Published in IVIS with the permission of the editor
The laboratory diagnosis
of feline kidney disease
Redun Heine, DVM, PhD
Department of Companion Animal Clinical
Sciences, Norwegian School of Clinical Sciences,
Oslo, Norway
Dr. Heine graduated from the Norwegian School of
Veterinary Science (NSVS) in 1988. She did a small animal
internship in Utrecht, the Netherlands, in 1989-1991 and
completed her PhD degree in nephrology at NSVS in
1996. She carried out post-doctoral research at UC Davis,
California in 1997-98 and is currently associate professor
in internal medicine at NSVS. Dr. Heine is president of
ESVNU, board member of IRIS and a member of the
WSAVA Renal Standardization Group.
Introduction
Kidney disease in cats often gives rise to vague and
nonspecific clinical signs. For example, the owner
may only have noted that the cat sleeps more than
before, or has shown reduced physical activity.
These signs are vague and may be attributed to a
lazy lifestyle or increasingly old age in the same
animal. Given the paucity of a detailed history,
whether it starts with a very sick animal with
severe azotemia and clear evidence of chronic
kidney disease (CKD) or just mild azotemia as
an incidental finding on a pre-anesthetic blood
screen, laboratory diagnostics are always import-
ant in a cat with kidney disease.
Unexplained polyuria/polydipsia (PU/PD) in an
otherwise healthy cat may provide an indication for
diagnostic imaging and laboratory tests. Ultrasound
16 / / Veterinary Focus / / Vol 18 No 2 / / 2008
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provides invaluable information in most patients,
and diagnostic samples may be collected by ultra-
sound guidance. Also with increasing frequency,
abnormal findings on abdominal ultrasound
performed for other reasons, raises the question
whether or not renal function is normal. Sometimes
abnormal kidneys can be detected by abdominal
palpation, or increases in plasma creatinine may
be noted on serial samples.
In obvious and severe kidney disease, knowledge
about the nature of the disease process may be
important for prognosis and optimal treatment. It
is important to distinguish between acute renal
failure and CKD, or a potential acute component
on top of a chronic disease process. It may also be
important to know whether a Pre-or Post-renal
component contribute to the severity of the clinical
picture. Underlying primary causes or secondary
complications need to be evaluated before optimal
patient care is possible.
Recently, the concept of “renoprotection” has
received increasing attention. Hopefully, we
should soon gain more knowledge about factors
that provide an indication for precautionary and
reno-protective measures. This should prompt
us as clinicians to give advice on these for the
dedicated owner. For instance, for decades it was
controversial whether or not a “renal” diet would
just alleviate the clinical signs of uremia, or also
prolong life by providing reno-protection. Carefully
designed studies have shown the beneficial
effect of these diets, and sometimes angiotensin
converting inhibitors (ACE inhibitors), in being able
to prolong life in cats with CKD (1-4). Although
several issues need further elucidation in research,
many owners may want to act according to a
precautionary principle in early kidney disease.
Proteinuria and high blood pressures are risk
factors for rapid progression.
Published in IVIS with the permission of the editor
While high quality renal ultrasound is of great
importance in patient work-up, it is also highly
operator-dependent and clearly not all clinicians
working with patients suffering from kidney
disease are board-certified ultrasonographers. On
the other hand, the laboratory diagnostics for
kidney disease discussed are available to most
clinicians, whether simple or advanced. Hopefully
this paper can provide some useful guidelines on
how to use various tests for individual patients.
Urinalysis
Urine dipstick glucose, pH, bilirubin, protein, heme
or ketones are very useful screening tests. Care must
be taken to avoid the use of damaged test strips,
or dilution artefacts due to dilute urine or long
exposure to the urine, so that the chemical reagent
in the pad disappears by diffusion. The blood/
heme pad can cross-react if there is contamination
with fecal contents. The nitrite, leucocyte and
specific gravity test pads are of no value in cats. In
cats, the renal threshold for bilirubin is lower
than in dogs and in humans, and low positive
reaction is always abnormal. Alkaline urine can
be produced after a meal or by urease-producing
bacteria (Staphylococcus spp. or Proteus sp.) or in
alkalosis. Acidic urine is normal in carnivores
but can also be observed in acidosis, infection
caused by acid-producing bacteria, hypokalemia
or by use of loop diuretics (5).
For accurate determination of urine specific gravity
a refractometer is used. As is well known, cats
concentrate urine to a greater extent than dogs and
humans. While urine osmolality is more accurate,
the specific gravity is much easier to measure and
the values are accurate enough for most clinical
purposes. Generally if a cat cannot concentrate
urine above a specific gravity (USG) of 1.035 it is
considered abnormal. PU/PD can be defined as
drinking more than 100 mL/kg/day or not being
able to concentrate urine to a specific gravity
above 1.035.
Note that only approximately half of cats with CKD
and uremia have clinically apparent PU/PD noted
by the owner. The owner may be asked to measure
water intake accurately over the day and also look
for subtle changes in the cats’ behavior which
could point to increased drinking. In the rare
instances where central diabetes insipidus is
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suspected, the PU/PD is generally more severe
than observed in CKD (Figure 1).
So-called “microalbuminuria” has been evaluated
in the dog and the cat in several studies. The term
refers to levels of proteinuria in the range of 30-
300 mg/L and has been a focus of several studies
after a semiquantitative laboratory method became
commercially available a few years back. While
some published studies point to specific situations
where microalbuminuria can be found, some un-
published data demonstrate that microalbinuria
is present in up to half of old cats or cats with any
disease (not necessarily kidney disease), thus
making interpretation of a positive test difficult. An
animal with a negative test is likely to be truly non-
proteinuric. A cat with CKD may well be non-
proteinuric, although the higher the serum crea-
tinine, the more likely the cat is to be proteinuric (6).
As knowledge about the urine protein creatinine
ratio (UPC) in the cat and other species is increas-
ing, some concepts are changing. It is worth paying
attention to the following:
1. The level of proteinuria is of clinical importance.
The greater the magnitude of the proteinuria,
the greater the risk for progression to end stage
renal disease and euthanasia or death (6,7).
2. The greater the magnitude of proteinuria, the
greater the benefit from therapeutic intervention
(2).
3. The levels of what is considered “normal” urine
protein creatinine ratios in cats are lower than
before. Since the use of urine protein creatinine
ratios in spot samples were validated in the 1980s
Figure 1. Cat exhibiting aberrant drinking behavior suggesting of
PU/PD.
Vol 18 No 2 / / 2008 / / Veterinary Focus / / 17
Published in IVIS with the permission of the editor
it has been common to consider UPC above
1 abnormal, below 0.5 normal and values
between 0.5 and 1.0 “borderline”. These values
are specified in many textbooks and review
articles. However, recent research indicates that
we should pay attention to UPC levels as low as
0.2 in cats. In a series of 136 cats (6) survival
was shorter with increasing UPC when cats were
classified according to UPC < 0.2, between 0.2
and 0.4 and > 0.4.
4. While dipstick testing has been the major screen-
ing method for proteinuria, unfortunately it is
quite inaccurate. The IRIS group, while classify-
ing kidney disease (see below) also focus upon
UPC levels. The IRIS group has not given re-
commendations upon the optimal screening
for urinary protein at this point in time, because
research is scarce and the average owner motiva-
tion for extensive screening may vary somewhat
from country to country. The major screening
methods, urine dipstick, sulfosalicylic acid test,
microalbuminuria, and UPC are discussed in
recent reviews (8). The clinician may choose
to use UPC, a screening test for proteinuria,
particularly if kidney disease is suspected.
5. Although logically attractive, there is limited
data in the cat to support a hypothesis that a
reduction of the magnitude of proteinuria will
prolong life of the cat with low levels of protein-
uria (2). Proteinuria could be merely a marker
for the severity of the disease. However, the
consensus in human medicine currently is that
reducing proteinuria will slow progression (9).
Urine sediment
Urine sediment analysis is crucial for the evaluation
of kidney disease. Young clinicians initially may
find it difficult to interpret urine sediments because
of various amounts of debris and stain precipit-
ations, however it is not difficult when a systematic
approach is followed (5).
1. It is wise to use a standard amount of urine or, if
the volume is low, a standard proportion of the
supernatant (i.e. 20% of the total volume) for
resuspending the sediment pellet, in order to be
able to evaluate the amount of sediment.
2. Examination of native wet mounts is used to look
for bacteria and to obtain an undisturbed picture
of other elements, as color stain precipitants or
stained debris may interfere with interpretation.
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3. Examination of a stained wet mount is used
to evaluate cellular elements because nuclei
will stain, so that it is possible to differentiate
between various types of cells or old dead cells
of less significance.
4. Focus upon recognizable elements and follow a
logical approach to what can be present in urine:
Epithelial, blood or inflammatory cells, bacteria,
crystals, or rarely fungi or parasite eggs.
5. Feline kidney tubular cells may be rich in lipid
droplets in normal animals, so the urine or casts
may contain abundant lipid droplets under
normal circumstances.
6. Renal tubular cells may be observed, and if
present in large amounts or in cellular casts
they point to acute kidney injury (Figure 2).
However, they do not often occur in casts and as
individual cells they may be confused with small
transitional epithelial cells or leucocytes.
Urine culture
One recent study in cats with CKD revealed that
17 of 77 cats had urinary tract infection (UTI) when
urine was cultured, although only 4 of them showed
clinical signs of LUTD and a substantial number
did not have WBC or bacteria in their urinary
sediment (10). It is thus recommended to culture
urine from any cat with CKD. Cystocentesis urine
can easily be obtained during renal ultrasound.
A routine should be established that whenever renal
abnormalities are detected, cystocentesis urine is
collected for urinalysis and bacterial culture.
Normal urine is inhibitory to bacterial growth, due to
the high osmolality and salt content, among other
things. Whenever urinary composition is changed,
such as lower osmolality or other changes in CKD, or
the appearance of mild glycosuria, it will predispose
to bacterial growth. Also anatomical/mechanical
properties of damaged urinary tract epithelium
may provide surfaces for bacterial growth.
In a few cases, chronic pyelonephritis may be
present. Bacterial culture from the renal pelvis
may be positive even if culture of urine from the
bladder is negative due to the bacterial inhibitory
factors present in normal urine. Although rare, the
clinician should be aware of this, because proper
case handling in those circumstances may be life
saving if progression of CKD is halted by interfering
with such a detrimental infectious process.
Published in IVIS with the permission of the editor
THE LABORATORY DIAGNOSIS OF FELINE KIDNEY DISEASE
Figure 2. Renal tubular cells in a cast in urine sediment.
Serum chemistry
Plasma or serum urea and creatinine are routinely
measured to evaluate the severity of renal in-
sufficiency. Azotemia may be Pre-renal, renal or
Post-renal. Any severe cause of Pre- or Post-renal
azotemia may progress to renal azotemia and thus
requires careful attention. A rule of thumb is that
the higher the level of plasma urea relative to
plasma creatinine, the more likely the cause is Pre-
renal (circulatory, such as in dehydration, heart
failure or shock). This is because urea is reabsorbed
from the renal tubuli in the medulla and relatively
higher levels of urea accumulate in plasma if the
renal medullary circulation is slow.
Mild azotemia due to CKD does not give rise to
clinical signs. Thus, if a cat presents with a crea-
tinine concentration of 200 μmol/L (2.62 mg/dL)
and severely depressed clinical condition, look for
other causes for the depression. Although, in most
cases, the clinical signs get more severe the more
severe the azotemia (as defined by the IRIS staging
system described on page 21) there is tremendous
individual variation in at what level of azotemia
severe clinical signs develop. While most cats will
show vague clinical signs such as anorexia and
weight loss, listlessness and occasional vomiting
with creatinine levels of 300-500 μmol/L (3.93-
6.56 mg/dL), the author has in exceptional cases
observed cats with clinical symptoms with a
creatinine of 250 μmol/L (3.28 mg/dL) and also
one cat without general depression with creatinine
values of 2000 μmol/L (26.23 mg/dL). Cats can
sometimes, especially in cases of acute kidney injury
secondary to obstructive FLUTD, develop creatinine
values of 1600-1800 μmol/L (20.98-23.6 mg/dL)
and yet recover; as opposed to dogs where such
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levels indicate a horrible prognosis. One recent
study defined clinicopathological parameters prog-
nostic for outcome in cats with CKD, pointing to
serum urea and creatinine, phosphate, packed cell
volume and UPC as important factors (7).
Serum creatinine is less influenced by factors other
than glomerular filtration and is thus generally
considered a better screening test for renal function
than serum urea (Figure 3). Serum creatinine is
higher in the cat than in the dog and the cut-off
point for reference ranges varies from laboratory to
laboratory. There is also some variation in creatin-
ine values in the same individual due to changes in
food and water intake, adding to some analytical
variation. Thus, borderline results may be worth
a repeat sample before extensive and expensive
investigations are instituted.
Increased serum phosphorus is generally known
to be observed in severe CKD. Although severe
hyperkalemia is a universally recognized finding
which will raise suspicion of acute renal failure,
phosphorus levels may also get very high in acute
renal failure.
While hyperkalemia as mentioned often indicates
acute renal failure, the distinction between lone
acute renal failure and acute-on-chronic renal
failure may be of clinical importance, with respect
to prognosis and thus how long it is recommended
to pursue aggressive treatment. High quality ultra-
sound or renal biopsy may provide guidance in
such cases.
Log plasma
concentration
AUC =
area under the curve
Time
Figure 3. A typical plasma clearance curve for a glomerular
filtration marker. Clearance = Dosage/AUC. If limited-sample
approaches are to be used, corrections are usually made for the
upper “lost” area under the curve, when the straight portion of
the curve is used only.
Vol 18 No 2 / / 2008 / / Veterinary Focus / / 19
Published in IVIS with the permission of the editor
IRIS staging system
The International Renal Interest Society (IRIS)
staging system for CKD has gained wide accept-
ance in recent years. Previously, a lot of poorly
defined and overlapping terms were in use, such
as renal disease, renal insufficiency, renal failure
and nephrotic syndrome.
Thus, the IRIS classification system makes it pos-
sible to communicate about patients in a more
accurate manner in scientific literature and in case
discussions. This work has been supported by
Novartis for some years, and an overview of the
staging system is given in Figure 4. The IRIS staging
system classifies renal disease in 4 stages and within
each stage a subclassification is made with respect
to urinary protein level and blood pressure (11).
IRIS Stage 1 and some of Stage 2 patients have
serum creatinine within reference ranges. Never-
theless, by definition there is some sign of kidney
disease, as outlined in the introduction to this paper.
GFR estimation by clearance methods
The estimation of glomerular filtration rate (GFR)
may allow the early identification of renal disease
(Table 1), thereby allowing earlier institution
of reno-protective measures such as dietary or
medical therapy. Indications for the measurement
of GFR include screening for the presence of renal
disease in animals with non-azotemic polyuria or
mild elevations in plasma creatinine, screening
in breeds with a predisposition to familial renal
disease, pre-surgical or post-treatment monitoring
and dosage guidance when using renally excreted
drugs (12). Sequential measurements of GFR
may guide evaluation of the effects of therapeutic
interventions on renal function over time.
GFR is regarded as the best overall index of renal
function in health and disease, and is optimally
estimated by measuring clearance of a marker
substance. The urinary clearance of the fructose
polymer inulin has long been regarded as the
reference method for determining GFR in humans,
dogs and cats.
An alternative to urine collection procedures is to
determine the plasma clearance of a marker, such as
inulin, the iodine-containing radiographic contrast
medium iohexol, radionucleides or creatinine.
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All have been evaluated in cats (13-20). The ex-
pense, laboratory analysis and lack of availability
generally preclude the use of inulin, whilst the
use of radionucleides requires access to a nuclear
medicine facility. The radiographic contrast media
iohexol, has been extensively used in human
nephrology. Contrary to findings in humans, where
creatinine undergoes more extensive interaction
with various body systems, plasma clearance of
exogenous creatinine seems to produce reliable
GFR estimates in dogs and cats.
The main advantage of creatinine is that it can be
analyzed in-clinic. The main advantage of iohexol
is that the excretion times is 1/3 of creatinine, so it
is a more rapid test and possibly more reliable if
renal function is low, and it may be more accurate if
the degree of dehydration is unknown. Thus, the
two methods will likely complement each other
for use in clinical practice. Reference values in
cats for limited-sample approaches (2-4 samples
after injection of creatinine or iohexol) have been
determined in cats of various sizes and ages.
Kidney biopsy
Kidney biopsy in the cat is technically relatively
easy, because of the kidney’s caudal location in the
abdomen and the ability to manually immobilize
the kidney, percutaneously, with one hand. The
biopsy still poses a risk for hemorrhage or other
complications related to the biopsy as such, or
to circulatory compromise during sedation and
anesthesia (21). Thus a biopsy should only be
collected if it is necessary with respect to treatment.
The two most important clinical situations where
treatment may differ based upon an accurate
biopsy diagnosis are cases of suspected acute renal
failure or in cases where glomerulonephritis
is a likely diagnosis. Acute renal failure can be
suspected if the chronic ultrasound changes in the
kidney are mild in nature relative to severe clinico-
pathologic findings or if the kidney is large. The
biopsy may accurately define the severity of the
changes or possible etiologies, or the nature of
possible underlying disease.
Glomerulonephritis can be suspected based
upon high urine protein: creatinine ratios (UP/C).
If a glomerulonephritis is present then treatment
may be pursued and the prognosis may be fair.
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THE LABORATORY DIAGNOSIS OF FELINE KIDNEY DISEASE

STAGING SYSTEM FOR CHRONIC KIDNEY DISEASE (CKD)

STEP 1. Staging is initally based on fasting plasma creatinine assessed on at least two occasions in the stable patient.

Plasma
creatinine
Renal function μmol/L Old terminology*
remaining* mg/dL
Normal renal function
100%
Early renal disease:
no biochemical evidence.
STAGE 1
<140
<1.6 Renal insufficiency: no azotemia. Decreased GFR;
poor concentration ability.

33%

STAGE 2 140 - 249 Early renal failure: mild azotemia. Mal-adaptions

1.6 - 2.8 can lead to hyperparathyroidism and hypokalemia.

25%
250 - 439
2.9 - 5.0 Uremic renal failure: moderate to severe azotemia.
Systemic signs present: e.g. bone pain, uremic
STAGE 3 gastritis, anemia, metabolic acidosis.

>440
<10% ≥ 5.0
STAGE 4
End-stage renal failure: increasing risk of systemic
clinical signs and uremic crisis.

STEP 2. Cases are then sub-staged based on proteinuria and blood pressure.
Note that UP/C and blood pressure vary independently of each other and the stage of CKD, so that any level of proteinuria or hypertension can occur at any
stage of CKD i.e. at any level of azotemia.

Urine protein/creatinine ratio (UP/C)

0 0.1 0.2 0.3 0.4 0.5 0.6

NON-PROTEINURIC BORDERLINE PROTEINURIC PROTEINURIC

Risk of end organ damage from hypertension (Systolic blood pressure mmHg)
130 140 150 160 170 180 190

MINIMAL RISK LOW RISK MODERATE RISK HIGH RISK

Adapted from the Manual of Canine & Feline Nephrology & Urology (Fig : 5.5) 2nd Edition edited by J. Elliott & G. Grauer (2006) with permission of the British
Small Animal Veterinary Association.

*The relative percentages of residual function are conceptual estimates only. This terminology has been used previously without precise definition and should
be replaced by the numerical staging system.

Supported by Novartis Animal Health Inc.

Based on IRIS 2006 staging of CKD.

Figure 4. Overview of the IRIS staging system in cats.

Vol 18 No 2 / / 2008 / / Veterinary Focus / / 21

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THE LABORATORY DIAGNOSIS OF FELINE KIDNEY DISEASE

Table 1.
Overview of data published for GFR during the last 10 years
Marker substance Number of cats Data given as Values (mL/min/kg) Reference

Inulin 99mTc
-DTPA n=8 Mean (range) 3.01 (1.9-4.6) 2.84 (1.82-4.19) 16

Creatinine, Iohexol n = 12 Mean ± SD 2.30 ± 1.32 1.83 ± 0.64 20

Creatinine, Iohexol n=6 “ 2.3 ± 0.73 1.8 ± 0.32 15

Iohexol n = 19 “ 2.75 ± 0.74 13

Inulin n = 30 Median (range) 2.72 (2.07-3.69) 14

Iohexol n = 17 Median (range) 3.68 (3.22-6.22) 18

Iohexol, Creatinine n=4 Mean ± SEM 3.64 ± 0.13 3.34 ± 0.13 19

Inulin, Creatinine n = 10 Mean ± SD 3.60 ± 0.67 4.24 ± 0.94 17

Feline glomerulonephritis is often thought to be if amyloidosis is the histological diagnosis, the

membranous, as in man, and optimal treatment of
membranous glomerulonephritis remains contro-
versial in human medicine. However, a recent
WSAVA kidney biopsy project is likely to improve
access to more detailed pathological diagnoses
(22) in the years to come. On the other hand,
prognosis is poor and immunosuppressive treat-
ment will be of no value.
Other rare conditions such as inheritable kidney
disease or ethylene glycol toxicosis may also be an
indication for kidney biopsy.

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