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HOW I APPROACH...
The azotemic cat
Jonathan Elliott, MA, Vet MB, PhD,
Cert SAC, Dipl. ECVPT, MRCVS
Royal Veterinary College, London, UK
Dr. Elliott is a graduate of the department of veterinary
medicine at Cambridge University. After completing
a year's internship in Medicine and Surgery in Small
Animals at the Veterinary Clinic of the University of
Pennsylvania, he returned to Cambridge and submitted
his PhD thesis. Since 1990 he has been on the staff at
the Royal Veterinary College in London, where he is
currently Professor of Veterinary Clinical Pharmacology.
His research work is dedicated to chronic kidney
disease and hypertension in cats and laminitis in horses.
In 2004 he was appointed Vice-Principal for research.
Dr. Elliott is a Diplomate of the European College of
Veterinary Pharmacology and Toxicology (ECVPT) and
a member of the Veterinary Products Committee.
A case study
A 15 year old neutered female domestic short
haired cat presents to your practice with a three
month history of polydipsia. The owners had also
noted some weight loss over the same period but
were primarily concerned that over the last week
the cat’s appetite had decreased and she seemed
weak and lethargic.
On physical examination your findings include:
• Condition score 2/5 – under weight (3.0 kg)
• Dull hair coat
• Hydration status – slightly dehydrated (mucous
membranes a little tacky)
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• A systolic heart murmur loudest over the sternum
on the left side (grade 2/6)
• Small and slightly irregular kidneys on palpation
• A moderately full bladder was detected on
abdominal palpation.
Blood was taken for a chemistry screen and a
complete blood count. Urine was collected by cysto-
centesis and an in-house urinalysis performed.
The results of the chemistry screen were as shown
in Table 1.
The hematology profile was all within the reference
range – the hematocrit was 33% (27-48%).
The urinalysis results undertaken in your labora-
tory were as follows: Urine specific gravity:
1.014, Protein: +2, Blood: +2, pH: 5.0.
All other stick test results were negative.
Ask yourself
• How would you classify the azotemia identified
in this case and on what basis would you make
this classification?
• What further routine diagnostic tests would
you undertake in this case, and what is the
justification for these tests?
Azotemia
Azotemia indicates a ‘failure’ of the kidney to
excrete nitrogenous waste products from the
body and can be categorized as:
• Pre-renal: reduced glomerular filtration rate
(GFR) due to reduced blood flow to the
glomeruli; often secondary to hemodynamic
disturbances resulting from circulatory shock
and/or severe dehydration leading to systemic
hypotension.
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THE AZOTEMIC CAT

Table 1.
Initial chemistry screen and after 7 days from a 15 year-old cat

Initial values Values after 7 days Normal values

Total protein g/L (g/dL) 82 (8.2) 75 (7.5 mg/dL) 55 - 80 (5.5 - 8)

Albumin g/L (g/dL) 33 (3.3) 30 (3.0 mg/dL) 24 - 43 (2.4 - 4.3)
Sodium mmol/L 152 150 140 - 156
Potassium mmol/L 2.8 3.3 3.5 - 5.5
Chloride mmol/L 112 115 110 - 130
Calcium mmol/L (mg/dL) 2.67 (10.68) 2.62 (10.48 mg/dL) 2.25 - 2.75 (9 - 11)
Phosphate mmol/L (mg/dL) 3.77 (11.67) 2.56 (7.93 mg/dL) 0.7 - 1.86 (2.17 - 5.76)
Total CO2 mmol/L (mg/dL) 13.0 17.0 14.0 - 23.0
Urea mmol/L (mg/dL) 33.0 (92.44) 24.0 (67.23 mg/dL) 4.0 - 15.0 (11.2 - 42.02)
Creatinine μmol/L (mg/dL) 386.0 (4.37) 283.0 (3.71 mg/dL) 40 - 177 (0.45 - 2.0)
Glucose mmol/L (mg/dL) 7.8 (140.54) 6.5 (117.12 mg/dL) 3.5 - 5.8 (63.06 - 104.5)
Cholesterol mmol/L (mg/dL) 5.75 (222.01) 5.52 (213.13 mg/dL) 1.8 - 5.0 (69.5 - 193.05)
ALT U/L 84 76 20 - 100
ALK-P U/L 56 52 10 - 60
Total T4 nmol/L 21 _ 19 - 55

• Primary intrinsic renal: primary disease of
the kidneys leading to loss of functioning
nephrons and, as a result, a reduced GFR. The
kidney disease could be affecting the vascular
supply, the glomeruli, the tubules or the inter-
stitial compartment and might be acute or
chronic (see below).
• Post-renal: (i) obstructive problem in the
urinary drainage/storage systems leading to
back pressure in the urinary system that is
transmitted to Bowman’s space in the glomeruli
and reduces or prevents filtration; (ii) leakage
of urine from the collection/storage system into
the peritoneal cavity preventing elimination of
waste products from the body.
In this case, the azotemia should be tentatively
classified as due to primary intrinsic renal disease
leading to failure to excrete waste products al-
though we do not have all the necessary inform-
ation that would be desirable. There are no clinical
signs suggestive of obstructive urinary tract
disease leading to azotemia nor is there a history of
blunt abdominal trauma that often accompanies
cases where there is leakage of urine into the
abdomen. Further investigation would help to rule
out bilateral ureteral obstruction as a cause of the
azotemia in this case (see below under further
diagnostic tests). The cat does not have clinical
signs of severe circulatory compromise leading
to reduced GFR although it is clinically mildly
dehydrated. Despite this, however, the cat is
producing dilute urine (based on its urine specific
gravity) and so is not able to respond to the
dehydration by conserving water and concentrating
its urine. In the face of dehydration, cats should
concentrate to a urine specific gravity of ≥1.040.
Having decided this case is most likely to have
azotemia due to a primary intrinsic kidney disease,
one should then ask whether this is an acute
or chronic problem. It is important to recognize
that none of the laboratory tests in this case can
distinguish between a decompensated chronic
kidney disease (CKD) case and an acute renal
failure case. The cat has become inappetant,
weak and lethargic over the last few days prior to
presentation but there are several features that
suggest it has a CKD including:
• Chronic history of weight loss and polydipsia
that has existed for three months or more
• The finding of small shrunken and irregular
kidneys on physical examination
• The finding of a dull hair coat and low body
condition score on physical examination

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Published in IVIS with the permission of the editor
HOW I APPROACH...
Figure 1. Photomicrograph of a urine smear from the cat
reported in this clinical case, at the time of presentation.
All these features suggest this cat has a CKD
leading to azotemia and has recently suffered
an exacerbation of the problem leading to
decompensation (loss of appetite, mild dehy-
dration, weakness and lethargy). Whether this
decompensation is due to a further extrinsic insult
to the kidneys (another episode of the primary
disease that damages the kidney) or intrinsic
progressive renal injury caused by the adaptive
mechanisms of the remaining functioning nephrons
is not possible to determine in many cases although
attempts to identify an active extrinsic disease
process should be made (see below).
What further routine diagnostic tests would
you undertake in this case?
Having identified this case as a case of decompens-
ated CKD, further diagnostic tests should be
aimed at:
• Identifying a primary (hopefully treatable)
extrinsic disease that may be responsible for
this episode of decompensation
• Identifying complications of the uremic syn-
drome that lead to:
- Reduced quality of life of the cat
- May contribute to the process of progressive
renal injury and so intrinsic progression of
the renal failure towards end stage.
The tests undertaken so far have identified
hypokalemia, hyperphosphatemia and metabolic
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acidosis as complications of the uremic syndrome
which may be influencing the quality of life of
the cat and certainly could be addressed in the
therapy of this case. There is reasonable evidence
to suggest that hyperphosphatemia contributes to
progressive renal injury and equivocal evidence
to suggest hypokalemia and metabolic acidosis
could contribute. As a routine in these cases, the
following additional diagnostic tests should be
undertaken:
• Urine sediment examination (+/- urine
culture)
Quite often we find the presence of significant
bactiuria, particularly in female cats presenting
to us for the first time. Bacteria are often visible
on sediment examination as they are usually
rod-shaped bacteria (Figure 1). It is difficult to
say whether bacterial infection of the urinary
tract caused the decompensation in these cases
but it is a treatable problem and infected cats
often improve clinically on antibacterial drug
therapy. This cat had evidence of a bacterial
urinary tract infection despite the fact it was not
showing clinical signs of lower urinary tract
disease. This is typical and is why this problem
is often missed unless urine sediments are
routinely examined in these cases or urine
collected by cystocentesis is routinely cultured.
• Assessment of urine protein excretion
If the urine sediment examination is inactive
and/or the culture results are negative, we
would usually measure the urine protein to
creatinine ratio, regardless of the results on
the dipstick analysis. Most cat urine samples
screened by standard dipstick analysis show
1+ protein in the urine. This can be associ-
ated with normal levels of protein (urine
protein to creatinine ratio <0.2), borderline
proteinuria (UPC >0.2 but <0.4) or signifi-
cant proteinuria (UPC >0.4) (1). Urine protein
to creatinine ratio is an important parameter
to determine when assessing or staging a case
of CKD since it has been shown to be predict-
ive of all cause mortality (2). The implications
of this finding is that proteinuric animals
(provided this is renal proteinuria) might benefit
from anti-proteinuric therapy (e.g. ACE inhibitor
treatment). In this case, because the urine
sediment was active and evidence of a bacterial
Published in IVIS with the permission of the editor
a b
Figure 2a and 2b. A cat undergoing Doppler assessment of systemic arterial blood pressure, with gentle restraint.
urinary tract infection was present, we de-
layed assessing proteinuria until this had
been successfully treated and the infection
had resolved.
• Measurement of arterial blood pressure
All cats with a diagnosis of CKD are at risk of
being hypertensive and should have their
blood pressure measured by one of the available
indirect methods. We use the Doppler technique
and measure systolic arterial blood pressure
(SABP) only (Figure 2). Blood pressure measure-
ment is undertaken in conjunction with a retinal
examination to determine whether there is
evidence of target organ damage. SABP below
150 mmHg is considered normotensive in our
clinic (minimal risk of target organ damage). If
the SABP is between 150 and 159 mmHg the cat
would be considered to be at mild risk of target
organ damage; SABP between 160 and 179
mmHg is associated with moderate risk of target
organ damage and pressures >180 mmHg are
associated with high risk of target organ damage
(3). This particular cat has a heart murmur
which is not uncommon in normotensive cats
with CKD (30% prevalence in our clinic (4))
but is more common in cats with hypertension
(70% prevalence). In addition, hypokalemia is a
significant risk factor associated with feline
hypertension (4).
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THE AZOTEMIC CAT
© Pr. Valérie Chetboul, Unité de Cardiologie
d’Alfort
Blood pressure was measured initially in this
case and was 146 mmHg. It is important to
monitor blood pressure in these cases over
time particularly in those cats which have de-
compensated and present in a dehydrated state.
Assessment of their blood pressure after they
have been rehydrated and are back in a more
compensated state would be very important.
• Diagnostic imaging of the kidneys and urinary
tract +/- renal biopsy
When looking for a primary disease process, the
use of diagnostic imaging of the kidneys and
ureters can sometimes yield useful diagnostic
information (Figure 3). The likelihood of finding
abnormalities on such investigations increases in
younger cats and in cats with palpably enlarged
kidneys on physical examination. For example,
ureteral obstruction by calcium oxalate uretero-
liths can occur - bilateral obstruction can lead to
azotemia and this tends to occur in younger cats
(<10 years of age), possibly with a history of
recurrent lower urinary tract signs. Renal biopsy
would be the ultimate diagnostic test to identify
the pathological processes going on in the
kidney. However, aged cats presenting as this
one did often only have evidence of chronic
interstitial fibrosis with glomerular sclerosis and
renal biopsy does not inform the management
or prognosis of these cases.
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HOW I APPROACH...
© Gagemont Animal Hospital, Hamilton, Ontario (Canada)
a
b
1.5 mm
c
Figure 3. A lateral radiograph of a cat with ureteral blockage
and nephrolithiasis, subsequently shown to be calcium
oxalate (a).
Note the post mortem pictures demonstrating the urolith within
the renal medulla (b) and the size of the urolith within the
ureter (c).
How would you manage this case?
There are several problems that have been
identified in this case that require immediate
attention. These are the things that may be
related to the acute decompensation of CKD.
They consist of:
* Usually the maintenance requirements are set at 50 mL/kg/24 h. With a cat with CKD that is polyuric, urinary losses will be high
and 75 mL/kg takes this into account.
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• Dehydration which will be exacerbating the
azotemia
• Hypokalemia probably resulting from the
anorexia and continued polyuria
• Urinary tract infection which, if untreated may
extend to the kidneys (it could already have
done so)
Fluid therapy to rehydrate the cat and correct the
metabolic acidosis and hypokalemia is important
in this case. It should be remembered that cats
with CKD are susceptible to over-hydration as
well as to dehydration since their kidneys can
not excrete a large fluid over-load. Great care is
necessary to make sure fluid therapy is accurately
administered (e.g. use of an infusion pump). This
cat is not vomiting and so the oral route can be
used to replace potassium and it may be possible
to follow-up initial intravenous treatment in
hospital with subcutaneous fluid on an out-patient
basis. Most cats are happier in their own environ-
ment and are far more likely to eat when at home
than when in the hospital environment.
One approach would be to provide sufficient
fluids to rehydrate the cat over 48 hours. In this
case assuming the cat is 10% dehydrated this
would be 300 mL (0.1 x 3 = 0.3 mEq) plus 75 x 3
x 2 (maintenance requirements – 75 mL/kg/24 h)*.
The total fluid requirements over the first 48 hr
would be 750 mL. Lactated ringers solution would
be appropriate to rehydrate the cat although its
sodium concentration is high and for prolonged
maintenance a lower sodium containing fluid
(with added potassium chloride) would be ideal.
Depending on the cat’s response to treatment,
subcutaneous fluids could be continued to provide
part of the maintenance requirements each day
on an outpatient basis.
To correct the hypokalemia an oral potassium
supplement was used. Potassium gluconate is the
one most commonly used in clinical practice in
the UK. A dose rate of 3 mEq of potassium twice a
day would be appropriate initially in this cat with a
follow-up blood test being advisable after 5 to 7
days. The owner of this cat felt unable to admin-
ister the potassium gluconate tablets and the gel
form was not available at the time. As the cat was
Published in IVIS with the permission of the editor
not eating much at all initially the powdered form
added to the food was not an option. We used
potassium citrate (available from pharmacies)
since tablets can be dissolved to make a liquid
formulation to syringe-dose the cat by mouth.
Both citrate and gluconate are bicarbonate pre-
cursors so act to provide bicarbonate replacement
therapy, addressing the problem of metabolic
acidosis demonstrated by the low total CO2 in
this cat.
Antibiotic treatment was essential in this case. The
choice of antibiotic should be made on the basis of
culture and sensitivity testing in this case since a
long course of treatment is usually recommended
(at least 4 week) on the assumption that the
infection has extended to the kidneys and we are
dealing with pyleonephritis. The organisms
cultured in our clinic are usually E coli and the
majority are sensitive to amoxicillin potentiated
with clavulanate. Palatable tablets are available
containing this drug combination and the owner
was able to administer these in this case. We
would routinely follow-up with an examination of
the urine sediment after a week on treatment.
Assuming there is no evidence of inflammation in
the urine sediment at that stage we would treat for
4 weeks and culture the urine again after the cat
had been off treatment for 7 days to determine
whether there had been a bacteriological cure.
Potentiated amoxicillin is well concentrated
in urine and even in cats with CKD reaches urine
concentrations which are 100 times higher than
its plasma concentration. It also has a time
dependent bactericidal action. Prolonged treat-
ment is required to clear any pockets of infection
within the renal parenchymal tissue. It is not
uncommon for urinary tract infections to recur
in cats with CKD and routine monitoring of the
urine sediment on a regular basis (+/- routine
cultures) are to be recommended. If potentiated
amoxicillin is not effective in managing these
infections our second line treatment would be a
fluoroquinolone. We have most experience of
using marbofloxacin for this purpose and most
uropathogenic E coli seem to be sensitive to this
group of antibiotics.
No attempt was made to change the cat’s diet at this
stage to address the hyperphosphatemia. The most
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THE AZOTEMIC CAT
important treatment targets are to get the cat
over the acute exacerbation of its CKD, correcting
the dehydration, managing the hypokalemia and
treating the urinary tract infection. Once the cat is
back in a more stable state, management of the
more chronic problems associated with chronic
kidney disease is then appropriate.
Progression of this case with the above
management
After a week of the treatment described above,
this cat was much improved and was eating more
of her normal diet. The urine sediment was non-
active. Systolic arterial blood pressure measured
at this point was 192 mmHg, placing her in the
high risk group for target organ damage. A retinal
examination (not performed when the cat first
presented) revealed evidence of hypertensive
choroidoretinopathy with patchy areas of edema
and small retinal hemorrhages around the retinal
blood vessels in both eyes.
A repeat plasma biochemistry profile showed
the values presented in Table 1.
The urine sediment examination at this visit was
unremarkable with very few red cells or white
cells seen and no bacteria identified. Thus the
response to treatment has been good and the
acute problems are under control in this case
allowing us to turn our attention to the more
chronic problems associated with CKD. Antibiotic
therapy should continue for a further 3 weeks
before assessment of whether a bacteriological
cure has been achieved and at that point, an
assessment of the urine protein to creatinine
ratio would be appropriate also. Potassium
supplementation was reduced from 3 mEq twice
a day to 3 mEq once a day at this point.
Management of more chronic problems
associated with chronic kidney disease
At this point there are two longer term problems
identified namely hyperphosphatemia and
hypertension. This cat has been stabilized with a
plasma creatinine concentration of 283 μmol/L
(3.71 mg/dL). This would place it in the early Stage
3 of CKD according to the IRIS classification (5).
Its blood pressure gives it a high risk of suffering
target organ damage and ocular complications
associated with this are evident. Sub-staging based
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HOW I APPROACH...
on proteinuria should be postponed until treatment
for the urinary tract infection has been completed.
Anti-hypertensive treatment
Our preference is to institute treatments one at a
time and assess response to these treatments,
getting the owner used to each new treatment. This
also means that not too many changes are made
too suddenly so the response of the cat to these
treatments can be adequately assessed. In this case
we prescribed amlodipine besylate to treat the
hypertension. The starting dose was 0.625 mg once
daily and the response to this treatment was
assessed after 14 days of therapy. Empirically, our
post-treatment target blood pressure is 160 mmHg.
If the SABP is above this value we would increase
the dose to 1.25 mg once a day and reassess.
Usually this is sufficient to achieve the target, if
not we would consider adding benazepril as an
additional treatment to aid in achieving the target.
Hypotension is a theoretical possibility with anti-
hypertensive treatment but one we rarely see
provided these drugs are not started in cats that
are dehydrated and decompensated. Hypotension
would be a SABP of <110 mmHg measured under
clinic conditions.
Management of hyperphosphatemia
In this case when we measured the SABP after
14 days on amlodipine it was 142 mmHg. At this
point it was appropriate to address the hyper-
phosphatemia problem. This was done initially
by reducing phosphate intake in the diet and
prescribing a renal clinical diet. The owner was
advised to introduce this gradually by mixing a
small quantity of the clinical diet with the cat’s
normal food and gradually increasing the
proportion of the clinical diet and reducing the
proportion of the cat’s normal food over a period
of 7 to 14 days. We recognize that palatability
can be an issue with these clinical diets and
suggest owners find the maximum proportion
of clinical diet that is acceptable and feed this
if it is not possible to transfer the cat onto the
clinical diet as the sole source of food. The
post-treatment target in this case is to achieve a
plasma phosphate concentration of <1.6 mmol/L
(4.95 mg/dL) (for Stage 3 cats) and ideally less
than 1.45 mmol/L (4.49 mg/dL) (for Stage 2
cats). In Stage 3 cats it may be necessary to use
both clinical diets and intestinal phosphate
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binding agents to achieve this post-treatment
target. There are a number of intestinal phosphate
binding agents available (calcium carbonate,
aluminium hydroxide, lanthanum carbonate).
These need to be mixed with the ration that is
fed so they can interact with the phosphate in
the food and reduce its bio-availability.
When we have changed the diet we measure
plasma phosphate concentration after 4 to 6 weeks
to assess response to treatment. This is a chronic
therapy that reverses the whole body phosphate
overload that occurs in chronic kidney disease
and leads to hyperparathyroidism and soft tissue
mineralization (including nephrocalcinosis). It
has been shown to be associated with increased
interstitial fibrosis and mineralization in experi-
mental cats (6) and phosphate restriction through
diet and phosphate binders is associated with
improved survival in cats with naturally occurring
chronic kidney disease (7). In addition to monitor-
ing plasma phosphate concentration against
the post-treatment targets, it is also important to
monitor plasma calcium concentration as some
cats (5% of those treated) develop hypercalcemia
(total calcium >3 mmol/L) (12 mg/dL) when
dietary phosphate is restricted. Theoretically it
might also be possible to induce hypophospha-
temia, which would be undesirable although that is
much less likely to occur particularly in a cat in
Stage 3 chronic kidney disease.
Response to dietary treatment
In this cat after 4 weeks of feeding a renal clinical
diet, the plasma phosphate concentration had
reduced to 1.85 mmol/L (5.73 mg/dL) (from
2.56 mmol/L) (7.93 mg/dL). This was considered
to be a good response to treatment and the cat
was eating the diet to the exclusion of everything
else. We decided to continue to feed the diet and
monitor the plasma phosphate concentration
rather than trying to introduce phosphate binding
agents at this point in time. The plasma creatinine
concentration was 275 μmol/L (3.11 mg/dL) and
plasma potassium concentration was 4.2 mmol/L.
SABP remained below the target at 150 mmHg.
Urinalysis post-antibiotic treatment yielded an
inactive urine sediment and bacterial culture was
negative. At this point a urine protein to creatinine
ratio was measured and found to be 0.56. The cat’s
body weight had stabilized at 3.2 kg.
Published in IVIS with the permission of the editor
At this point the potassium supplementation
therapy was stopped. After another 6 weeks
of dietary and antihypertensive treatment a
reassessment of this cat was undertaken. The
plasma phosphate concentration was 1.55 mmol/L
(4.8 mg/dL) (below the 1.6 mmol/L (4.95 mg/dL)
target)), plasma creatinine remained stable at
290 μmol/L (3.28 mg/dL), the blood pressure was
still within the target at 138 mmHg, the urine
sample had benign (inactive) sediment and the
urine protein to creatinine ratio was 0.68. At this
point we discussed with the owners about instituting
further treatment to manage the persistent protein-
uria. This would involve administering another
oral medication (benazepril; 2.5 mg once daily) to
manage the proteinuria. The post-treatment target
would be to reduce the UPC to below 0.4. We would
also need to monitor blood pressure carefully to
make sure the combination of amlodipine and
benazepril did not induce systemic hypotension.
Benazepril does consistently reduce proteinuria in
cats with CKD (8) and in our experience does not
lead to systemic hypotension when combined
with amplodipine.
Outcome in this case
This cat remained stable on dietary treatment,
amlodipine and benzepril for a further six months.
Post-treatment UPCs following initiation of
benazepril therapy were 0.36 and 0.42. After six
months this cat suffered from another uremic
crisis presenting severely dehydrated and suffering
from a recurrence of its urinary tract infection. The
owners at this point decided euthanasia was
REFERENCES
1. Lees GE, Brown SA, Elliott J, et al. Assessment and management of
proteinuria in dogs and cats; 2004 ACVIM Forum Consensus Statement
(Small Animal). J Vet Intern Med 2005; 19(3): 377-385.
2. Syme HM, Markwell PJ, Pfeiffer DU, et al. Survival of cats with
naturally occurring chronic renal failure is related to severity of
proteinuria. J Vet Intern Med 2006; 20(3): 528-535.
3. Brown S, Atkins C, Bagley R, et al. American College of Veterinary
Internal Medicine. Guidelines for the identification, evaluation, and
management of systemic hypertension in dogs and cats. J Vet Intern
Med 2007; 21(3): 542-558.
4. Syme HM, Barber PJ, Rawlings JM, et al. Incidence of hypertension in
cats with naturally occurring chronic renal failure. J Am Vet Med Assoc
2002; 220: 1799-1804.
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THE AZOTEMIC CAT
the best option rather than a further period of
hospitalization and fluid therapy.
Take home messages
• The finding of azotemia (raised creatinine and
urea) on a chemistry screen requires careful
consideration of the history and physical
examination findings to classify the case
appropriately.
• A full urinalysis is required in all azotemic
patients and this must include microscopic
examination of the urine sediment.
• In cats with CKD, which is a heterogeneous
syndrome, measurement of urine protein to
creatinine ratio (if the urine sediment is benign)
and of systemic arterial blood pressure is
important to identify therapeutic targets in the
management of these cases.
• Re-assessment and monitoring of laboratory test
results (including urine protein to creatinine
ratio) and blood pressure is important as part of
the monitoring process. In animals that have
recently deteriorated, reassessment once they
have stabilized again is very important as blood
pressure and plasma creatinine may change
substantially once the cat is feeling better and
more stable.
• Tailoring treatment to the individual case is
important. Dealing with acute problems first
and then, once the cat is stable again assessing
what chronic therapeutic targets there are and
dealing with these sequentially so that responses
to treatment can be adequately assessed is
important.
5. Elliott J. Staging of chronic kidney disease. In: Manual of canine and
feline nephrology and urology. Eds. Elliott J & Grauer GF. BSAVA
Publication, Cheltenham, Glos 2007.
6. Ross LA, Finco DR, Crowell WA, et al. Effect of dietary phosphorus
restriction on the kidneys of cats with reduced renal mass.
Am J Vet Res 1982; 43: 1023-1026.
7. Elliott J, Rawlings JM, Markwell PJ, et al. Survival of cats with naturally
occurring renal failure: effect of conventional dietary management.
J Small Anim Pract 2000; 41: 235-242.
8. King JN, Gunn-Moore DA, Tasker S, et al. Benazepril in renal
insufficiency in cats study group. Tolerability and efficacy of benazepril
in cats with chronic kidney disease. J Vet Intern Med 2006; 20(5): 1054-1064.
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