❖ PEER-RE VIE WED CE

Differentiating between
acute and chronic
kidney disease
When dogs and cats have kidney disease, it can be a puzzle in this article, aKi and cKd are used
to include pre-azotemic (disease) and
determining whether the problem has just developed or has azotemic (failure) conditions. dogs and,
been ongoing. These diagnostics can help you piece the puzzle especially, cats may have compensated
together to make that distinction so you can provide optimal cKd in which they exhibit no clinical
care and give owners the most accurate prognosis for their pets. signs until an acute uremic crisis is
superimposed. this “acute-on-chronic”
Meghan Myott, DVM, and Cathy Langston, DVM, DACVIM kidney disease may have clinical features
of both aKi and cKd.

D
ifferentiating between acute
and chronic kidney disease
can be a complicated task. the
recommended tests, treatments, and
short- and long-term prognoses differ
depending on whether the patient has
acute or chronic disease.
in this article, we review important
components of the diagnostic process that
aid in differentiating acute kidney injury
(aKi) and chronic kidney disease (cKd).
We discuss historical, physical examina-
tion, laboratory, and histologic findings
and diagnostic imaging results. common
clinical findings and diagnostic test results
in cases of aKi or cKd are summarized
in Table 1. We also briefly discuss a few less
common diagnostic techniques.
OvErviEw Of AKi vs. CKD
Multiple definitions of aKi are used in the
human medical and veterinary literature.
Specific criteria for the severity of dam-
Meghan Myott, DVM
Cathy Langston, DVM, DACVIM
The Animal Medical Center
510 East 62nd St.
New York, NY 10065
age range from an increase in creatinine
concentration of 0.3 mg/dl (compared with
a previous reading) to the need for renal
replacement therapy.1-5 the time frame for
increased creatinine concentrations var-
ies from hours to weeks.6 the term acute
kidney injury has been adopted in lieu of
acute renal failure to accentuate that dam-
age to the kidney is a continuum—even
mild decreases in glomerular filtration
rate, even if they do not lead to overt
azotemia, are associated with adverse
clinical outcomes.6,7 aKi may be reversible.
Most definitions of cKd specify that
renal disease has been present for at
least three months,8,9 although some
sources suggest that four to eight weeks
may be sufficient time for stabilization
after an acute insult to allow accurate
categorization.10 after an acute insult to
the kidney, compensatory hypertrophy
may gradually improve renal function,
but this adaptation is generally maximal
within three months. renal dysfunc-
tion that persists after three months is
typically not reversible. the term chronic
kidney disease is preferred to chronic renal
failure to accentuate the concept that renal
disease may be present in the absence
of azotemia. For azotemia to develop,
over 75% of the nephrons must be lost.11
the diagnostic and therapeutic ap-
proach to aKi differs from the approach
to cKd. With aKi, an aggressive diag-
nostic plan is recommended to uncover
any ongoing process that requires a
specific treatment in addition to sup-
portive therapy. aKi frequently requires
aggressive treatment in the hospital,
whereas cKd may be treated on an
outpatient basis in many cases.
Prognosis varies considerably between
acute, chronic, and acute-on-chronic kid-
ney disease. Giving clients prognostic in-
formation allows them to make informed
decisions about their pets’ care. in one
study, 53% of cats survived an episode of
aKi.12 Of these surviving patients, 47%
were discharged from the hospital with
a normal serum creatinine concentration,
whereas the remaining 53% of surviving
cats had persistent azotemia.12 therefore,
25% of the total study population were
discharged without azotemia.12 a similar
study in dogs with aKi revealed compa-
rable results in dogs, with 44% of the study
population surviving to be discharged
from the hospital.13 nineteen percent of
the total study population had creatinine
concentrations that returned to normal.13
although cure is impossible with cKd,
long-term survival (i.e. years) is possible

illustration by Kip carter dvm360.com Veterinary Medicine June 2011 295

Acute vs. chronic kidney disease ❖ PEER-REVIEWED

TAbLE 1

Common Clinical Findings and Diagnostic Test Results in Cases

of Acute Kidney Injury or Chronic Kidney Disease*

Acute Kidney Injury Chronic Kidney Disease

Patient History
Polyuria/polydipsia Yes Yes
Decreased appetite Yes Yes
Vomiting Yes Yes
Oliguria/anuria Maybe Unlikely
Physical Examination
Oral ulcers Yes Yes
Weight loss/poor body condition No Yes
Small kidneys No Maybe
Normal to large kidneys Yes Maybe
Hypertension Yes Yes
Laboratory Findings
Nonregenerative anemia No Yes
Hyperphosphatemia Yes Yes
Hypercalcemia/hypocalcemia Maybe Maybe
Hypokalemia Yes Yes
Hyperkalemia Maybe No
Active urine sediment Maybe Maybe
Diagnostic Imaging Results
Small kidneys No Maybe
Normal to large kidneys Yes Yes (maybe)
Uroliths Yes Yes
Renal osteodystrophy No Yes
Parathyroid gland hyperplasia No Yes
*Because of possible concurrent diseases and individual manifestations of kidney disease, not all of these findings
will be present in all patients.

in many patients. Patients with acute-on-
chronic disease may require aggressive
treatment in the hospital but will have
residual cKd requiring some degree of
long-term management.
PATiENT HisTOrY
Obtaining a thorough clinical history
is useful in determining the chronicity
of a patient’s kidney disease. Polydipsia
and polyuria are classic signs of kidney
disease but are not present in all cases.
their presence does not differentiate
aKi from cKd, but their duration may
help distinguish between the two. in
one study, 70% of cats with cKd pre-
sented with an owner complaint of
polydipsia and 31% with polyuria.14
the discrepancy in owners’ reporting
of polydipsia more frequently than
polyuria is likely because owners are
better able to detect abnormalities in
water consumption than abnormali-
ties in urination volume or frequency.
about half of dogs and cats with aKi
are oliguric or anuric.12,13,15
decreased appetite, vomiting, or other
gastrointestinal signs can be associated
with both aKi and cKd, but these signs
would be of recent onset with aKi. in one
study, decreased appetite was present in
33% and vomiting in 22% of cats with
cKd.14 Often these signs were waxing
and waning for months. in addition to
complete refusal of food, other common
signs include taking longer to eat or
showing interest in food without actu-
ally eating. Historical weight loss sug-
gests chronic disease, although owners
frequently do not recognize weight loss
when it is slowly progressive and subtle.
compensatory mechanisms can mask
a great degree of the patient’s clinical
signs at home, leading owners to miss
subtle changes. the history should also
include questions about exposure to
medications (administered or accidental)
or possible toxins.
PHYsiCAL EXAMiNATiON
a thorough physical examination can
help differentiate between aKi and cKd.
initially, most patients with aKi with-
out concurrent disease processes have

296 June 2011 Veterinary Medicine dvm360.com

 Acute vs. chronic kidney disease ❖ PEER-REVIEWED
FELIMAZOLE (methimazole)
TM

Coated Tablets
2.5 mg and 5 mg strengths
For oral use in cats only

BRIEF SUMMARY (For Full Prescribing Information,

see package insert.)

CAUTION: Federal (USA) law restricts this drug to

use by or on the order of a licensed veterinarian.

DESCRIPTION: Methimazole is a thioureylene

antithyroid drug, which inhibits the synthesis of
thyroid hormones. Methimazole (1-methylimidazole-
2-thiol) is a white, crystalline substance that is freely
soluble in water. The chemical formula is C4H6N2S.
Molecular weight is 114.16.

INDICATIONS: FELIMAZOLE (methimazole)

Coated Tablets are indicated for the treatment
of hyperthyroidism in cats.

CONTRAINDICATIONS: Do not use in cats with

hypersensitivity to methimazole, carbimazole or
the excipient, polyethylene glycol. Do not use
in cats with primary liver disease or renal failure,
autoimmune disease, hematological disorders, or
coagulopathies. Do not use in pregnant or lactating
queens. Laboratory studies of methimazole in rats
and mice have shown evidence of teratogenic and

1. A cat with poor body condition secondary to CKD. Note the generalized severe
embryotoxic effects.

WARNINGS: Methimazole has anti-vitamin K activity muscle wasting, including the epaxial muscles.
and may induce bleeding diathesis without evidence
of thrombocytopenia.

HUMAN WARNINGS: Not for use in humans.

Keep out of reach of children. Methimazole is a
human teratogen. Wash hands with soap and water
after administration of methimazole or contact with
the litter of treated cats. Do not break or crush
tablets. Wear protective gloves to prevent direct
contact with litter, feces, urine, or vomit of treated
cats, and broken or moistened tablets. Methimazole
may cause vomiting, gastric distress, headache,
fever, arthralgia, pruritus, and pancytopenia. In the
event of accidental ingestion/overdose, seek medical
advice immediately and show the product label
to the physician.
PRECAUTIONS: Use of FELIMAZOLE Coated
Tablets in cats with renal dysfunction should be
carefully evaluated. Reversal of hyperthyroidism
may be associated with decreased glomerular
filtration rate and a decline in renal function,
unmasking the presence of underlying renal disease.
Cats on methimazole therapy should be monitored
closely for any sign of illness including fever,
lymphadenopathy, or signs of anemia, as these
may be associated with serious adverse reactions.
ADVERSE REACTIONS: The most common
adverse reactions reported are lethargy, anorexia,
vomiting, diarrhea/loose stool, abnormal vocalization,
and self-induced excoriations of the head and
neck. Serious, but less common, adverse reactions
may include lymphadenopathy, hepatopathy,
immune mediated anemia, thrombocytopenia, and
agranulocytosis. Depression/withdrawn behavior,
weight loss, hair coat abnormalities, increased blood
urea nitrogen (BUN), weakness, and agitation have
also been reported as associated with long-term use.
Distributed by:
Dechra Veterinary Products
7015 College Boulevard, Suite 525
Overland Park, KS 66211
www.dechra-us.com
866-933-2472
FELIMAZOLE is a trademark of
Dechra Ltd. © 2009, Dechra Ltd.
NADA 141-292, Approved by FDA
a normal body condition. However,
because kidney disease is a highly
catabolic disease, muscle loss can oc-
cur rapidly. although weight loss and
poor body condition are not specific
for kidney disease, a poor body con-
dition with diffuse muscle wasting
and an unkempt coat are often some
of the first characteristics noted on
physical examination of a patient
with cKd (Figure 1). Palpation of the
epaxial muscles often reveals subtle but
marked muscle loss. Small, irregular
kidneys on abdominal palpation sup-
port a diagnosis of cKd, while normal
or large kidneys can be associated
with either aKi or cKd.
the prevalence of hypertension is
9% to 93% in dogs with cKd16-21 and
19% to 65% in cats with cKd.22-24 With
aKi, 87% of dogs25 and 30% of cats are
hypertensive (Worwag S, Langston
ce, Unpublished data, 2009). thus,
the presence of hypertension does
not distinguish between aKi and
cKd. Because the eyes are a target
of hypertensive damage, retinal ex-
amination is indicated in any patient
with renal disease and is quick and
easy to do with an indirect lens. the
most common ocular manifestation
of systemic hypertension is exudative
retinal detachment.26 retinal edema
can be seen as an early manifestation
of systemic hypertension and appears
as “pseudonarrowing” of retinal arte-
rioles. dilation and tortuosity of retinal
vessels, retinal hemorrhage, retinal
detachment, and retinal degeneration
are seen more commonly with chronic
hypertension.26,27 identification of any
of these ocular signs should prompt
blood pressure measurement. Ocular
lesions are identified in between 48%
and 100% of cats and 20% and 62% of
dogs with hypertension.24,28-32 Hyper-
tensive retinopathy tends to gradually
progress with chronic hypertension,
but an acute rise in blood pressure may
precipitate an acute exudative retinal
detachment or hyphema.27
clinical signs of cKd may be less
pronounced when compared with
those of aKi with the same level of
azotemia,33 although we have observed
that some patients with early aKi
have minimal clinical signs, which
worsen over the subsequent several
days if recovery is not prompt. as
with the patient history, the physical
examination is just one of multiple
pieces in this clinical puzzle.
LAbOrATOrY fiNDiNgs
although initial laboratory testing
(a serum chemistry profile, complete
blood count [cBc], and urinalysis) is
essential to diagnosing kidney disease,

298 June 2011 Veterinary Medicine dvm360.com

these tests cannot, by themselves, dif-
ferentiate between aKi and cKd. these
two disease processes often have similar
initial laboratory findings. But patients
with results consistent with renal fail-
ure may have additional findings that
support further characterization of the
disease process as acute or chronic, such
as an elevated parathyroid hormone
(PtH) concentration.
serum chemistry profile
Calcium concentrations. Hypercal-
cemia has traditionally been associated
with cKd. it can develop in the presence
of renal tertiary hyperparathyroid-
ism, if the hyperplastic parathyroid
gland autonomously starts secreting
PtH despite normal to high serum ion-
ized calcium concentrations. this only
occurs with cKd. However, because
ionized hypercalcemia can cause aKi
and because hypercalcemia can also be
secondary to either aKi or cKd, it is
not useful in distinguishing between
acute and chronic disease. no cats in
one study of 32 cats with aKi were
hypercalcemic (Worwag S, Langston
ce, Unpublished data, 2009), although
total hypercalcemia was present in
62.5% of dogs with aKi from grape or
raisin intoxication and in 30% of dogs
with aKi in another study.34,35 With
cKd, 9% to 22% of dogs and cats have
total hypercalcemia,17,35-39 whereas 0% to
30% have ionized hypercalcemia.14,35-37,40
total hypocalcemia occurs in 7%
to 23% of dogs with cKd,17,35,41,42 com-
pared with 10% to 15% of dogs with
aKi.37-39 in cats with cKd, 8% to 15%
have total hypocalcemia, compared
with 30% of cats with aKi (Worwag S,
Langston ce, Unpublished data, 2009).
Given these similar ranges for both aKi
and cKd, total hypocalcemia cannot be
used to differentiate acute from chronic
kidney disease.
in the presence of cKd, the total cal-
cium concentration is poorly predictive
of ionized calcium, the metabolically
active fraction.37 thirty to forty percent
of dogs and 10% to 26% of cats with cKd
Renal imaging CE
Focus on your imag-
ing skills in Dr. Laura
Ambrust’s presenta-
tion “Renal ultraso-
nography: Kidneys
big, small, and in between” on Aug.
28 during the CVC in Kansas City. For
more information and to register to
attend, visit thecvc.com.
have ionized hypocalcemia.35,37,40,41,43
data on ionized calcium concentrations
in aKi are not available.
Unfortunately, because of the preva-
lence of both hypercalcemia and hypo-
calcemia with both acute and chronic
kidney disease, the value of calcium
concentrations in differentiating be-
tween acute and chronic kidney disease
is quite low.
CbC
evidence of a nonregenerative anemia
on a cBc should trigger suspicion that
the azotemia is long-standing. Seventy
percent of dogs with cKd in one study
presented with a nonregenerative, normo-
cytic, normochromic anemia,44 compared
with 25% of dogs with aKi present-
ing with anemia in another study.13
erythropoietin is an important factor
in replacing senescent red blood cells,
and erythropoietin production decreases
in the face of cKd. a relative or abso-
lute erythropoietin deficiency leads to
chronic, nonregenerative anemia. With
severe aKi, erythropoietin production
may be decreased, but anemia would
not be expected to occur unless there is
dvm360.com Veterinary Medicine June 2011
accelerated red blood cell loss (bleeding
or hemolysis).
conditions that contribute to anemia
include low-grade hemolysis secondary
to uremic toxin accumulation causing
increased erythrocyte fragility; blood
loss associated with platelet dysfunc-
tion, especially from gastrointestinal
ulcers; and increased PtH concentra-
tions inhibiting hematopoiesis.44 Patients
with renal disease may have less severe
clinical signs from anemia compared
with patients with anemia associated
with other disease processes, since
concurrent increases in serum phos-
phate concentrations and erythrocyte
2,3-diphosphoglycerate concentrations
may improve tissue oxygenation in the
face of a lower hematocrit.44
Urinalysis
Similar to the serum chemistry profile
and cBc, urinalysis is indispensable in
diagnosing kidney disease. However,
it often does not shed enough light on
whether the kidney disease is acute
or chronic. an active urine sediment
with evidence of pyuria, hematuria,
bacteriuria, and proteinuria can be seen
with either form of kidney disease. re-
nal epithelial cells may be present in
a urine sample in a patient with aKi.
However, it is not possible to definitively
distinguish whether the cells originated
in the kidney or lower in the urinary
tract unless they are formed into casts.45
Occasional renal epithelial cells may be
normal. However, larger numbers may
indicate acute infiammation, infection,
or neoplasia of the renal pelvis.45
casts may be evident in both aKi
and cKd and indicate active damage.
casts rapidly disintegrate, frequently
precluding identification at the labora-
tory.46 Hyaline casts are present with
acute or chronic proteinuria and may
not represent marked renal pathology.43
cellular casts are more common in
aKi.43 White blood cell casts are usu-
ally associated with acute nephritis,
pyelonephritis, or toxins that damage
the renal tubular epithelium, and red
blood cell casts often support a diagnosis
299
Acute vs. chronic kidney disease ❖ PEER-REVIEWED
2. Radiographic examination can allow efficient evaluation of kidney
size. In this ventrodorsal radiograph of a neutered male cat, the
length of the L2 vertebra measures about 2.2 cm. The length of the
right kidney measures about 4 cm, and the length of the left kidney
measures 6.6 cm. The right kidney is slightly smaller than normal,
and the left kidney is enlarged. This radiograph also reveals bilateral
nephroliths (arrows) and an irregular margin to the right kidney.
Bilateral ureteral obstructions secondary to proximal ureteroliths
were diagnosed in this cat. Severe hydronephrosis of the left kidney
and mild pelvic dilation were identified with ultrasonography.
of glomerulonephritis or renal hematuria,47 although both
types of casts are uncommon in cats and dogs. casts with
kidney tubular epithelial cells signal tubular damage.48
Granular casts can be present in cases of aKi and are com-
posed of cells that have degenerated such that the cell type
cannot be distinguished.47 Fatty casts are course granular
casts with lipid granules that are seen with glomerular
disease or diabetes mellitus.47 Waxy casts indicate chronic
renal tubular degeneration47 as they are the final stage of
granular cast degeneration.46
Additional laboratory testing: PTH assay
an increased serum phosphorus concentration decreases
the serum ionized calcium concentration, which stimulates
secretion of PtH to return the ionized calcium concentration
to normal. With progressive cKd, PtH concentrations tend
to increase. in one study, 47% of asymptomatic cats with cKd
had elevated PtH concentrations, compared with 100% of
cats with severe end-stage cKd.14 in another study, 100% of
dogs with cKd or aKi had elevated PtH concentrations.35
although the mean PtH concentration was higher in the
dogs with cKd compared with those with aKi, this differ-
ence was not significant.35
300 June 2011 Veterinary Medicine dvm360.com
Acute vs. chronic kidney disease ❖ PEER-REVIEWED
iMAgiNg
radiography and ultrasonography can be useful tests in dif-
ferentiating aKi from cKd as well.
radiographic examination
an abdominal radiographic examination allows evaluation of
renal size and shape. normal canine kidneys should measure
2.5 to 3.5 times the length of the second lumbar vertebra in
a ventrodorsal view.49 the kidneys of neutered cats should
measure 1.9 to 2.6 times and the kidneys of intact male and
female cats 2.1 to 3.2 times the length of the second lumbar
vertebra on a ventrodorsal view.50
Small kidneys in comparison to the patient’s size suggest
cKd (Figure 2). One study showed 33% of cats with cKd
had small kidneys, 40% had normal-sized kidneys, and 27%
had enlarged kidneys.51 renal asymmetry can be caused by
chronic damage to one kidney leading to scarring, fibrosis,
and small size with hypertrophy of the contralateral side.
acute obstruction of one kidney could lead to enlargement
of that side with a normal-sized contralateral kidney, but
azotemia would not be expected if the normal-sized kidney
were functioning normally. an irregular renal contour can
be caused by an acute or chronic infarction, cystic diseases,
or, rarely, renal masses. Symmetrically enlarged kidneys sug-
gest acute disease. Uroliths in the kidney or ureters indicate
a chronic disease process but may have caused acute uremia
from acute obstruction or pyelonephritis.
evaluation of bone density throughout the radiograph
is important in diagnosing any concurrent renal osteodys-
trophy secondary to renal secondary hyperparathyroidism.
radiography alone is 60% sensitive and 100% specific for
detecting nephroliths or ureteroliths in cats.52 Ultrasonog-
raphy alone is 77% to 100%53,54 sensitive and 33% specific,52
and the combination of radiography and ultrasonography
is 90% sensitive.55
Ultrasonographic examination
an abdominal ultrasonographic examination allows for the
evaluation of kidney size, shape, and architecture. a normal
feline kidney is about 3.8 to 4.4 cm in length and has no pelvic
dilation.56 Ultrasonographic determination of renal volume
(by measuring renal length, width, and depth) and the ratio
of renal length to aortic diameter have been evaluated to
determine normal renal size parameters in dogs.57 although
both the renal volume and the ratio methods provide some
utility, the amount of normal variation is large, especially in
very small or very large dogs, and these techniques are not
commonly used.54,57
during an ultrasonographic examination, cKd will fre-
quently appear as small irregular kidneys with hyperechoic
cortices and decreased corticomedullary distinction (Figure
3). Pelvic dilation, renal mineralization (nephrocalcinosis), or
nephroliths may also be present. renal asymmetry, with one
Acute vs. chronic kidney disease ❖ PEER-REVIEWED
3. Ultrasonographic images of cats with diseased kidneys. Panel A: Normal renal shape and internal architecture with good corticomedul-
lary distinction in a cat with AKI. Panels b and C: Reduced corticomedullary distinction (arrowheads), renal asymmetry (right larger than
the left), irregular renal contour bilaterally, and a caudal infarct on the left kidney (flattened caudal pole, arrow) in a cat with CKD.
small and one normal or large kidney,
suggests chronic disease of the small
kidney, but the contralateral kidney
may have chronic disease (e.g. compen-
satory hypertrophy, hydronephrosis
from obstruction) or acute disease (acute
obstruction, pyelonephritis, ischemic
or toxic insult). renal cysts typically
denote chronic disease.58 the kidneys
may appear structurally normal in the
presence of cKd.
in the presence of aKi, the kidneys
may appear normal or may be enlarged,
hydronephrotic, and hyperechoic on ul-
trasonographic examination. Perinephric
fiuid generally is associated with acute
disease.59 enhanced corticomedullary
distinction does not distinguish between
acute or chronic disease, nor does the
presence of a medullary rim sign (a hy-
perechoic band at the corticomedullary
junction), which has also been seen in
normal animals.56 decreased cortical
echogenicity can be seen in both acute
and chronic renal disease.56 Varying de-
grees of renal pelvic dilation or ureteral
dilation occur with partial or complete
obstruction, which can be acute or chronic.
Ultrasonographic examination
can also be used to evaluate the size
and echogenicity of the parathyroid
glands. in cKd, chronically increased
phosphorus and decreased calcium
concentrations stimulate chronic in-
creases in PtH production. this renal
secondary hyperparathyroidism leads
to parathyroid gland hyperplasia. in one
study, parathyroid glands in dogs with
cKd were larger (2.8 to 7.1 mm) than
parathyroid glands in healthy control
dogs or dogs with aKi (1 to 3.5 mm).60
Parathyroid gland size varies with pa-
tient size. although ultrasonographic
examination of the parathyroid gland
is not part of the routine evaluation of
patients with kidney disease in most
practices, it is helpful to determine chro-
nicity in experienced hands.
rENAL biOPsY
Fibrosis, sclerosis, and atrophy are histo-
logic indicators of chronicity of injury.61
Because these changes are irreversible,
renal biopsy rarely affects the manage-
ment or outcome of cKd.62 Biopsy is
typically reserved for suspected cases
of aKi when a diagnosis cannot be con-
flrmed by less invasive testing, and it is
used to attempt to deflnitively diagnose
histologic lesions causing protein-losing
nephropathy, providing appropriate
technique is used. Fibrosis and other
evidence of chronicity may not be uni-
formly distributed throughout the kidney,
so biopsies may miss the lesion. it is
prudent to inspect a core biopsy with a
dissecting microscope to ensure that at
least 10 glomeruli have been collected.
if the sample is insufflcient, additional
tissue should be collected.
Good-quality kidney biopsy samples
are more likely to be obtained in anesthe-
tized patients compared with those that
are only sedated.63 a complication rate
dvm360.com Veterinary Medicine June 2011
of 13.4% in dogs and 18.5% of cats was
noted in one large study.62 ten percent of
dogs and 17% of cats required transfu-
sion because of post-biopsy hemorrhage,
and 2.5 % of dogs and 3% of cats died.62
renal function does not decrease in
healthy dogs and cats after unilateral
renal biopsy.64,65
OTHEr TEsTs
Various other tests have been investi-
gated to help distinguish between aKi
and cKd but are not commonly used in
veterinary medicine. an elevated urea
concentration causes hemoglobin to
become carbamylated, and this abnor-
mal hemoglobin accumulates over time
within red blood cells. the carbamylated
hemoglobin concentration can be corre-
lated to the duration of azotemia. in one
study, cKd was accurately diagnosed in
dogs with a carbamylated hemoglobin
concentration exceeding 108 µg of valine
hydantoin per gram of hemoglobin with a
positive predictive value of 71.2%.66 if the
blood urea nitrogen concentration is not
elevated, this test will not be predictive.
the creatinine concentration at the
distal end of the flngernails is another
method for differentiating aKi and cKd
in people. nails do not change in their
chemical makeup after they leave the
cuticle.67 Fingernail growth from proximal
to distal end takes about three months.67
therefore, the creatinine concentration
at the distal tip indicates the creatinine
concentration three months before, with a
301
Acute vs. chronic kidney disease ❖ PEER-REVIEWED
false positive result rate of 6.12% with no
false negative test results.67 to our knowl-
edge, no veterinary study has evaluated
toenail creatinine concentrations.
sUMMArY
identifying whether a patient’s kidney
disease is acute or chronic in origin is
not always easy. all the clinical evidence
must be evaluated. in our experience, a
long-standing history of clinical signs
consistent with kidney disease, poor
body condition, and identification of
small, irregular kidneys are the most
useful in confirming that kidney disease
is chronic. in the absence of these find-
ings, evaluation of other parameters such
as PtH concentration or parathyroid
gland size, presence of anemia, presence
of urinary casts, presence of uroliths,
renal ultrasonographic architecture,
and renal biopsy may be used to fur-
ther characterize the disease and may,
in aggregate, help differentiate acute
from chronic disease. differentiating
between aKi and cKd in each patient
will ensure that the patient is getting
optimal care and that clients are well-
informed about their pets’ condition to
make optimal decisions. ❖
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