 5% Dextrose plus 0.18% NaClwith added KCl).

Disclaimer
Although every effort has been made to ensure the completeness and accuracy of theinformation provided herein, the IRIS Board assumes no responsibility for thecompleteness or accuracy of the information. All information is provided “as is” without
any warranties, either expressed or implied.

16© 20192023 International Renal Interest Society (IRIS) Ltd. IRIS Ltd. is an independent non-profit organization limited by guarantee in the UK (Registered Number 10213173).