Journal of Feline Medicine and Surgery (2012) 14, 785–793

CLINICAL REVIEW

FELINE ACUTE KIDNEY INJURY

2. Approach to diagnosis,
treatment and prognosis
Kelly Monaghan, Benjamin Nolan and Mary Labato

Prompt recognition – a priority Practical relevance: Feline acute

Acute kidney injury (AKI) is a term used to describe the condition in
which there is an abrupt reduction in renal function. This can occur
due to several causes, as discussed in Part 1 of this article. In all cases
prompt recognition of AKI is important to maximize the chance of a
favorable outcome.
Diagnosis
Diagnosis of AKI should focus on attempts to identify an underlying
cause and establish the severity of disease.
History and physical examination
A thorough history should be obtained from the owner regarding time
course, previous therapies, medication history and potential exposure
to toxins. Physical examination may reveal various degrees of lethargy
and depression depending on the severity of systemic illness. With
severe disease, patients may have
Patients with AKI may have oral ulceration and a ‘uremic breath’
odor (ammonia-like smell). Melena
pre-existing chronic kidney may be noted in patients with sec-
disease as well. ondary gastrointestinal ulceration
and bleeding. Attention should be
paid to the size of the urinary bladder
to evaluate for obstruction as well as hint towards urine production.
Kidneys are often palpably normal or enlarged, and may be painful.
A patient with a renal tumor or a ureteral obstruction may have asym-
metry in renal size and shape. However, it should not be forgotten that
patients with AKI may have pre-existing chronic kidney disease (CKD)
as well and this must be considered when evaluating physical exami-
nation findings, as well as laboratory and imaging results.
kidney injury (AKI) is a commonly
recognized problem in small animal
practice that requires prompt
diagnosis and directed therapy. There
are many treatment methods with which
practitioners should be familiar, including medical
options, surgical interventions and
renal replacement therapy (dialysis). It is important
to know which option is most appropriate for
each cause and stage of AKI to deliver the most
effective therapy.
Clinical challenges: AKI can cause vague
clinical signs, but a vast array of life-threatening
sequelae. Rapid recognition of potential
complications and knowledge of treatment options
is imperative for successful management.
Feline patients also require an understanding
of their unique physiology as it relates to the
therapeutic plan.
Audience: This two-part review article is directed
at small animal practitioners as well as specialists.
Part 2 discusses the diagnosis of AKI in cats using
physical examination findings, clinicopathologic
results and imaging modalities. The treatment of
AKI and its sequelae is also reviewed, with
information on recent advances in this area.
Evidence base: While there is very limited data
comparing the outcomes of various treatment
options, there is literature addressing the use of
several medications, as well as renal replacement
therapy, in cats.

Kelly N Monaghan
DVM*
Department of Medical Sciences,
University of Wisconsin–Madison, School of Veterinary
Medicine, Madison, Wisconsin, USA
PART 1
Benjamin G Nolan Part 1 of this review article, discussing
DVM DACVIM (SAIM) PhD mechanisms underlying AKI in the cat,
Veterinary Specialty Center, Middleton, Wisconsin, USA as well as etiologies and treatments
Mary A Labato related to some specific causes of AKI,
DVM DACVIM (SAIM) appears on pages 775–784 of this
Department of Clinical Sciences, Tufts Cummings issue of J Feline Med Surg and at:
School of Veterinary Medicine, North Grafton, DOI: 10.1177/1098612X12464458
Massachusetts, USA
*Corresponding author.
Email: KMonaghan@svm.vetmed.wisc.edu

DOI: 10.1177/1098612X12464460
© ISFM and AAFP 2012 JFMS CLINICAL PRACTICE 785
R E V I E W / Feline AKI – diagnosis, treatment and prognosis

Clinicopathologic assessment
Complete blood count results are often non-
specific and may show an inflammatory or
stress leukogram. Non-regenerative anemia is
Figure 1 (a) Ureterolithiasis
more typical of CKD, but could be found in an resulting in dilation of the
AKI patient, particularly if acute gastric ulcer- ureter. (Ureter is between
calipers; arrow indicates
ation is present. Chemistry profile results may ureterolith.) (b) Short-axis
be within reference intervals and show a ris- view of the left kidney
showing severe
ing serum creatinine over serial monitoring or hydronephrosis secondary
may demonstrate varying degrees of azotemia to ureteral obstruction.
and hyperphosphatemia. Hyperkalemia is These ultrasound images are
from a 10-year-old castrated
common in patients with oliguria or anuria. male domestic shorthair cat
However, potassium may also be increased that presented for acute
severe exacerbation of CKD
with post-renal diseases (eg, urinary obstruc- resulting from a ureteral
tion or urinary tract rupture), so this finding obstruction. Traditional
medical management
is not specific to AKI. Alterations in other bio- was unable to resolve the
chemical values may occur, dependent on the a obstruction and a ureteral
stent was placed surgically
underlying etiology (see discussion on ethyl-
ene glycol [EG] in Part 1). Isosthenuria is the
most typical abnormality on urinalysis but
other findings may be useful in identifying an
underlying etiology, such as proteinuria,
glucosuria, hematuria, pyuria, bacteriuria,
crystalluria or casts.
Culture and sensitivity is recommended in
all patients with an unknown cause of AKI
prior to treatment with antibiotics. Unfortu-
nately, a negative culture does not necessarily
rule out pyelonephritis and it may be benefi-
cial to repeat the culture, consider pyelocente-
sis or continue antibiotic therapy if a positive
response is documented and pyelonephritis is
suspected clinically.
Additional clinicopathologic testing, such
b
as toxin/drug levels (eg, EG, non-steroidal
anti-inflammatory drugs [NSAIDs], amino-
glycosides), may be considered on a case- kidney insufficiency, pyelonephritis or out-
by-case basis. Doppler blood pressure meas- flow obstruction.1 Antegrade pyelography or
urement and a fundic examination should be computed tomography may further delineate
performed in all patients with kidney disease the presence of a ureteral obstruction if not
given the high prevalence of hypertension in visible with ultrasonography, as is the case for
this patient population. Depending on the dried solidified blood calculi or blood clots.2
underlying cause and severity of disease,
patients with AKI may also suffer from Biopsy and GFR estimation
hypotension, which could exacerbate their Biopsy is not commonly employed in patients
kidney injury. with AKI but may have potential benefit in
determining the extent of insult, the prog-
Imaging nosis, and whether the disease is purely
Abdominal radiography and ultrasound acute in nature. It is likely required for
imaging may be helpful to further char- the diagnosis of neoplasia; however,
acterize the etiology of injury. Radi- in the case of renal lymphoma a
ography is useful for evaluation of Future diagnostics diagnosis is often possible through
There are numerous novel biomarkers of kidney
kidney size and shape, and may also injury currently under investigation in human fine needle aspiration alone.
be used to identify radiopaque stones medicine but limited study has been performed in vet- Additionally, estimations of
within the urinary tract. Abdominal erinary patients. One such biomarker is N-acetyl-β-D- glomerular filtration rate (GFR)
ultrasound can be used to evaluate glucosaminidase, which has thus far only been evalu- are rarely indicated in patients
ated in cats with CKD.3,4 The advantage of these
further for obstruction (particularly novel biomarkers is improved sensitivity and speci-
with AKI as GFR is difficult to
with non-radiopaque calculi), neopla- ficity for diagnosis of AKI as compared with determine in a patient that is not
sia or signs of pyelonephritis (Figure 1). serum creatinine and blood urea nitrogen in a steady state, as is the case with
Mild renal pelvic dilation can be detected (BUN). Further research is needed to this condition. GFR reduction in these
assess the utility of these diagnos-
in dogs and cats with clinically normal kid- patients is implied by an elevation in
tics in cats with AKI.
ney function, but pelvic size will increase with creatinine and alterations in urine output.

786 JFMS CLINICAL PRACTICE


Treatment and monitoring
Treatment of AKI should be initiated as soon
as possible and requires intensive patient
monitoring. Any potentially nephrotoxic
medications should be discontinued immedi-
ately. If the cause of AKI is known, specific
interventions should be started immediately
(eg, see Part 1 for discussion of treatments for
EG toxicity).
Fluid therapy
Intravenous fluid therapy is the cornerstone
of treatment for AKI, but it also requires care-
ful monitoring to ensure appropriate use.
Most commonly, a replacement solution (eg,
PlasmaLyte A, lactated Ringer’s solution,
Normosol-R) is chosen during initial manage-
ment. Normal saline 0.9% can be considered
in cats with severe hyperkalemia; however,
caution should be exercised in using this
potentially acidifying solution in patients that
are frequently acidemic. As most cats with
AKI also present with some degree of dehy-
dration, it is important to correct this to ensure
adequate renal blood flow.
Generally, fluid volume deficit can be
assessed by multiplying the cat’s weight in
kilograms by the estimated percentage dehy-
dration based on clinical assessment to obtain
an estimated deficit volume in liters. The time
over which this volume should be replaced
will vary depending on several factors such as
cardiac status, the underlying disease process,
and whether the dehydration is acute or
chronic, but in general ranges from 4–12 h.
After this is completed, intravenous fluids
should be given to replace ongoing losses and
potentially stimulate diuresis. Controversy
exists regarding the benefit of forced diuresis
There are several parameters used to help assess volume status, such as urine output, central
venous pressure (CVP), weight change, changes in packed cell volume (PCV) and total solids,
and presence of peripheral edema.
✜ Urine output Urine output is the most helpful
of these tools in AKI patients as it allows tailoring
of fluid therapy based on urine production. Urine
production can most easily be measured through
sterile placement of a closed system urinary
catheter, which is a relatively easy procedure
in both male and female cats with moderate
sedation. Alternatively, diaper/incontinence pads
or litter can be weighed before and after urination
to estimate total urine volume.
✜ Central venous pressure CVP is most helpful
when assessed as a trend, but in general a CVP
R E V I E W / Feline AKI – diagnosis, treatment and prognosis
Fluid therapy is the cornerstone of treatment
for AKI, but close monitoring is essential
to prevent volume overload.
in patients with AKI, as this may put the
patient at increased risk of morbidity associ-
ated with fluid overload. Importantly,
the fluid plan should be tailored to the indi-
vidual patient’s maintenance needs and
continued losses, and not necessarily aim to
exceed that.
The duration of intravenous fluid therapy
depends on the response of the patient.
Ideally, the kidney values would normalize,
but it is not uncommon to see partial
improvement after several days of intra-
venous fluids with a plateau in azotemia. In
general, the renal values are considered to
have reached a plateau when no further
change is noted over a 24 h period in a well-
hydrated patient. Although renal recovery
can take several months to reach its full
extent, once the plateau is identified this is
generally recognized as the point beyond
which additional fluid diuresis has diminish-
ing returns. Patient status and tolerance of
tapering fluid therapy will help determine the
next step.
Monitoring of fluid therapy should be
undertaken, both to ensure adequate volume
and to prevent overhydration (see box). Fluid
overload is associated with increased morbid-
ity and mortality in human AKI patients5 and
likely has similar impacts on veterinary
patients.
Monitoring of fluid therapy
<0 cmH2O is indicative of hypovolemia, whereas
a CVP >10 cmH2O is associated with volume
overload.
✜ Body weight Body weight should be monitored
at least three times per day as a crude estimate
of fluid gain or loss: 1 kg body weight is equal to
1 l of fluid.
✜ Packed cell volume and total solids Changes in
PCV and total solids are also crude measurements
of fluid balance, although it must be remembered
that these parameters are influenced by other
factors such as blood loss, proteinuria and effusion.6
JFMS CLINICAL PRACTICE 787
R E V I E W / Feline AKI – diagnosis, treatment and prognosis
Electrolyte disturbances
Electrolyte disturbances are common in AKI.
The most frequently encountered and
clinically important are hyperphosphatemia
and hyperkalemia.
Hyperphosphatemia
Hyperphosphatemia is a result of decreased
renal excretion and treatment consists of intra-
venous fluid therapy and administration of
enteral phosphate binders to reduce intestinal
absorption of dietary phosphorus if the
patient is eating.
Hyperkalemia
Hyperkalemia is a result of metabolic acidosis
shifting potassium into the extracellular
space, as well as decreased urinary excretion
in patients with oliguria or anuria. Myocardial
cells and other muscle tissue are the most
clinically affected by hyperkalemia. Elevated
potassium results in an alteration in resting
membrane potential and deactivation of the
sodium–potassium channels, with a resultant
prolongation of the action potential and
inability of myocardial cells to repolarize.7
Consequently, there is a loss of cellular
excitability. This can result in bradycardia,
loss of P waves, a prolonged QRS complex, a
peaked and narrowed T wave, a shortened QT
interval, sinoventricular rhythm, ventricular
flutter or fibrillation, and asystole.7 Clinical
severity is not at all predictable based on the
degree of potassium elevation, so treatment
considerations should be based on electrocar-
diographic (ECG) findings.7
Treatment for hyperkalemia is aimed at
cardioprotection and reduction of serum potas-
sium levels. Calcium gluconate can be given
intravenously to antagonize the membrane
effects of hyperkalemia by decreasing the mem-
brane threshold potential. This will immediate-
ly improve ECG changes, but the duration of
effect is only about 20–30 mins. Calcium should
be given over several minutes, with careful
monitoring of the electrocardiogram during
administration. Caution is required when
administering calcium to patients with altered
kidney function and hyperphosphatemia due
to the risk of soft tissue mineralization.
Reduction of serum potassium can be
achieved through a variety of means including
administration of insulin, dextrose, sodium
taline (a β2 agonist) stimulate movement of
bicarbonate or terbutaline. Insulin and terbu-
potassium from the extracellular to the intra-
cellular compartment by activation of Na+/K+-
ATPase membrane pumps. Dextrose works in
a similar way in that it induces release of
insulin. Bicarbonate alkalinizes the blood,
causing exchange of extracellular potassium
ions for intracellular hydrogen ions.
788 JFMS CLINICAL PRACTICE
If the patient is hyperkalemic secondary to
urethral or bilateral ureteral obstruction, this
should be relieved as soon as possible. If the
patient does not produce adequate urine and
hyperkalemia is refractory to treatment, dialy-
sis should be considered.
Acid–base disturbances
Metabolic acidosis is common in patients with
AKI due to a decreased ability to reabsorb and
recycle bicarbonate and reduced excretion of
hydrogen ions by the renal tubules. Other
The terms contributors to acidosis include lactic acid
production due to decreased perfusion;
oliguria and decreased elimination of phosphate, resulting
anuria are only in decreased urinary excretion of acid; and EG
metabolites, if present.
applicable to a Treatment with sodium bicarbonate can be
considered if the patient’s pH is <7.1 or
well-hydrated TCO2 is <12 mEq/l despite improved perfu-
patient that is sion through fluid administration. However,
in most cases this is not necessary as diuresis
appropriately often helps address acidosis. Sodium bicar-
bonate administration is associated with
volume several potential complications, including
resuscitated. iatrogenic alkalosis, paradoxical central nerv-
ous system (CNS) acidosis, hypokalemia and
hypernatremia, and so this is an infrequently
used therapy.
Oliguria or anuria
Oliguria is defined as urine production
<1 ml/kg/h in a well-hydrated, normo-
tensive, euvolemic patient receiving intra-
venous fluid therapy. Anuria implies zero
urine production. Relative oliguria is another
term that is frequently used to describe a
patient that produces 1–2 ml/kg/h of urine
despite infusion of higher volumes of intra-
venous fluids. These terms are only applicable
to a well-hydrated patient that is appropriate-
ly volume resuscitated, and treatment inter-
ventions to convert to a non-oliguric state
should only be attempted in such patients.
Medications for hyperkalemia
Regular insulin and dextrose
Calcium gluconate ✜ In a patient without diabetes,
✜ 0.5–1 ml/kg IV, given slowly to 0.25–0.5 g/kg dextrose IV will
effect, with ECG monitoring induce endogenous insulin release
✜ For more severe hyperkalemia, or
if patient is diabetic, give 0.5 U/kg
Sodium bicarbonate
✜ The dose of sodium
regular insulin IV, followed by
1–2 g dextrose/U insulin IV bolus
bicarbonate is based on the
and 1–2 g dextrose/U insulin in IV
base deficit, or an empirical
fluids for the next 4–6 h
dosage of 1–2 mEq/kg IV
over 10–20 mins can be used
Terbutaline
✜ 0.01 mg/kg SC or IM

If oliguria or anuria persist despite correc-
tion of dehydration, hypovolemia and
hypotension, there are various medications
such as diuretics and dopaminergic agonists
that are used in patients with AKI to attempt
conversion to a non-oliguric state. There is
currently no evidence that these medications
improve outcome in human or veterinary AKI
patients, but it is thought that if a patient is
able to respond to these medical interven-
tions, their kidney injury is likely less severe
and, as such, they tend to have a better prog-
nosis. If these therapies are unsuccessful, renal
replacement therapy (RRT) is the only viable
treatment option.
Treatments to consider
✜ Furosemide Furosemide is a loop
diuretic that exerts its effect through
inhibition of the renal Na+-K+-2Cl–
cotransporter found on the luminal
membrane of the thick ascending limb
Cats that remain oliguric/anuric after
of the loop of Henle. Inhibition of this no more than 6–12 h of medical inter- vasodilation, and promote natriuresis and
cotransporter results in increased renal vention should be considered as
excretion of water, sodium, chloride,
potassium and calcium. It is one of the first-
line treatments used by many to attempt
to induce diuresis in AKI patients. While
conversion to a non-oliguric state using
furosemide has benefits in regard to ease of
management, its use has not been shown to
improve renal recovery or mortality in human
medicine.8 In one study in healthy cats,
furosemide combined with dopamine did
increase urine output but had no effect on renal
blood flow or GFR.9 If furosemide treatment is
elected, it is prudent to start with a bolus of 1–2
mg/kg IV and, if an effect is seen, instigate a
continuous rate infusion at 0.25–1 mg/kg/h.
✜ Mannitol Mannitol is an osmotic diuretic
that promotes natriuresis and has been shown
to increase renal blood flow in healthy cats.9
It also increases tubular flow and is thought to
be beneficial in flushing tubular obstructions
caused by casts and cellular debris. Additionally,
mannitol has free radical scavenging properties
and is thought to reduce cellular swelling.
Despite these potential benefits, however, no
studies have been performed in cats with AKI to
determine whether there is truly a positive effect
on outcome. Furthermore, mannitol can have
deleterious effects by contributing to volume
overload and exacerbating intracellular
dehydration. If mannitol is given, an initial
bolus dose of 0.5–1 g/kg is recommended. If
urine production improves with this, a
continuous rate infusion can be started at 1–2
mg/kg/min. Doses exceeding 2–4 g/kg/day
should be avoided as this may contribute to
AKI.10 If urine production is not achieved with
initial dosing, further administration should not
be performed.
R E V I E W / Feline AKI – diagnosis, treatment and prognosis
Medications for oliguria/anuria
Furosemide
✜ 1–2 mg/kg IV bolus
✜ 0.25–1 mg/kg/h IV as a CRI
Mannitol
✜ 0.5–1 g/kg IV bolus
✜ 1–2 mg/kg/min IV as a CRI
Fenoldopam
✜ 0.1–1 µg/kg/min IV as a CRI
✜ Fenoldopam Fenoldopam is a specific D1
agonist that is used to treat emergency
hypertension in people and has gained
popularity for use in oliguric or anuric AKI
Failure to respond due to its actions that induce systemic
diuresis. It has been demonstrated to exhibit a
failing to respond. RRT (dialysis) 300-fold greater affinity for the feline D1
is the only therapeutic option receptor compared with dopamine.11 A study in
at 0.5 µg/kg/min documented an increase in
for these patients.
healthy cats using a 2 h infusion of fenoldopam
urine output, sodium excretion, fractional
excretion of sodium and creatinine clearance
within 6 h that lasted for at least 24 h.12 While
further research is needed to evaluate the use of
fenoldopam in cats with AKI, this preliminary
range is 0.1–1 µg/kg/min as a constant rate
data holds promise. The recommended dosage
infusion.
Dopamine – the case against
agonistic effect on dopaminergic receptors, β-
Dopamine is a catecholamine that exerts an
Dopamine is adrenergic receptors and α-adrenergic recep-
dopamine (0.5–5 µg/kg/min) has historically
tors in a dose-dependent fashion. Low dose
no longer
recommended been recommended as a treatment for dogs
and people with oliguric or anuric AKI due
for treatment to its supposed effect on only D1 and D2
receptors. However, its use has become
of oliguric or increasingly controversial due to a lack of
anuric AKI. proven benefit and possible deleterious
effects. It has not been shown to positively
Fenoldopam influence morbidity, need for dialysis or mor-
tality in human patients.13 Additionally, in
may be a more critically ill patients dopamine’s dose-depend-
effective ent response may be less predictable and
tachyarrhythmias, vasoconstriction or hyper-
alternative. tension could result.13 It is no longer recom-
mended for human AKI.
Cats were previously believed to lack renal
dopamine receptors, but it is now known that
they possess a putative renal D1 receptor in
reduced quantities compared with dogs and
people.11 This may explain their lack of
JFMS CLINICAL PRACTICE 789
R E V I E W / Feline AKI – diagnosis, treatment and prognosis

channel blocker, is considered the first-line

treatment for hypertension in cats.17 However,
response to dopamine infusion with regard to

caution should be exercised when decreasing

urine output, sodium excretion, heart rate,

the blood pressure so as not to induce

mean arterial blood pressure and creatinine

hypotension and compromise renal perfusion.

clearance.14 Given the lack of beneficial effect

The use of angiotensin-converting enzyme

seen in feline patients, the potential for side

inhibitors such as enalapril or benazepril is

effects and the changing recommendations

not recommended in critically ill AKI patients

in human AKI, dopamine cannot be recom-

due to their negative effect on GFR; these

mended for feline oliguric or anuric AKI.

agents should be reserved for stable patients

Systemic hypertension is a commonly recog- after recovery from AKI.
Hypertension

nized sequela in dogs with AKI, affecting

37–87% of this population.15,16 The prevalence
of hypertension in cats with AKI has not been
Gastrointestinal sequelae

investigated to date but it is likely that this is

Vomiting and anorexia are common complica-

an under-recognized condition that requires

tions associated with uremia due to AKI in

recognition and intervention. Blood pressure

cats and are frequently the reason for presen-

should be evaluated in these patients both at

tation. The cause of these sequelae is multifac-

presentation and throughout their hospital-

torial. Uremic toxins stimulate peripheral and

ization (Figure 2). It is imperative that proper-

central receptors that trigger nausea, which
Blood pressure
ly trained personnel utilize a standardized
can be treated by a variety of antiemetic

technique to ensure accurate assessment. A

should be medications (metoclopramide, dolasetron,

patient may present with a normal blood

ondansetron, maropitant). The kidneys are
evaluated in
pressure which subsequently increases to a
important for elimination of gastrin, a stimu-

hypertensive range (>150/95 mmHg) with

lator of gastric acid secretion; hypergastrin-
AKI patients
fluid resuscitation. Additionally, a fundic
emia can cause gastric inflammation and

examination should be performed in all

at presentation ulceration is common in these patients.18

patients to evaluate for the presence of target

As such, treatment with medications to
and throughout
organ damage of hypertension (eg, retinal
inhibit gastric acid production may be benefi-

hemorrhage or detachment) (Figure 3).

their cial. These medications include histamine-2

Amlodipine, a dihydropyridine calcium

antagonists (famotidine, ranitidine) and pro-
hospitalization. ton pump inhibitors (omeprazole, pantopra-
zole). If uremic complications secondary to
AKI persist, malnutrition is another potential
problem and supplemental nutrition may be
required either through placement of a feed-
ing tube or via total parenteral nutrition. It is
imperative that the fluid volume adminis-
tered through parenteral or enteral feeding is
taken into consideration with regard to vol-
ume status and risk of fluid overload, particu-
larly in oliguric or anuric patients.

Renal replacement therapy

RRT is indicated for cats with AKI that are
oliguric or anuric despite appropriate medical
therapy, those with refractory hyperkalemia
Figure 2 Doppler blood pressure monitoring in a cat. Here or acid–base disturbances, patients experienc-
the cuff was measured and placed just above the right tarsus,
with the transducer positioned over the dorsal pedal artery ing volume overload, or for removal of certain
dialyzable toxins (eg, EG). These therapies
essentially allow stabilization of the patient
while awaiting renal recovery; or, in the
case of toxin removal, they may prevent
development of disease by removal of a harm-
ful substance.
There are three different types of RRT —
peritoneal dialysis (PD), intermittent
hemodialysis (IHD) and continuous renal
replacement therapy (CRRT) (see box on page
791). The latter two modalities are only avail-
a
able at a limited number of veterinary facilities
Figure 3 Hypertensive retinopathy (a) (see Supplementary data) and require exten-
and retinal hemorrhage (b) seen on fundic b
examination secondary to hypertension sively trained personnel and a dedicated team.

790 JFMS CLINICAL PRACTICE

 R E V I E W / Feline AKI – diagnosis, treatment and prognosis

Renal replacement therapies

Dialytic therapies employ a semipermeable membrane, dialysate solutions, and the principles of diffusion, convection
and adsorption to remove unwanted solutes (eg, BUN, creatinine), correct acid–base imbalances, remove excess fluid and
correct electrolyte disorders.

Peritoneal dialysis
PD can be performed at many 24 h referral facilities without ded-
icated equipment although it is labor-intensive and necessitates
experience and an advanced understanding of the technique.
PD requires placement of a peritoneal catheter attached to a
closed collection system to allow infusion of dialysate, which is
allowed to dwell for a specified amount of time in the peritoneal
space, and is then removed (Figure 4). In this case, the peri-
toneum acts as the semipermeable membrane. The technique
has been utilized in several cats and outcomes have been retro-
spectively reported with regard to survival and complications.
The most recent such study reported 22 cats with AKI that were
treated with PD. Overall survival in this group was 45%,
although the median survival time of those cats was 774 days.19
Still, PD is considered an effective option for treatment of refrac-
tory AKI when other RRT modalities are unavailable.
Figure 4 A 6-year-old castrated male domestic longhair cat being
treated with peritoneal dialysis for an oliguric acute exacerbation of
Intermittent hemodialysis chronic kidney disease secondary to severe pyelonephritis
IHD employs an extracorporeal filter to remove solutes and
excess fluid, and to balance acid–base and electrolyte distur-
bances (Figure 5). It is generally performed for about 4–8 h per
day, several times per week up to once daily as dictated by
patient needs. This modality is effective for rapid removal of tox-
ins as well as treatment of refractory AKI. It can also be used for
long-term therapy if the patient fails to recover kidney function
or needs more time to do so.

Continuous renal replacement therapy

CRRT functions similarly to IHD but in a slower fashion that is
thought to better approximate natural kidney function (Figure 6).
It is administered for 24 h per day and is potentially more suit-
able for hemodynamically unstable patients that may not toler-
ate the rapid fluid and electrolyte shifts associated with IHD.
However, this remains a controversial topic in the human litera- Figure 5 A 14-year-old castrated male Siamese cat receiving
intermittent hemodialysis using a Fresenius 2008H hemodialysis
ture. In many facilities, hybrid therapies using daily, extended machine after experiencing an acute exacerbation of chronic kidney
intermittent therapies may be employed during the initial treat- disease and subsequent volume overload. The cause of AKI was
undetermined in this patient
ment of critical patients as an alternative to CRRT.
There is still much debate among human physicians as to
which therapy is better and, to date, there is no definitive bene-
fit to treatment with CRRT versus IHD. However, there is a bias
toward use of CRRT for more critically ill patient populations. In
veterinary medicine, the data is even more limited and there are
no prospective studies on the use of any of these treatments
and certainly no studies comparing therapies.

Indications for renal replacement therapy

✜ AKI refractory to medical management
✜ Oliguria or anuria
✜ Life-threatening electrolyte imbalances
✜ Life-threatening acid–base disturbances
✜ Exposure to dialyzable toxins such as EG Figure 6 A 6-year-old castrated male domestic shorthair cat with lily-
✜ Fluid overload induced nephrotoxic anuric AKI receiving continuous renal replacement
✜
therapy using Gambro’s Prismaflex system
Stabilization prior to renal transplantation

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R E V I E W / Feline AKI – diagnosis, treatment and prognosis

Prognosis
Summary of treatment considerations for AKI
The prognosis for cats with AKI is guarded to
✜ Discontinue nephrotoxic medications and begin specific therapy poor overall and there is a reported mortality
for known etiology (eg, antibiotics, fomepizole, relief of obstruction) of 47–64% if all causes of AKI are consid-
✜ Correct dehydration and induce diuresis ered.20,21 Factors associated with decreased
survival include elevated serum potassium,
low serum albumin, low serum bicarbonate
Is the patient producing an appropriate amount of urine? and decreased urine production. The severity
of increase in the initial BUN and creatinine
values is not prognostic.20,21 However, consis-
Yes No tently decreased BUN and creatinine within
3 days has been associated with a lower case
fatality rate.21
✜ Continue intravenous fluids and ✜ Diuretics (furosemide, The prognosis is considerably worse for
etiology-specific therapy until renal mannitol) oliguric or anuric patients as compared with
values plateau ✜ Fenoldopam non-oliguric cats and dialysis is required for
✜ Address sequelae of AKI ✜ RRT treatment if they do not respond to initial
– Electrolyte abnormalities medical management.20 Reported survival for
– Acid–base disturbances cats receiving RRT is 44–60%.19,22,23 However,
– Hypertension it is important to keep in mind that the cats
– Gastrointestinal complications that received dialysis would likely die with-
✜ If azotemia, electrolyte abnormalities out that therapy. Despite appropriate therapy,
or acid–base disturbances are residual kidney disease or incomplete recov-
refractory to therapy, consider RRT ery is common and affects about 50% of
patients that survive an acute event.20

KEY POINTS
✜ The diagnostic approach to patients with acute kidney injury (AKI) includes a thorough
history, physical examination, complete blood count, chemistry profile, urinalysis, urine
culture, blood pressure measurement and imaging.
✜ Abdominal ultrasonography yields the most information regarding kidney architecture,
but abdominal radiographs can be useful for evaluating kidney size and investigating for
urolithiasis/ureterolithiasis.
✜ Intravenous fluids are the cornerstone of therapy for AKI. However, close monitoring of
hydration status is essential to ensure that a patient is receiving enough fluids to induce
diuresis, but not so much that volume overload ensues. Parameters that are useful for
evaluating hydration status include urine output, jugular venous distension/pulsation,
body weight, central venous pressure, respiratory rate and effort, and packed cell volume
and total solids.
✜ Electrolyte and acid–base abnormalities are common in patients with AKI and should be
addressed. This is primarily achieved with intravenous fluid therapy, but more directed
treatments may be necessary with severe derangements such as hyperkalemia.
✜ Urine production needs to be closely monitored in patients with AKI. If there is any
concern about low urine output a urinary catheter should be placed to quantify
production. Identification of oliguria or anuria in the face of adequate hydration is an
emergency situation and carries a guarded prognosis. If medical treatments are not
successful in stimulating urine production, renal replacement therapy (RRT) is required.
✜ RRT is available at only a limited number of referral institutions but is the best option
when certain complications of AKI develop. It can take the form of peritoneal dialysis,
intermittent hemodialysis or continuous renal replacement therapy.
✜ The prognosis for cats with AKI is guarded, but may depend on the exact cause.
Cats with oliguria or anuria have a worse prognosis than those with normal
or increased urine production.

792 JFMS CLINICAL PRACTICE


Supplementary data
A list of dialysis centers is available online as
supplementary data. This is based on a regularly
updated list provided by Dr Cathy Langston at
www.QueenoftheNephron.com.
Funding
The authors received no specific grant from any
funding agency in the public, commercial or not-for-
profit sectors for the preparation of this article.
Conflict of interest
The authors do not have any potential conflicts of
interest to declare.
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