V 20TH ANNIVERSARY
8 August 1999
CE Refereed Peer Review
FOCAL POINT
★ Determining the stage of chronic
renal disease (CRD) provides a
framework for managing affected
patients.
KEY FACTS
■ The use of a single therapeutic
approach in all animals with CRD
routinely leads to treatment
failure.
■ Therapy for CRD may be
palliative (symptomatic or
uremolytic), directed at the
primary renal disease (specific),
or designed to protect the kidney
from damage (renoprotective).
■ CRD can be categorized as stage
I (renal disease), stage II (renal
insufficiency), or stage III (renal
failure).
■ Mechanisms for disease
progression, appropriate
diagnostic testing, and
therapeutic goals vary
dramatically among the
stages of CRD.
Vol. 21, No.
Evaluation of Chronic
Renal Disease:
A Staged Approach
University of Georgia
Scott A. Brown, VMD, PhD
ABSTRACT: Chronic renal disease (CRD) generally is progressive and produces a sequence of
relatively identifiable stages. Stage I is characterized by the relative absence of clinical and lab-
oratory abnormalities. Stage II is identified by the presence of mild to moderate azotemia.
Stage III is characterized by moderate to marked azotemia and the development of clinical
signs attributable to uremic toxins. This article describes these stages of CRD and the appro-
priate therapy for each.
C
hronic renal disease (CRD) is a leading cause of illness and death in pet
dogs and cats. The prevalence of renal disease in dogs has been estimated
at 0.5% to 1%.1,2 Cats, particularly older ones, are more commonly af-
fected than are dogs, and the prevalence of feline CRD may be increasing.3 Esti-
mates of the prevalence vary from approximately 1.6%3 to 1.9%1 of cats present-
ed to U.S. veterinary clinics to 10% to 30% of elderly animals presented to
referral veterinary hospitals.4
In affected animals, CRD is generally progressive, producing a sequence of
clinical and laboratory findings. Traditionally, the terms renal disease, renal insuf-
ficiency, and renal failure have been used interchangeably to describe this disease
process. However, the use of a single therapeutic approach in all animals with
CRD routinely leads to treatment failure. The approach outlined in this article
suggests a revision of this terminology as recommended by othersa and presents a
clinically useful division of the various phases that occur during the course of
CRD. Considering CRD in stages provides a framework for approaching the
management of patients at any time during the course of the disease. This article
introduces this staged approach and focuses on the general approach to animals
with CRD.
DEFINITION OF TERMS
Primary renal disease (PRD) is caused by any factor or process that elicits renal
damage. A number of common disease processes, including inflammatory (e.g.,
glomerulonephritis or bacterial infection), metabolic (e.g., hypercalcemic
nephropathy), hereditary (e.g., hereditary nephritis), hemodynamic (e.g., hyper-
tensive nephropathy), and neoplastic (e.g., renal lymphosarcoma), may be
a
Personal Communication: Watanabe T, Azabu University, Kanagawa, Japan, 1998.
Compendium August 1999 20TH ANNIVERSARY Small Animal/Exotics

causative. Diagnosing the

PRD generally requires uri- Primary Renal Mechanisms of Inherent Progression
nalysis, serum biochemistry Disease —Glomerular hypertension and hypertrophy
profile, and/or renal imag- —Derangements of homeostasis
ing studies. Accurate charac-
terization of renal disease Prerenal Progressive Renal Injury
may depend on histologic
Factors
evaluation of renal tissue,
which is often more reliable
Progression of Renal Disease
early in the course of the
disease. (declining GFR)
Making a distinction be- Figure 1—Progression of chronic renal disease or progressively declining glomerular filtration
tween acute renal disease rate (GFR) is reflected clinically as rising serum creatinine and blood urea nitrogen concentra-
and CRD is based on the tions. The primary renal disease and inherent mechanisms of progression combine to cause in-
time course of the disease jury to the kidney leading to progressive decrements in GFR. In the latter stages of chronic re-
process. Acute renal disease nal disease, superimposed prerenal factors (e.g., dehydration, systemic hypotension) further
is marked by a sudden on- contribute to observed decrements in GFR.
set, and the diagnosis is gen-
erally established within a
few days of the insult. Nephrotoxicity is a common pressure and glomerular size, referred to as glomerular
cause of acute renal disease in dogs and cats. CRD is hypertension and glomerular hypertrophy, respectively.
presumed to be present whenever the time course of re- According to proponents of this theory, these maladap-
nal disease exceeds 2 weeks. In most cases of CRD, tations cause local hypertension and disordered in-
however, careful historical evaluation demonstrates a trarenal growth, which in turn contribute to a self-per-
much more protracted clinical course. Classically, CRD petuating cycle of renal damage.5,6 The other proposed
is characterized by nonregenerative anemia, a long-term cause of inherent progression, termed derangements of
history of polyuria and polydipsia, weight loss, palpably homeostasis, includes some of the secondary changes
small or irregularly surfaced kidneys, and poor haircoat (e.g., systemic hypertension, mineral imbalances) ob-
and body condition. In contrast, animals with acute re- served in animals with renal failure. Although un-
nal disease often exhibit normal or elevated hematocrit proven, some evidence supports a role for both of these
values; although they may have evidence of recent ex- processes in inherent renal injury in dogs and/or cats.5–13
posure to a nephrotoxin, there is generally no other his- In addition, prerenal factors, such as dehydration, can
torical evidence of preexisting renal disease or its mani- lead to marked reductions in GFR, particularly when
festations. superimposed on CRD. Consequently, to prevent on-
Progression of CRD refers to sequential decrements going damage to the kidney, veterinarians must attempt
in renal function, generally reflected as declining to minimize the effects of three types of factors: PRD,
glomerular filtration rate (GFR) leading to end-stage re- inherent progression factors (e.g., renal maladapta-
nal failure.5 Decrements in GFR may be caused by renal tions and derangements of homeostasis), and prerenal
injury or the superimposition of prerenal factors on factors.
CRD (Figure 1). Renal injury has two general causes: Azotemia is the accumulation of nitrogenous wastes
the PRD and inherent progression. The first and most in the bloodstream. Renal azotemia occurs as a result of
obvious cause of progressive renal injury is the PRD it- decrements in GFR from destruction of renal tissue.
self. If not properly treated, the primary disease contin- Azotemia is identified clinically by measurement of the
ues to destroy nephrons, leading to progressive decre- nontoxic nitrogenous compounds serum creatinine
ments in GFR. The kidney is intriguing in that the (SCr) and blood urea nitrogen (BUN). Because the
consequences of CRD often activate mechanisms that normal ranges for SCr and BUN are broad, generally
cause further renal injury. Inherent or spontaneous pro- more than 75% of nephrons are destroyed before clini-
gression refers to renal damage that occurs by these cally detectable azotemia occurs.
mechanisms, which are often independent of the PRD. Uremic syndrome (or uremia) is the constellation of
Two proposed mechanisms contribute to inherent clinical signs observed in animals with severe reductions
progression in dogs and cats (Figure 1). First, the renal in GFR. Common clinical manifestations of uremia in-
compensatory response to a decrease in GFR may lead clude lethargy, depression, inappetence, and vomiting.
to maladaptive increases in glomerular intracapillary The uremic syndrome is generally not manifest until

INHERENT PROGRESSION ■ DERANGEMENTS OF HOMEOSTASIS ■ AZOTEMIA ■ UREMIC SYNDROME

Small Animal/Exotics 20TH ANNIVERSARY Compendium August 1999

TABLE I
Therapeutic Strategies Employed in Chronic Renal Disease
Type of Therapy Purpose
Specific Control or eliminate primary renal
disease
Disease-associated symptomatic Ameliorate clinical manifestations
specifically associated with the
primary renal disease
Renoprotective Delay or stop mechanisms causing
inherent progression of chronic renal
disease
Uremolytic symptomatic Ameliorate clinical manifestations
caused by uremic toxins
Examples
Antibiotics for renal infection; control
of plasma Ca++ for hypercalcemic
nephropathy; chemotherapy for renal
neoplasia
Diuretics for edematous animals with
glomerulonephritis; antihypertensive
therapy for systemic hypertension;
treatment of mineral, electrolyte, and
acid–base imbalances
Dietary phosphorus restriction;
dietary omega-3 polyunsaturated fatty
acid supplementation; angiotensin-
converting enzyme inhibition
Dietary phosphorus restriction;
dietary protein restriction; treatment
of mineral, electrolyte, and acid–base
imbalances; encouragement of food
intake; antiemetics; erythropoietin;
intermittent parenteral fluid
administration; intermittent
or chronic dialysis

BUN exceeds 80 mg/dl and/or SCr exceeds 4.0 mg/dl.
Because clinical abnormalities have a variety of causes
(some of which are present only at certain phases of
CRD), the therapeutic approach varies as the disease
progresses. In this article, specific therapy (Table I) is
defined as therapy aimed at the PRD, such as antibiotic
therapy for renal infection or chemotherapy for renal
neoplasia.
Symptomatic therapy refers to treatment directed at
ameliorating a clinical abnormality in a patient with
CRD (Table I). Clinical abnormalities seen in animals
with CRD may be disease associated, such as systemic
hypertension in a dog with renal vascular disease,
nephrotic syndrome in a cat with glomerulonephritis
and marked proteinuria, or metabolic acidosis in a dog
with Fanconi’s syndrome. These clinical manifestations
are caused by the specific renal disease but are not sole-
ly attributable to severe decrements in GFR. In con-
trast, the manifestations of uremia (e.g., vomiting in a
dog with markedly elevated BUN) are nonspecifically
attributable to loss of renal function (i.e., severe de-
crease in GFR) due to destruction of renal tissue by any
cause.
Disease-associated symptomatic therapy is directed at
ameliorating the specific manifestations of the PRD
(e.g., administration of a diuretic in an edematous,
nephrotic cat; alkali therapy in a dog with Fanconi’s
syndrome). Uremolytic therapy refers to symptomatic
treatment directed at ameliorating the manifestations of
the uremic syndrome (e.g., administration of antiemet-
ics in a uremic dog). Examples of therapy designed to
limit the extent of clinical abnormalities from uremia
include dietary phosphorus and/or protein restriction,
antihypertensive therapy, administration of recombi-
nant erythropoietin, and dietary supplementation with
fiber.
Systemic hypertension refers to elevated hydrostatic
pressure within systemic arteries and is commonly pre-
sent in animals with CRD. Antihypertensive therapy is
symptomatic therapy to lower blood pressure in dogs or
cats with CRD and systemic hypertension. Vasodila-
tors, such as angiotensin-converting enzyme inhibitors
or calcium-channel antagonists, are commonly used as
antihypertensive agents in patients with CRD.
Renoprotective therapy is directed at preventing in-
herent progression (Table I). Examples of therapy that
might be employed to limit inherent progression in-
clude dietary phosphorus restriction,7,11 antihyperten-
sive therapy,8,12 and dietary supplementation with omega-3
polyunsaturated fatty acids.13

SPECIFIC THERAPY ■ SYMPTOMATIC THERAPY ■ UREMOLYTIC THERAPY ■ RENOPROTECTIVE THERAPY

Compendium August 1999 20TH ANNIVERSARY Small Animal/Exotics

TABLE II
Characteristics of Chronic Renal Disease Stages
Causes of Progression
(Declining GFR)
Primary
Usual Method Renal Inherent Prerenal
Stage Azotemia Clinical Signs of Diagnosis Treatment Disease Progression Factors
Stage I: renal No Usually absent Urinalysis; Specific therapy + – –
disease renal imaging; for primary
renal biopsy; renal disease;
measurement symptomatic
of GFR therapy for
disease-associated
conditions

Stage II: renal Yes: SCr = Frequently Azotemia of Specific therapy + + –

insufficiency 2.4–4.0; absent renal origin for primary renal
BUN = disease; symptomatic
25–80 therapy for disease-
associated conditions;
renoprotective therapy

Stage III: Yes: SCr Initially Uremia of Specific therapy for + + +

renal failure >4.0; intermittent renal origin primary renal disease;
BUN >80 symptomatic therapy
for disease-associated
conditions; renoprotective
therapy; uremolytic
therapy

BUN = blood urea nitrogen (mg/dl); GFR = glomerular filtration rate; SCr = serum creatinine (mg/dl); + = present; – = absent.

STAGES OF CHRONIC RENAL DISEASE
Stages of CRD are defined here as phases in the pro-
gression of renal disease. Although not distinct in every
case, these stages can be identified in most patients. A
thorough understanding of the differences among these
stages is necessary for veterinarians to make appropriate
diagnostic and therapeutic choices.
Renal Disease
Stage I CRD, or renal disease, is the initial stage
wherein renal tissue is being damaged by the PRD (Fig-
ure 1) but compensatory processes generally mask the
injury and minimize clinical and laboratory signs. Al-
though azotemia is absent (Table II), animals begin to
lose renal concentrating ability late in stage I CRD; this
is manifest as polyuria and polydipsia. Diagnostic tests,
such as urinalysis, renal imaging, renal biopsy, and/or
measurement of GFR, are usually required to detect the
presence of a renal disease in this stage. However, be-
cause there are frequently no clinical signs in patients
during stage I CRD, these specialized tests frequently
are not conducted and the disease is unrecognized for
months or even years. In fact, it is unusual to recognize
CRD in this early stage. The use of routine biochemi-
cal panels and urinalyses in patients with an increased
prevalence of CRD, such as dogs and cats older than 10
years of age, enhances the likelihood of identifying pa-
tients at this stage.
If CRD is identified in stage I, the main goals of diag-
nostic testing are to identify the primary cause of the renal
injury and the disease-associated manifestations thereof
(e.g., systemic hypertension [by measuring blood pressure]
or the nephrotic syndrome [by measuring urine
protein:creatinine ratio and serum albumin concentra-
tion]). In stage I disease, inherent progression of CRD and
prerenal factors are generally presumed to be absent (Table
II), and these causes of sequential decrements in GFR are
not a focus of patient management. Because the therapeu-
tic approach varies among the stages of CRD (Table II),
specific therapy directed at control or eradication of the
PRD (if it can be identified) should be instituted in stage
I. Clinical signs attributable to the specific PRD may be

STAGE I CRD ■ POLYURIA ■ POLYDIPSIA ■ ROUTINE BIOCHEMICAL PANELS

Small Animal/Exotics 20TH ANNIVERSARY Compendium August 1999

TABLE III
Guidelines for Diagnostic Evaluation of Patients with Chronic Renal Diseasea
Test/Evaluation Stage I (Renal Disease) Stage II (Renal Insufficiency) Stage III (Renal Failure)
Historical evaluation and 6 3–6 1–3
physical examination
(including body weight)

Serum creatinine and 6 3–6 1–3

blood urea nitrogen

Biochemical panel 6 3–6 1–3

Urinalysis 6 3–6 1–3

Urine culture 6 6 3–6

Blood pressure and retinal examination 6 6 3–6

aThese guidelines represent the minimal evaluation intervals (in months) in stable patients. Where ranges are provided, patients late in
that stage or with changing clinical status, unstable problems, or new clinical signs require more frequent evaluations.

present in some patients in this stage of CRD; disease-as-
sociated symptomatic therapy should be based on labora-
tory and clinical findings in each individual patient. Al-
though few or no clinical abnormalities are present in
stage I, routine patient evaluations should be directed at
early identification of abnormalities (Table III).
Renal Insufficiency
Stage II CRD, or renal insufficiency, occurs as a suffi-
clinical signs attributable to uremic toxins accompany
the azotemia. Patients can be classified as having stage
III CRD only if clinical signs attributable to uremic
toxins are present, which generally occurs when SCr ex-
ceeds 4 mg/dl and/or BUN exceeds 80 mg/dl (Table II).
Routine patient evaluation is required more frequently
in this stage and should be directed at early identifica-
Normal

cient loss of nephrons leads to renal azotemia without Primary Disease Stage I:
clinical signs attributable to uremia (Table II). The level Renal Disease
of azotemia is mild to moderate (SCr below 4 mg/dl,
BUN below 80 mg/dl). In general, both primary dis-
GFR

Inherent Stage II:

ease and inherent mechanisms of progression are pre-
sumed to be operating in this stage. If the PRD can be
identified, appropriate specific therapy should be insti-
tuted. Symptomatic therapy for systemic hypertension
and/or other disease-associated clinical manifestations
of the PRD should be maintained.
Even if the PRD has resolved or is effectively treated,
progression of CRD still occurs because of inherent pro-
gression (Figure 2). In stage II CRD, inherent mecha-
nisms of progression should be considered and appro-
priate therapy employed (Table I). Although clinical and
laboratory abnormalities observed in stage II are often
limited to polyuria and/or polydipsia, routine evalua-
tions (Table III) are essential to identify and manage
mineral, electrolyte, and acid–base abnormalities.
Renal Failure
Stage III CRD, or renal failure, is the phase in which
Progression Renal Insufficiency
Stage III:
Prerenal Factors Renal Failure
Time
Figure 2—In chronic renal disease (CRD), different factors
lead to progressive declines in glomerular filtration rate
(GFR) in each stage of the disease process. In stage I CRD
(renal disease), the primary renal disease is responsible for se-
quential losses in GFR. Stage II (renal insufficiency) develops
when azotemia is present; during this stage, inherent mecha-
nisms of renal injury, such as glomerular hypertension and
hypertrophy, are believed to contribute to spontaneous
decrements in GFR. In stage III CRD (renal failure), clinical
signs attributable to uremic toxins develop and associated
prerenal factors (e.g., dehydration) lead to an erratic pattern
of change in GFR.

DIAGNOSTIC GUIDELINES ■ STAGE II CRD ■ STAGE III CRD ■ UREMIC TOXINS

Compendium August 1999 20TH ANNIVERSARY Small Animal/Exotics

TABLE IV
Specific Therapeutic Recommendations in Chronic Renal Disease
Therapy Stage of Disease Type of Therapy Details
Antibiotic therapy I, II, III Specific Based on results of urine culture and sensitivity testing;
avoid nephrotoxic antibiotics; increase interdose intervala

Antihypertensive I, II, III Disease-associated Administer benazepril or enalapril (0.5 mg/kg PO every
therapy symptomatic; 12–24 hr) and/or amlodipine besylate (0.10–0.25 mg/kg
renoprotective PO every 24 hr) if systolic blood pressure >180 mm Hg or
if hypertensive retinopathy (hyphema, retinal hemorrhage,
retinal detachment) is present; discontinue if azotemia
worsens during therapy

Alkali therapy II, III Disease-associated Administer sodium bicarbonate (8–15 mg/kg PO every
symptomatic; 8–12 hr) or potassium citrate (10–30 mg/kg PO every
uremolytic 8–12 hr); adjust dosage to sustain plasma bicarbonate or
total carbon dioxide concentration within the normal range

Potassium II, III Disease-associated Administer potassium citrate or potassium gluconate (PO
supplementation symptomatic; or in food) to sustain plasma potassium concentration in
uremolytic the mid-normal range

Dietary phosphorus II, III Renoprotective <0.4% (dogs) or <0.6% (cats) phosphate on a dry-weight
restriction basis; add an intestinal phosphate binding agent (e.g.,
aluminum hydroxide; 30–60 mg/kg/day with food) if
animal remains hyperphosphatemic after 4 wk of dietary
restriction

Dietary protein III Uremolytic Goal is to maintain BUN ≤80 mg/dl; more severe renal
restriction dysfunction requires greater protein restriction

Antiemetics III Uremolytic Histamine-blocking agents (e.g., famotidine; 0.5 mg/kg

PO every 12–24 hr) for vomiting and/or inappetence
(presumptive diagnosis of uremic gastritis); consider adding
a central-acting antiemetic (0.2–0.4 mg metoclopramide
orally or SC every 6–8 hr) if antihistaminics are ineffective
or if is vomiting protracted

Erythropoietin III Uremolytic Use only when hematocrit <18% and clinical signs of
weakness, inactivity, or lack or sociability are present;
administer to effect (initial dose of 25–100 U/kg SC 1–3
times/wk) to sustain hematocrit of 30%–35%; iron
supplementation (ferrous sulfate; 5–20 mg/kg/day PO)
frequently required to support regenerative response; avoid
overtreatment, which induces polycythemia; development
of antierythropoietin antibodies is common when human
recombinant product is used

Subcutaneous fluids III Uremolytic Balanced electrolyte solution (e.g., lactated Ringer’s;
30–50 ml/kg SC every 1–3 days) to combat intermittent
inappetence and/or dehydration
aNew interval = Usual recommended interval × (Patient’s plasma creatinine concentration ÷ High-normal value for plasma creatinine
concentration).
BUN = blood urea nitrogen; PO = orally; SC = subcutaneously.
Small Animal/Exotics 20TH ANNIVERSARY Compendium August 1999

TABLE V
Clinical Examples of the Stages of Chronic Renal Disease
Normal
Parameter Findings Patient 1 Patient 2 Patient 3
Stage — Stage I (renal disease) Stage II (renal insufficiency) Stage III (renal failure)

Signalment Any 4-year-old male dog 10-year-old female dog 7-year-old female dog

Primary renal disease None Glomerular amyloidosis Unknown Unknown

Serum creatinine 0.5–1.5 1.2 3.1 5.8

(mg/kg)

Blood urea nitrogen 10–30 25 62 157

(mg/kg)

Clinical signs None None Polyuria Lethargy; inappetence;

occasional vomiting

Other laboratory Variable None Serum phosphate = 6.1 mg/dl Hematocrit = 22%;
abnormalities (normal, 3.0–5.2 mg/d) serum phosphate = 9.1
mg/dl; serum bicarbon-
ate = 9 mmol/L

tion of abnormalities (Table III). Although frequently
still present, the PRD is often unidentifiable at this
stage of CRD, even with renal biopsies. Even if the
PRD has resolved or is effectively treated, progression
of CRD nevertheless occurs because of inherent pro-
gression.
In addition to inherent progression, prerenal factors
(e.g., intermittent anorexia and/or vomiting) produce a
characteristically erratic course often seen as recurrent
cycles of improvement and decline in clinical condition
(Figure 2). Consequently, uremolytic therapy to mini-
mize these gyrations and improve the clinical status of
such animals plays a central role in this stage; efforts to
reduce the extent of uremia should be the focus of
managing patients with stage III CRD. Therapy to
slow inherent progression and symptomatic therapy for
systemic hypertension and/or other disease-associated
clinical manifestations of the PRD should also be used
in this stage (Table II).
APPLIED EXAMPLES
Applying this staged approach to clinical patients re-
quires classification of the disease stage in each patient.
The following discussion provides examples of specific
veterinary therapy (Table IV) for three patients with
CRD (Table V). Although all of these patients have
CRD, the appropriate diagnostic and therapeutic ap-
proaches vary.
Patient 1 is in stage I CRD, thus neither clinical signs
of uremic syndrome nor azotemia is present. Because
the cause of the PRD (glomerular amyloid deposition)
is known, specific therapy directed at this disease pro-
cess could be instituted. However, the effects associated
with amyloid therapy (e.g., dimethylsulfoxide, col-
chicine) are incompletely characterized in dogs, and
thus such therapy was not instituted in this patient.
Renoprotective therapy (e.g., dietary modification) is
not indicated at this stage. Prerenal factors are also un-
likely to be present in this phase of CRD. If urine cul-
ture and sensitivity reveal a urinary tract infection, ap-
propriate antibiotic therapy should be instituted (Table
IV). Similarly, systemic hypertension should be treated
only if systolic blood pressure is known to exceed 180
mm Hg.
The patient should be evaluated at least every 6
months and more frequently if there is evidence that
disease-associated clinical manifestations, such as
nephrotic syndrome (i.e., hypoalbuminemia or edema)
or hypercoagulability (i.e., hypoalbuminemia and/or
reduced circulating levels of antithrombin III), are de-
veloping. For the latter, low-dose aspirin therapy could
be used prophylactically.
Patient 2 is in stage II CRD. Because the PRD is un-
known, specific therapy is not possible. In this phase,
renoprotective therapy, such as dietary phosphorus re-
striction, should be considered (Tables I and IV). Some
veterinarians would recommend the routine use of anti-
hypertensive agents, such as angiotensin-converting en-

PRERENAL FACTORS ■ SYSTEMIC HYPERTENSION ■ DIETARY PHOSPHORUS RESTRICTION

Compendium August 1999 20TH ANNIVERSARY
zyme inhibitors, as renoprotective agents in such a pa-
tient (Table IV), regardless of the level of systemic
blood pressure. Whereas prerenal factors are also un-
likely to be present in this phase of CRD, mineral and
electrolyte imbalances (e.g., hypokalemia, metabolic
acidosis) should be identified and treated (Table IV).
Clinical signs attributable to uremic toxins are not ob-
served, and uremolytic therapy (e.g., dietary protein re-
striction) is not indicated. This patient should have
evaluations scheduled every 3 to 6 months regardless of
the clinical course. The emergence of any new or unsta-
ble clinical problems would mandate more frequent
evaluations.
Patient 3 has progressed to stage III CRD. Because
the PRD is unknown, specific therapy is not possible.
In this advanced stage of CRD, renoprotective therapy
should be considered but is now less important than
managing uremia (Tables I and IV). Thus renoprotec-
tive therapy, such as dietary phosphorus restriction,
should be instituted gradually and maintained only if
there is no adverse effect on clinical status, food intake,
or azotemia. Clinical signs attributable to uremic toxins
and prerenal factors are likely to be present in this
phase of CRD, producing an erratic course of uremic
crises followed by transient responses to symptomatic
therapy. Uremolytic therapy, such as dietary protein re-
striction, judicious use of antiemetics, or erythropoietin
(Table IV), should be considered.
Efforts to minimize prerenal factors become the focus
of veterinary care in this patient; thus, maintaining
careful records of body weight and instituting efforts to
sustain adequate food intake (e.g., warming food, pro-
viding different products or formulations, frequently
offering fresh food, and administering pharmacologic
appetite-enhancing agents) become critical in this stage.
This patient should have evaluations scheduled at least
every 1 to 3 months regardless of the clinical course.
The emergence of any new or unstable clinical prob-
lems would mandate more frequent evaluations.
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About the Author
Dr. Brown is a professor in the Department of Physiology
and Pharmacology, College of Veterinary Medicine, Uni-
versity of Georgia, Athens, Georgia.