Chronic Kidney Disease in Dogs and Cats: Joseph W. Bartges
Chronic Kidney Disease in Dogs and Cats: Joseph W. Bartges
Chronic Kidney Disease in Dogs and Cats: Joseph W. Bartges
and Cats
Joseph W. Bartges, DVM, PhD
KEYWORDS
• Chronic kidney disease • Geriatric • Nutrition • Treatment
• International Renal Interest Society
KEY POINTS
• Chronic kidney disease occurs commonly in dogs and cats.
• Chronic kidney disease is progressive; however, management utilizing dietary modification
and pharmacologic agents may improve quality of life and survival.
• Management of dogs and cats with chronic kidney disease is directed at minimizing the
excesses and deficiencies that occur.
• Specifically, management is directed at providing nutritional support, treating hypokalemia
and metabolic acidosis, decreasing the degree of proteinuria, maintaining hydration,
decreasing retention of wastes such as nitrogen containing compounds, avoiding other
renal insults, improving anemia, minimizing renal secondary hyperparathyroidism and
hyperphosphatemia, and decreasing blood pressure if systemic arterial hypertension is
present.
• Serial monitoring of dogs and cats with chronic kidney disease is essential because of the
progressive nature of the disease.
Chronic kidney disease (CKD) occurs commonly in older dogs and cats and is the
most common renal disease occurring in elderly patients. It is defined as structural
and/or functional impairment of one or both kidneys that has been present for more
than approximately 3 months. In most patients, there is loss of function and structure
with CKD; however, degree of functional impairment does not always mirror loss of
structure. CKD implies irreversible loss of renal function and/or structure that remains
stable for some period of time but is ultimately progressive. In some patients, CKD
may be complicated by concurrent prerenal and/or postrenal problems that may
worsen the condition, but if managed, they may improve the situation.
CKD is considered a disease of older animals, although it occurs at all ages. The
estimated incidence of CKD in the general population of dogs and cats is 0.5% to
1.5%.1 At the University of Minnesota Veterinary Medical Center, more than 10% of
dogs and 30% of cats over 15 years of age are diagnosed with CKD.1 One
retrospective study reported that 53% of cats with CKD were over 7 years old, but
animals ranged in age from 9 months to 22 years.2 In a study on age distribution of
kidney disease in cats based on data submitted from 1980 to 1990 to the Veterinary
Medical Data Base at Purdue University, 37% of cats with the diagnosis of “renal
failure” were less than 10 years old, 31% of cats were between the ages of 10 and 15,
and 32% of cats were older than 15 years.3 Similarly, in a study of cats with CKD
reported in 1988, the mean age was 12.6 years with a range of 1 to 26 years.4 Mean
age among 45 control cats in this study was 10.0 years. During 1990, the prevalence
of kidney disease was reportedly 16 cases for every 1000 cats of all ages, 77 cases
per 1000 cats over age 10 years, and 153 per 1000 among cats older than 15 years.2
Maine coon, Abyssinian, Siamese, Russian blue, and Burmese cats were dispropor-
tionately reported as affected.
The kidneys are involved with whole body homeostasis; therefore, CKD affects many
organ systems, is associated with many metabolic derangements, and affects general
well-being. Glomerular filtration results in formation of urine in Bowman’s space except
for cells and protein-bound compounds; a small amount of albumin is filtered. Bulk
reabsorption of the filtrate occurs in the proximal tubule with additional secretion or
reabsorption of anionic and cationic compounds. The loop of Henle concentrates then
dilutes the filtrate through selective reabsorption of water and sodium. The distal
convoluted tubule and collecting ducts fine-tune the solute and moisture content of urine.
In addition to these processes, the kidneys are intimately involved in metabolic regulation
of acid-base status, have endocrine function (eg, erythropoietin and vitamin D), and have
a role in blood pressure regulation (eg, renin production and adrenal secretion of
aldosterone). Therefore, when renal function declines there is disruption of these normal
processes resulting in retention of compounds that should be excreted (eg, phosphorous
and creatinine) and loss of compounds that should be retained (eg, water and protein).
TREATMENT OF CKD
Fig. 1. Uremic stomatitis and glossitis in a 20-year-old, spayed female domestic shorthair cat
with chronic kidney disease.
Table 1
International Renal Interest Society (IRIS) System
Stage of CKD based on serum or plasma creatinine concentration
Plasma Ccreatinine,
mol/L, mg/dL
Courtesy of Novartis Animal Health, Inc, Basel, Switzerland, sponsor of the International Renal
Interest Society (IRIS), with permission.
Chronic Kidney Disease in Dogs and Cats 673
Table 2
Body condition scoring systems
Descriptor Description 5 point 9 point
CACHECTIC Ribs are easily palpated with no fat cover; bony 1 1
structures are prominent and easy to
identify; muscle tone and mass often
decreased; little to no subcutaneous fat; hair
coat often poor; pronounced abdominal tuck
UNDERWEIGHT Ribs are easily palpated with little fat cover; 2 3
abdominal tuck present; bony structures are
palpable but not prominent; hair coat may
be poor; muscle tone and mass may be good
or slightly decreased
IDEAL Ribs are easily palpated, but fat cover is 3 5
present; hourglass shape present and
abdominal tuck is present, but not
pronounced; bony prominences are palpable
but not visible some subcutaneous fat, but
no large accumulations; muscle tone and
mass good; hair coat quality is good
OVERWEIGHT Ribs are difficult to palpate due to overlying fat 4 7
accumulation; hourglass shape is not
prominent and abdominal tuck is absent;
subcutaneous fat obvious with some areas of
accumulation; muscle tone and mass good;
hair coat quality may be decreased; cannot
identify bony prominences
OBESE Ribs are impossible to palpate due to overlying 5 9
fat; hourglass shape is absent and animal
may have a round appearance; subcutaneous
fat is obvious and accumulations are present
in the neck, tail-base, and abdominal
regions; muscle tone and mass may be
decreased; hair coat quality may be
decreased
N Nutrition
The main goal of nutritional support of any patient with a chronic disease is
maintenance of lean muscle mass and optimal body condition, and this is true of
patients with CKD. A thorough physical examination is performed and a body
condition score (BCS) and muscle condition score (MCS) are assigned.10 There are 5-
and 9-point BCS systems; either can be used.11–13 Assigning a BCS (Table 2)
provides more information than BW alone and estimates body fat content. The goal
for most pets is a BCS of 2.5 to 3 of 5 or 4 to 5 of 9.
An MCS may also be assigned and is an assessment of muscle mass and tone.10
Evaluation of muscle mass includes visual examination and palpation of muscles over
temporal bones, scapulae, lumbar vertebrae, and pelvic bones. Muscle condition is
an assessment of lean mass and loss of muscle mass may adversely affect strength,
immune function, wound healing, and ability to compensate for chronic conditions
such as CKD. A simple MCS has been suggested using a 0-to-3 scale where 0 ⫽
normal muscle mass and tone, 1 ⫽ slightly decreased muscle mass and tone,
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Table 3
Activity and life stage factors used to estimate MERs after RERs are estimated
Life Stage Canine Factor Feline Factor
Gestation 1.0–3.0 1.6–2.0
Dogs: first ½–2⁄3 1.0–2.0
Dogs: last 1⁄3 2.0–3.0
Lactation 2.0–8.0 1.0–2.0
Growth 2.0–3.0 2.0–5.0
Adult intact 1.8 1.4
Adult neutered 1.6 1.2
Senior 1.4 1.1
Work: light 2.0
Work: moderate 3.0
Work: heavy 4.0–8.0
Obese prone 1.4 1.0
Weight loss 1.0 0.8
Weight gain 1.2–1.4 ideal 0.8–1.0 ideal
Critical care (usually) 1.0 1.0
in fat compared with maintenance adult foods. Available diets contain 12% to 30%
crude fat (dry matter basis).
Nausea and anorexia associated with chronic renal failure may also occur because
of hypergastrinemia and gastric hyperacidity.17 Dietary protein stimulates gastric acid
secretion; therefore, dietary protein restriction may decrease gastric hyperacidity.
Administration of histamine2-receptor antagonists (famotidine: dogs and cats, 1.1
mg/kg po q 12–24 hours; ranitidine: dogs and cats, 1–2 mg/kg po q 8 –12 hours)19 or
other antacids are beneficial in dogs and cats with CKD; many phosphate binders
also bind gastric acid and act as antacids. Sucralfate (dogs, 0.5–2.0 g po q 6 –12
hours; cats, 0.25– 0.5 g po q 6 –12 hours)19 is an aluminum-containing compound that
binds to exposed submucosal collagen in an acidic environment and may have
cytoprotectant effects via prostaglandin E2. It is used to treat active gastric ulcers, but
may also act as an antacid and phosphate binder. Maropitant (dogs and cats: 2– 8
mg/kg po q24h; although not recommended for more than 5 days)19 is an anti-emetic
that inhibits neurokinin-1; it is used for motion sickness but is effective with many
other causes of vomiting including uremic gastroenteritis. Mirtazapine (dogs, 15–30
mg po q 24 hours; cats, 1.875–3.75 mg po q 48 –72 hours)19 is a noradrenergic and
serotonergic antidepressant that stimulates appetite and has antiemetic properties. In
cats with CKD, it should be administered every 48 hours.20 Metoclopramide (dogs
and cats, 0.1– 0.5 mg/kg po q 6 –24 hours),19 an intestinal prokinetic agent that has
central antiemetic effects via dopamine receptor antagonism, may also be used
although it is less effective than serotonin receptor antagonists in uremic human
beings.21
In patients that are unwilling or unable to eat, nutrition may be provided by feeding
tubes including nasogastric, esophagostomy, and gastrostomy feeding tubes.22–26 A
study of 56 dogs with renal failure were managed with gastrostomy feeding tubes; 10
were low profile and 46 were standard mushroom-tipped tubes.27 Gastrostomy tubes
were used for 65 ⫾ 91 days (range, 1– 438 days). Eight dogs gained weight, 11 did not
have a change in BW, and 17 lost weight; information was not available for 20 dogs.
Mild stoma-site complications included discharge, swelling, erythema, and pain in 26
(46%) of dogs. Twenty-six gastrostomy tubes were replaced in 15 dogs; 11 were
replaced because of patient removal, 6 were replaced because of tube wear, and 3
were replaced for other reasons. Three dogs were euthanatized because they
removed their gastrostomy tubes, 2 were euthanatized because of evidence of tube
migration, and 1 died of peritonitis. Based on this report, gastrostomy tubes appear
to be safe and effective for improving nutritional status of dogs with renal failure. In
another report, 96% of owners of dogs or cats managed with gastrostomy feeding
tubes had a positive experience and would use a gastrostomy feeding tube again in
their pet if necessary.28
In addition to providing calories (energy), there are specific nutrients that may
alter progression of CKD in dogs and cats. With a decrease in numbers of
functioning nephrons, pressure inside remaining nephrons increased; this is
termed intraglomerular hypertension.29,30 The intraglomerular hypertension in-
creases the filtration rate in the remaining nephrons. The tradeoff of intraglomeru-
lar hypertension is damage to these nephrons over time. In dogs with induced
CKD, feeding diets containing omega-3 fatty acids has been shown to decrease
intraglomerular hypertension, maintain glomerular filtration rate, and increase
survival.31–34 In dogs fed omega-3 long chain fatty acids, renal function actually
increased and remained above baseline over 20 months of the study. Glomeru-
losclerosis, tubulointerstitial fibrosis, and interstitial inflammatory cell infiltrates
were less in dogs fed an omega-3 fatty acid–supplemented diet compared with
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dogs fed an omega-6 fatty acid–supplemented diet.32 Omega-3 fatty acids reduce
hypercholesterolemia, suppress inflammation and coagulation, lower blood pres-
sure, and improve renal hemodynamics. An omega-6 –to– omega-3 fatty acid ratio
of 3:1 to 5:1 appears to be beneficial and is present in many renal failure diets.
B vitamins are water-soluble vitamins and may be decreased with CKD due to the
polyuric state. B vitamin deficiency may be associated, in part, with hyporexia/
anorexia, which occurs commonly with CKD. A recent study showed that B vitamin
deficiency is not common in patients with CKD.35 Nonetheless, diets formulated for
CKD in dogs and cats are supplemented with B vitamins.
Oxidative stress may be an important component of CKD. Renal cells, particularly
renal tubular cells, are among the most metabolically active cells. The kidneys
maintain persistently high levels of mitochondrial oxidative phosphorylation and
arterial blood flow, making them an environment in which reactive oxygen species
formation occurs.36 Important factors in generation of reactive oxygen species
include angiotensin II, glomerular hypertension, hyperfiltration, tubular hypermetab-
olism, systemic arterial hypertension, anemia, regional hypoxia, and renal inflamma-
tion.37,38 The result of reactive oxygen species formation may be glomerulosclerosis
and interstitial fibrosis, thereby promoting progression of CKD. Renal oxidative stress
may be decreased by treating systemic arterial hypertension, correcting anemia,
providing omega-3 fatty acids, and treating with angiotensin-converting enzyme
inhibitors.37 In a study of cats with induced CKD, feeding a diet with vitamins C and
E and beta-carotene for 4 weeks decreased evidence of oxidative stress as measured
by serum levels of 8-hydroxy-2=-deoxyguanasine and comet assay parameters.38
Supplementation with omega-3 fatty acids and antioxidants has not been ade-
quately evaluated in cats. A retrospective study on the effects of several renal diets
did find that survival was greatest among cats fed the diet with the highest omega-3
fatty acid content.39 The study, however, was retrospective and it is not possible to
accurately assess effects of dietary omega-3 fatty acids from these data.
Recently, an extract of medicinal rhubarb (Rheum officinale) has become available
for dogs and cats with CKD. Experimentally, it decreases renal fibrosis in an induced
CKD model in rats.40,41 One study of cats with CKD showed no benefit when
administered alone or in combination with benazepril.42
E Electrolytes
The kidneys are involved with regulation of electrolyte balance. Electrolytes are
filtered at the glomerulus, most of the filtered electrolytes are reabsorbed in the
proximal convoluted tubule, and the remainder of the nephron reabsorbs or secretes
electrolytes depending on status. A common electrolyte disturbance in cats and
occasionally in dogs with CKD is hypokalemia,43,44 which has been reported to occur
in 20% to 30% of cats with stage 2 or 3 CKD.2,4 Hypokalemia may occur because of
hyporexia or anorexia, excessive renal losses, transcellular shift due to chronic
metabolic acidosis, and activation of the renin-angiotensin-aldosterone system due
to dietary sodium restriction.45,46 Hypokalemia often manifests as polymyopathy.
Clinical signs include decreased activity and muscle weakness or classically as an
inability for the patient to lift its head while sitting sternally (Fig. 2). Additionally,
hypokalemia may result in hyporexia or anorexia and progression of CKD.2 The target
for plasma or serum potassium concentration should be in the middle to upper half of
reference range for the laboratory. Once hypokalemia is present, whole body
potassium content is low and it is difficult to replete in patients with CKD.47
Diets formulated for use in patients with CKD are supplemented with potassium,
typically using potassium citrate as it is a source of potassium and an alkalinizing
Chronic Kidney Disease in Dogs and Cats 677
agent. This is based, in part, on diets low in potassium and high in acid content being
implicated in impairing renal function and promoting development of lymphoplasma-
cytic tubulointerstitial lesions in cats.47–51 Potassium may be supplemented orally
using potassium gluconate or potassium citrate. If patients are receiving subcutane-
ously administered fluids, potassium may be added to the fluids up to 30 mEq/L as
potassium chloride.7 Irritation at injection site may occur with concentrations above
this. Potassium chloride may also be added to fluids administered intravenously
depending on blood potassium concentration (Table 4). Rate of administration should
not exceed 0.5 mEq/kg/h because cardiotoxicity may occur. Potassium may be
supplemented orally as well as gluconate or citrate salts; potassium citrate is used
more often as it provides alkalization as well. Potassium gluconate (dogs and cats, 2
mEq/kg po q 12 hours)19 or potassium citrate (dogs and cats, 75 mg/kg po q 12
hours)19 may be administered; dosage is adjusted to achieve a serum or plasma
potassium concentration in the middle to upper half of the reference range. If
hypokalemic polymyopathy is present, it usually resolves within 1 to 5 days after
initiating parenteral or oral potassium supplementation. Typical commercial modified
diets for CKD in dogs and cats contain 0.4% to 0.8% potassium on a dry matter basis
for dogs and 0.7% to 1.2% potassium on a dry matter basis for cats.52
Table 4
Suggested guidelines for intravenous potassium supplementation
Amount of Potassium to Add
Serum Potassium to Lactated Ringer’s Solution Maximum Fluid
(mEq/L) (mEq/L) Rate (mL/kg/h)
⬍2.0 80 6
2.1–2.5 60 8
2.6–3.0 40 12
3.1–3.5 28 18
3.6–5.0 20 25
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Blood sodium concentrations are typically normal in patients with CKD. Sodium
retention may occur with CKD because of intravascular volume contraction. This may
promote systemic arterial hypertension, in part; therefore, dietary sodium restriction
may be beneficial in patients with CKD. Furthermore, there is evidence that excessive
sodium intake may be harmful to the kidneys and excessive salt intake may impair
effectiveness of antihypertensive therapy.53 Excessive dietary sodium restriction may
be detrimental, however. In one study of experimentally induced CKD in cats, dietary
sodium restriction to 50 mg sodium/kg of diet promoted hypokalemia due to
activation of the renin-angiotensin-aldosterone system.46 Additionally, in one study,
dietary intake of sodium at 1.1% as fed was associated with increased azotemia in
cats with CKD54; however, other studies did not find this.55 Typical commercial
modified diets for CKD in dogs and cats contain 0.3% sodium or less on a dry matter
basis for dogs and 0.4% sodium or less on a dry matter basis for cats.52
P Proteinuria
Proteinuria occurring in association with CKD in dogs and cats is associated with
progression.5,6,60 Proteinuria is considered a hallmark of glomerular disease; how-
ever, proteinuria appears to be nephrotoxic even without overt primary glomerular
disease.61 In humans with CKD, reducing proteinuria slows progression; however, no
such evidence exists for dogs and cats with CKD.62– 65 Proteinuria may promote
progressive renal injury by several mechanisms including mesangial toxicity, tubular
overload and hyperplasia, toxicity from specific filtered proteins (eg, transferrin), and
Chronic Kidney Disease in Dogs and Cats 679
H Hydration
Patients with CKD are polyuric due to decreased ability to concentrate urine from
decreased nephron mass. Polyuria is offset by polydipsia. Because of polyuria,
dehydration may occur if water loss exceeds water intake. This occurs more often in
cats than in dogs with CKD. In patients that are dehydrated, parenteral fluid is
administered.68 Intravenous administration is preferred over other parenteral routes.
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R Retention of Substances
With CKD, substances that are eliminated normally in urine are retained. These
substances include nitrogenous compounds (blood urea nitrogen and creatinine)
among others. Elimination of nitrogenous compounds is a major function of the
kidneys and retained nitrogenous compounds are associated with clinical signs of
CKD. Azotemia is a hallmark of CKD. Thus, restriction of dietary protein is logical.
Results of studies are contradictory concerning the influence of dietary protein
restriction on progression of CKD.69 –72 Restricting dietary protein may be associated
with a decreased degree of azotemia, decreased dietary phosphorous as meat-based
protein is also high in phosphorous, decreased metabolic acids generated from
dietary protein, and decreased stimulus for gastric hydrochloric acid production and
may reduce dosage of antihypertensive agents and decrease requirement for
erythropoietin.73 Modified diets for managing CKD in dogs and cats typically contain
14% to 20% protein on a dry matter basis for dogs and 28% to 35% protein on a dry
matter basis for cats.52
There are 3 studies of dietary intervention in dogs and cats with spontaneously
occurring CKD: 2 in cats and 1 in dogs.74 –77 In these studies, a diet formulated to
contain lower quantities of protein, phosphorous, and sodium and higher quantities of
potassium, B vitamins, calories, alkalization potential, and omega-3 fatty acids were
compared with a diet that was formulated to be similar to maintenance over-the-
counter adult dog or cat foods. Results of these studies showed benefit in dogs and
cats with CKD: patients lived longer, had fewer episodes of uremia, time to onset of
Chronic Kidney Disease in Dogs and Cats 681
first uremic episode was longer, and owners perceived quality of life was better.
Although diets formulated for renal failure are lower in protein than over-the-counter
maintenance adult foods, they are still adequate and typically contain higher biologic
value protein.
Prebiotics and probiotics have been suggested to redistribute a small amount of
nitrogen into the gastrointestinal tract for elimination, thus decreasing the degree of
azotemia. Prebiotics are dietary fiber, typically soluble fiber that promotes prolifera-
tion of beneficial bacteria in the colon that metabolizes nitrogen and urea intraluminal.
The proliferation of bacteria also promotes uptake and utilization of intraluminal
nitrogen by the bacteria resulting in less absorption from the colon. Probiotics are live,
nonpathogenic bacteria that are presumed to populate the gastrointestinal tract,
providing the same benefit. One such probiotic (Azodyl; Vetoquinol, Lure Cedex,
France) is commercially available and marketed as “enteric dialysis.” A small
uncontrolled study showed decreased degree of azotemia; however, a controlled
study evaluating administration of the probiotic with and without food failed to show
a benefit.78
N Neuroendocrine Function
There are 3 abnormalities of neuroendocrine function that may occur with CKD:
renal secondary hyperparathyroidism, hypoproliferative anemia, and systemic
arterial hypertension.
osteodystrophy, particularly of the mandible and maxilla; this occurs more commonly
in dogs with congenital or juvenile-onset CKD but may occur in adult patients (Fig. 3).
It occurs, in part, because of phosphorous retention and decreased calcitriol
(1,25-dihydroxy vitamin D3) metabolism. Renal tubular cells contain 1␣-hydroxylase,
which is the enzyme that converts 25-hydroxyvitamin D to the active 1,25-dihy-
droxyvitamin D3. Calcitriol stimulates gastrointestinal absorption of calcium and
phosphorous and inhibits parathyroid hormone production. Parathyroid hormone
stimulates renal reabsorption of calcium and excretion of phosphorous, stimulates
calcium and phosphorous release from bone, and stimulates calcitriol production.
With CKD, there is decreased enzyme activation of calcitriol. In response to
decreased calcitriol, parathyroid hormone production and secretion are increased.
Parathyroid hormone may be considered a uremic toxin. With decreased glomerular
filtration rate, hyperphosphatemia occurs, which may result in dystrophic mineraliza-
tion and progression of CKD and further inhibits calcitriol production. Hyperphos-
phatemia is associated with progression of CKD and shortened survival.
Chronic Kidney Disease in Dogs and Cats 683
fibrosis.94,95 It has been shown that patients with CKD have increased survival if the
hematocrit is above 35%. Treatment includes maintaining good nutritional status,
minimizing gastrointestinal blood loss, and stimulating red blood cell production.
Patients with CKD may have blood loss due to uremic gastroenteritis. Hypergas-
trinemia occurs with CKD and gastrin stimulates hydrochloric acid production by
gastric parietal cells resulting in gastric hyperacidity.18,96 Histamine2-receptor– block-
ing agents may be beneficial in decreasing gastric acid production, although they are
not potent and the effect may be transient. Proton pump inhibitors (dogs and cats,
omeprazole: 0.7–2.0 mg/kg po q 12–24 hours; esomeprazole: 0.7 mg/kg po q 12
hours)19 decrease gastric acid secretion by inhibiting the potassium-hydrogen pump
located in the cell membrane; they are the most potent antacids. Sucralfate is also an
antacid that has phosphate binding properties and is used to treat active gastric ulcer
disease.
Red blood cell production by bone marrow may be stimulated pharmacologically.97
Anabolic steroids have been used to stimulate red blood cell production and to
stimulate appetite. While they may stimulate appetite and increase lean muscle mass,
they have minimal effect in promoting red blood cell production and may induce
hepatopathy. In addition to anabolic steroids, other hormones may be supplemented
including erythropoietin (dogs and cats, initial dose of 100 IU/kg subcutaneously 3
times per week and adjust based on hematocrit)19 and darbepoetin, a longer-acting
form of erythropoietin (induction phase: 1.5 g/kg subcutaneously q 7 days and when
desired target hematocrit is reached the dosage is decreased to q 14 days; frequency
or amount of dosage is adjusted depending on response).7,97–99 Studies with
erythropoietin have shown that dogs and cats with CKD feel better even before
hematocrit is increased. The main limitation of erythropoietin administration is
development of antierythropoietin antibodies, which occurs in 20% to 70% of
patients.98,100 There have been no controlled studies with darbepoetin. Because of
antibody production, it has been recommended to begin erythropoietin therapy when
the hematocrit is less than 20% or in patients that do not feel well that are anemic but
not to that degree. Darbepoetin may be started at a lesser degree of anemia because
of the decreased risk of antibody production. Because uremic gastroenteritis is
common, iron should be supplemented to offset the iron deficiency associated with
blood loss (ferrous sulfate: dogs, 100 –300 mg po q 24 hours; cats, 50 –100 mg po q
24 hours; iron dextran: dogs, 10 –20 mg IM q 3– 4 weeks; cats, 50 mg intramuscularly
q 3– 4 weeks).19 Additionally, infections should be treated to minimize iron seques-
tration that may result in decreased effectiveness of erythropoietin and darbepoetin
administration. It is the author’s opinion that a hematocrit of 35% to 40% is the goal.
This is based on results of a study in cats with CKD where the median packed cell
volume in the group with progressive disease was 32% (interquartile range of
29%–36%) compared with the group with nonprogressive disease where the median
packed cell volume was 36% (interquartile range of 34%– 41%).101 Once the target is
reached, the dosage can be slowly decreased to find the lowest amount necessary to
control anemia. Complications of administration may include irritation at injection site,
systemic arterial hypertension, and polycythemia.97 In patients that initially respond
but in whom the hematocrit begins to decline, suspect antibody production against
the recombinant human erythropoietin. Additionally, ensure iron deficiency has not
occurred, which would result in decreased red blood cell production.
Systemic arterial hypertension. Systemic arterial hypertension has been reported to
occur in up to 65% to 75% of dogs and cats with CKD.102 It occurs, in part, because
of activation of the renin-angiotensin-aldosterone system, increased vasopressin
(antidiuretic hormone) levels, and increased sympathetic tone. Indirect determination
Chronic Kidney Disease in Dogs and Cats 685
of systemic arterial blood pressure is indicated in all patients diagnosed with CKD and
is used to substage CKD. Systemic arterial hypertension may promote progression of
CKD and proteinuria; result in left ventricular hypertrophy and possibly left-sided heart
failure; neurologic signs such as ischemic encephalopathy, seizures, and death; and
ocular disease such as retinal vascular tortuosity and hemorrhage, hyphema, and
blindness (Fig. 4). The risk is moderate to high with a systolic blood pressure greater
686 Bartges
S Serial Monitoring
Because CKD is dynamic and progressive, serial monitoring should be performed on
all patients with CKD in order to adjust treatment. Monitoring should include body
condition, BW, muscle condition, thoracic auscultation, assessment of hydration
status, indirect measurement of systemic arterial blood pressure, complete blood
Chronic Kidney Disease in Dogs and Cats 687
count, biochemical analysis, urinalysis, and possibly aerobic microbial culture of urine
collected by cystocentesis. Frequency and extent of monitoring depend on how
rapidly CKD is progressing, any nonrenal influences that may affect renal function,
and owner satisfaction and finances.
SUMMARY
Many strides have been made in diagnosing and treating dogs and cats with CKD
including dietary modification and pharmacologic therapy. Use of the International
688 Bartges
Renal Insufficiency Society staging system provides a basis for diagnosis and
management and for assessing response to treatment as well as comparison of
results of studies for application to patients.
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