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8 August 1999

CE Refereed Peer Review

Evaluation of Chronic
FOCAL POINT Renal Disease:
★ Determining the stage of chronic
renal disease (CRD) provides a
framework for managing affected
A Staged Approach
University of Georgia
Scott A. Brown, VMD, PhD
ABSTRACT: Chronic renal disease (CRD) generally is progressive and produces a sequence of
■ The use of a single therapeutic relatively identifiable stages. Stage I is characterized by the relative absence of clinical and lab-
approach in all animals with CRD oratory abnormalities. Stage II is identified by the presence of mild to moderate azotemia.
routinely leads to treatment Stage III is characterized by moderate to marked azotemia and the development of clinical
failure. signs attributable to uremic toxins. This article describes these stages of CRD and the appro-
priate therapy for each.
■ Therapy for CRD may be

palliative (symptomatic or hronic renal disease (CRD) is a leading cause of illness and death in pet
uremolytic), directed at the dogs and cats. The prevalence of renal disease in dogs has been estimated
primary renal disease (specific), at 0.5% to 1%.1,2 Cats, particularly older ones, are more commonly af-
or designed to protect the kidney fected than are dogs, and the prevalence of feline CRD may be increasing.3 Esti-
from damage (renoprotective). 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
■ CRD can be categorized as stage referral veterinary hospitals.4
I (renal disease), stage II (renal In affected animals, CRD is generally progressive, producing a sequence of
insufficiency), or stage III (renal clinical and laboratory findings. Traditionally, the terms renal disease, renal insuf-
failure). 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
■ Mechanisms for disease CRD routinely leads to treatment failure. The approach outlined in this article
progression, appropriate suggests a revision of this terminology as recommended by othersa and presents a
diagnostic testing, and clinically useful division of the various phases that occur during the course of
therapeutic goals vary CRD. Considering CRD in stages provides a framework for approaching the
dramatically among the management of patients at any time during the course of the disease. This article
stages of CRD. introduces this staged approach and focuses on the general approach to animals
with CRD.

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
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
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


Small Animal/Exotics 20TH ANNIVERSARY Compendium August 1999

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


Compendium August 1999 20TH ANNIVERSARY Small Animal/Exotics

Characteristics of Chronic Renal Disease Stages
Causes of Progression
(Declining GFR)
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

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

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

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


Small Animal/Exotics 20TH ANNIVERSARY Compendium August 1999

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

Inherent Stage II:

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


Compendium August 1999 20TH ANNIVERSARY Small Animal/Exotics

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

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
BUN = blood urea nitrogen; PO = orally; SC = subcutaneously.
Small Animal/Exotics 20TH ANNIVERSARY Compendium August 1999

Clinical Examples of the Stages of Chronic Renal Disease
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


Blood urea nitrogen 10–30 25 62 157


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


Compendium August 1999 20TH ANNIVERSARY Small Animal/Exotics

zyme inhibitors, as renoprotective agents in such a pa- vate veterinary practices in the United States. JAVMA 214:
tient (Table IV), regardless of the level of systemic 1336–1341, 1999.
2. MacDougall DF, Cook T, Steward AP, et al: Canine chronic
blood pressure. Whereas prerenal factors are also un-
renal disease: Prevalence and types of glomerulonephritis in
likely to be present in this phase of CRD, mineral and the dog. Kidney Int 29:1144–1151, 1986.
electrolyte imbalances (e.g., hypokalemia, metabolic 3. Lulich JP, Osborne CA, O’Brien TD, et al: Feline renal fail-
acidosis) should be identified and treated (Table IV). ure: Questions, answers, questions. Compend Contin Educ
Clinical signs attributable to uremic toxins are not ob- Pract Vet 14(2)127–151, 1992.
served, and uremolytic therapy (e.g., dietary protein re- 4. Polzin DJ, Osborne CA: Update—Conservative medical
striction) is not indicated. This patient should have management of chronic renal failure, in Kirk RW (ed): Cur-
rent Veterinary Therapy IX. Philadelphia, WB Saunders Co,
evaluations scheduled every 3 to 6 months regardless of 1986, pp 1167–1173.
the clinical course. The emergence of any new or unsta- 5. Brenner BM, Meyer TW, Hostetter TH: The role of hemo-
ble clinical problems would mandate more frequent dynamically mediated glomerular injury in the pathogenesis
evaluations. of progressive glomerular sclerosis in aging, renal ablation,
Patient 3 has progressed to stage III CRD. Because and intrinsic renal disease. N Engl J Med 307:652–659,
the PRD is unknown, specific therapy is not possible. 6. Brown SA, Finco DR, Crowell WA, et al: Single-nephron
In this advanced stage of CRD, renoprotective therapy adaptations to partial renal ablation in the dog. Am J Physiol
should be considered but is now less important than 258:F495–F503, 1990.
managing uremia (Tables I and IV). Thus renoprotec- 7. Brown SA, Crowell WA, Barsanti JA, et al: Beneficial effects
tive therapy, such as dietary phosphorus restriction, of dietary mineral restriction in dogs with marked reduction
of functional renal mass. J Am Soc Nephrol 1:1169–1179,
should be instituted gradually and maintained only if 1991.
there is no adverse effect on clinical status, food intake, 8. Brown SA, Walton CA, Crawford P, et al: Long-term effects
or azotemia. Clinical signs attributable to uremic toxins of antihypertensive regimens on renal hemodynamics and
and prerenal factors are likely to be present in this proteinuria. Kidney Int 43:1210–1218, 1993.
phase of CRD, producing an erratic course of uremic 9. Brown SA, Brown CA: Single-nephron adaptations to partial
renal ablation in cats. Am J Physiol 269:R1002–R1008,
crises followed by transient responses to symptomatic 1995.
therapy. Uremolytic therapy, such as dietary protein re- 10. Brown SA, Crowell WA, Brown CA, et al: Pathophysiology
striction, judicious use of antiemetics, or erythropoietin and management of progressive renal disease. Br Vet J
(Table IV), should be considered. 154:93–109, 1997.
Efforts to minimize prerenal factors become the focus 11. Finco DR, Brown SA, Crowell WA, et al: Effects of dietary
phosphorus and protein in dogs with chronic renal failure.
of veterinary care in this patient; thus, maintaining Am J Vet Res 53:2264–2271, 1992.
careful records of body weight and instituting efforts to 12. Gaber L, Walton C, Brown S, et al: Effects of antihyperten-
sustain adequate food intake (e.g., warming food, pro- sive agents on the morphologic progression of diabetic
viding different products or formulations, frequently nephropathy in dogs. Kidney Int 46:161–169, 1994.
offering fresh food, and administering pharmacologic 13. Brown SA, Brown CA, Crowell WA, et al: Beneficial effects
of chronic administration of dietary omega-3 polyunsaturat-
appetite-enhancing agents) become critical in this stage. ed fatty acids in dogs with renal insufficiency. J Lab Clin
This patient should have evaluations scheduled at least Med 131:447–455, 1998.
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. About the Author
Dr. Brown is a professor in the Department of Physiology
REFERENCES and Pharmacology, College of Veterinary Medicine, Uni-
1. Lund EM, Armstrong JP, Kirk CA, et al: Health status and versity of Georgia, Athens, Georgia.
population characteristics of dogs and cats examined at pri-