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Renal DiseaseCase Studies
IDEXX Laboratories
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Authors
Dennis DeNicola, DVM, PhD, DACVPChief Veterinary Educator, Clinical
Pathologist, IDEXX LaboratoriesDr. DeNicola completed his DVM in 1978 and his PhD in1981, both at Purdue University. For more than twenty
years, he served as educator in clinical and surgicalpathology. In addition, he directed the primary cytol-ogy and surgical pathology service at the veterinary
school laboratory and ran a private pathology servicefor 15 years. A speaker at more than 100 national and
international education symposia, Dr. DeNicola also hasauthored or co-authored more than 150 publications in
various aspects of veterinary clinical pathology.
Fred Metzger, DVM, DABVPOwner, Metzger Animal HospitalDr. Metzger is a 1986 graduate of the Purdue Schoolof Veterinary Medicine and a diplomate of the American
Board of Veterinary Practitioners, with specialties incanine and feline medicine. He is an adjunct
professor at Pennsylvania State University and serveson the practitioner advisory boards of Veterinary
Economics and Veterinary Medicine magazines. Herecently co-authored Guide to Hematology in Dogs and
Cats with Dr. Alan Rebar. Dr. Metzger owns the Metzger
Animal Hospital, a four-doctor practice in StateCollege, Pennsylvania, that received the 1998 Veterinary
Economics/Pfizer Practice of Excellence award.
Pete Fernandes, DVM, DACVPClinical Pathologist, IDEXX LaboratoriesDr. Fernandes completed his DVM at the University ofWisconsin-Madison, followed by an internship in small-
animal medicine and surgery at South Shore AnimalHospital in Boston. Dr. Fernandes residency was in
clinical pathology at Texas A&M University and theUniversity of Florida. He is a diplomate of the American
College of Veterinary Pathologists.
Brian Poteet, DVM, DAVCR, DABSNMDirector, Gulf Coast Veterinary Diagnostic
ImagingDr. Poteet received his DVM from Texas A&M University
and completed his radiology residency at the Universityof Tennessee. In addition to being board-certified
with the American College of Veterinary Radiology,Dr. Poteet is also a member of the American Board of
Science in Nuclear Medicine. Dr. Poteet is a member
of several local and national veterinary medicalassociations, Vice President of the Veterinary Cancer
Associates, and holds two adjunct faculty positions atTexas A&M University.
Richard Goldstein, DVM, DACVIM,DECVIM-CAAssistant Professor, Small-Animal Medicine,
Cornell UniversityDr. Goldstein received his DVM from the Koret School
of Veterinary Medicine, the Hebrew University ofJerusalem, Israel. He completed his residency in small-animal internal medicine at the University of California,
Davis. He is a diplomate of the American College ofVeterinary Internal Medicine and the European College
of Veterinary Internal MedicineCompanion Animals.He joined the faculty at Cornell in 2001. Dr. Goldsteins
clinical and research interests include nephrology and
leptospirosis and Lyme nephritus in dogs.
Roberta Relford, DVM, MS, PhD, DACVIM,DACVP
Divisional Vice President of Worldwide
PathologyCoagulation, Cytology, Internal
Medicine, IDEXX LaboratoriesDr. Relford received her DVM from Auburn University
in 1982 and worked as a small-animal practitioner forfour years before pursuing her advanced training. She
started her residency training in clinical pathology andobtained an MS in pathology from Mississippi State
University. She then transferred to Texas A&M, whereshe completed her pathology residency training and
obtained a PhD in pathology. While completing her
PhD, Dr. Relford pursued a residency in small-animalinternal medicine.
Dr. Relford is board-certified in internal medicine by theAmerican College of Veterinary Internal Medicine and inclinical pathology by the American College of Veterinary
Pathologists. She currently serves as Divisional VicePresident of Worldwide Pathology for IDEXX Reference
Laboratories. Dr. Relford has given numerous lectureson a wide variety of topics including clinical pathology,
internal medicine, infectious diseases, cytology, platelet
disorders, health maintenance programs and zoonoticdiseases.
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Case Study 1
Patient
Three-year-old intact male Labrador retriev
Presenting Complaints
Rear leg lameness
History
Traveling hunting dog with recent trips to
Texas and New Mexico four months ago
Physical Exam
Dehydration (~10%), fever, edema, genera
peripheral lymphadenopathy, uveitis, bilate
swollen hocks and right stifle
Jake Douglas
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HematologyHct = 32.2 % LOW 37 55
Hgb = 10.1 g/dL LOW 12.0 18.0
RBC = 4.9 L LOW 5.50 8.50
MCV = 63.5 fL 60.0 77.0MCH = 21.33 pg 19.50 24.50
MCHC = 33.2 g/dl 32.0 37.0
RDW = 17.3 % HIGH 12.0 16.0
% RETIC = 0.6 %
RETIC = 40,000 L
WBC = 18,237 L HIGH 5,500 16,950
NEU = 14,200 L HIGH 2,000 12,000
LYM = 900 L LOW 1000 4,900
MONO = 2,900 L HIGH 100 1,400
EOSIN = 223 L 100 1,490
BASO = 14 L 0 100
PLT = 360 K/L 175 500
Biochemical profileAlk Phos = 899 U/L HIGH 23 212
ALT (SGPT) = 201 U/L HIGH 10 100
Albumin = 1.6 g/dL LOW 2.2 3.9
Total Protein = 8.1 g/dL 5.2 8.2
Globulin = 6.5 g/dL HIGH 2.8 4.5
Total Bilirubin = 0.2 mg/dL 0.0 0.4
BUN = 37 mg/dL HIGH 7 27
Creatinine = 2.2 mg/dL HIGH 0.5 1.8
Glucose = 99 mg/dL 77 125
Calcium = 10.3 mg/dL 7.9 12.0
Phosphorus = 9.0 mg/dL HIGH 2.5 6.8
Sodium = 150 mEq/L 144 160
Potassium = 5.1 mEq/L 3.5 5.8
Chloride = 111 mEq/L 109 12
Complete Urinalysis: CystocentesisDipstick Tests Urine Sediment Examination
Color Yellow WBCs/hpf 0
Transparency Clear RBCs/hpf 0
Specific Gravity 1.013 Epithelial cells/hpf 0
Protein 3+ Casts/hpf 5 to 7, granular
Glucose Negative Crystals 0
Bilirubin Trace Bacteria 0
Blood Negative
pH 6.5 UPC Ratio 5.1
Case Study 1
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Cytology Arthrocentesis (hock and stifle):
suppurative inflammatory joint fluid
Lymph node FNA (inguinal & popliteal):
lymphoid hyperplasia, consistent with reactive lymph nodes
SerologyLeptospirosis negative
SNAP 3Dx Test Heartworm antigen negative
E. canis antibody negative
Lyme C6 antibody positiveRocky Mountain spotted fever negative
Case Study 1
Lyme-positive SNAP 3Dx Te
Cytology: fine-needle aspirate Renal biopsy 10x
Renal biopsy 60x
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DiagnosisThe clinical diagnosis is Lyme
nephritis.
Treatment/Plan
Blood was sent to a reference
laboratory for quantitative C6
antibody testing.
The patient was treated with
doxycycline, intravenous fluid
support and a renal diet.
Recheck renal panel in 35 days.
Renal biopsy
Prevention
Prevention of Lyme disease includes
reducing tick exposure, utilizing tick
repellant products and vaccinating
at-risk patients.
Zoonotic Potential
Since pets share our environment,
they may incidentally become our
sentinels; therefore, borreliosis inour canine companions should be a
warning to increase vigilance and
re-evaluate tick-prevention protocols.
Lyme disease is not transmissible
directly from the canine patient to the
owner. However, the owners should
be educated that they are living in a
tick-endemic area and the ticks may
be infected with Lyme disease.
Interpretive Summary
Hematology
There is mild nonregenerative anemia. The most common cause of
mild nonregenerative anemia is anemia of chronic disease. The modest
leukocytosis composed of mature neutrophilia and monocytosis with
concurrent lymphopenia is consistent with an established inflammatory
condition. The thrombon/platelets are within normal limits
Biochemical profile
Hypoalbuminemia and azotemia with an elevated UPC and the presence of
granular casts support renal disease. The positive Lyme serology along with
the hyperglobulinemia suggests Lyme nephritis. The specific gravity 1.013
indicates some, yet inadequate, concentrating ability, and hypoalbuminemia
may be masked somewhat by dehydration. Significant hypoalbuminemia
is caused by protein-losing glomerulopathy and worsened by systemic
vasculitis, severe hepatic insufficiency and hyperglobulinemia related to
antigenic stimulation.Azotemia is likely of mixed origins or primarily of renal origins with some
degree of a prerenal component. Decreased urine concentrating ability
in the face of dehydration is an indication of renal azotemia. Confounding
renal azotemia, severe hypoalbuminemia can decrease colloidal osmotic
pressure and essentially decrease vascular volume or renal perfusion. In
the later stages of Lyme nephritis, lesions can include some combination
of interstitial lymphoplasmacytic nephritis, tubular necrosis and diffuse
glomerulonephritis, all of which can be a cause of proteinuria.
The pathogenesis of the tubular changes in canine Lyme nephritis is
questionable, but immune-mediated glomerular disease, decreased
perfusion and hypoxia, and the toxic effects of severe proteinuria are
all postulated as potential causes. Liver enzymes are increased by
hepatocellular damage, systemic or intrahepatic vasculitis, and vacuolar
hepatopathy associated with chronic inflammation or infection and ischemia.
Urinalysis
Urine specific gravity shows inappropriate concentrating ability caused
by glomerular and tubular dysfunction. Observation of granular casts can
confirm coexisting tubular damage, but the density of casts in urine cannot
reliably measure severity, reversibility or duration of lesion. The pathogenesis
of the tubular changes in canine Lyme nephritis is questionable, but immune-
mediated glomerular disease, decreased perfusion and hypoxia, and the
toxic effects of severe proteinuria are most likely responsible.
Additional testingSerology
Follow-up with quantitative C6
antibody test aids in determining when
treatment is warranted, accurately tracking response to therapy and,
eventually, as an indicator of when treatment has been effective.
Lyme C6
antibody to the C6
antigen is a highly specific for Borrelia
burgdorferiinfection. Dogs with leptospirosis, Rocky Mountain spotted
fever, babesiosis, ehrlichiosis and heartworm disease do not have
antibodies to C6, nor are antibodies to C
6produced in response to
immunization with currently available canine Lyme vaccines.
Case Study 1
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Case Study 2
Patient
Nine-year-old DSH female cat
Presenting Complaints
Mild PU/PD, intermittent vomiting sometime
containing hair, weight loss
Physical Exam
Moderate dental tartar, unkempt coat,
evidence of diarrhea on tail, tachycardia,
dehydration and palpable thyroid nodule
Muriel Jones
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Case Study 2
HematologyHct = 47 % HIGH 30 45
Hgb = 10 g/dL 0.0 15.1
RBC = 10.97 L HIGH 5.0 10.0MCV = 49 fL 41.0 58.0
MCH = 15 pg 12.50 17.60
MCHC = 33 g/dl 29.0 36.0
RDW = 19 % 17.3 22.0
% RETIC = 0.2
RETIC = 15.3 K/L 0.0 60
WBC = 18,025 L 5,500 19,500
NEU = 16,680 L HIGH 2,000 12,500
LYM = 1,000 L 900 7,000
MONO = 230 L 100 790
EOSIN = 115 L 100 790
BASO = 0 L 0 100
PLT = 220 K/L 175 600
Biochemical profileAlk Phos = 86 IU/L HIGH 0 62
ALT (SGPT) = 80 IU/L HIGH 28 76
Albumin = 2.6 g/dL 2.3 3.3
Total Protein = 6.8 g/dL 5.9 8.5
Globulin = 4.2 g/dL 3.6 5.2
Total Bilirubin = 0.2 mg/dL 0.0 0.4
BUN = 39 mg/dL HIGH 15 34
Creatinine = 2.7 mg/dL HIGH 0.8 2.3
Cholesterol = 145 mg/dL 82 218Glucose = 148 mg/dL 70 150
Calcium = 9.3 mg/dL 8.2 11.8
Phosphorus = 5.9 mg/dL 3.0 7.0
Sodium = 152 mEq/L 145 156
Chloride = 116 mEq/L 111 125
Potassium = 3.8 mEq/L LOW 3.9 5.8
Total T4 = 7.9 ug/dL HIGH 0.7 5.2
Complete Urinalysis: CystocentesisDipstick Tests Urine Sediment Examination
Color Yellow WBCs/hpf 0
Transparency Clear RBCs/hpf 0
Specific Gravity 1.045 Epithelial cells/hpf 0
Protein Negative Casts/hpf 0
Glucose Negative Crystals 0
Bilirubin Negative Bacteria 0
Blood Negative
pH 6.7 UPC Ratio 2.7
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Case Study 2
Thoracic radiograph: lateral
Thoracic radiograph: DV
Nuclear scintigraphy
SNAP T4
Test
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Interpretive Summary
Hematology
Very mild polycythemia, which can be either relative or absolute.Relative polycythemia is associated with dehydration; absolute can be
associated with polycythemia vera or causes of increased erythropeitin.
Slight leukocytosis composed of mature neutrophilia (a lack of immature
neutrophils on the blood film) with lymphopenia suggests a stress
leukogram.
Biochemical profile
Mild increases in alkaline phosphatase (ALKP) and alanine
aminotransferase (ALT) are present. Azotemia is present (BUN, creatinine
increased). Deciding if azotemia is prerenal, renal or postrenal can be
difficult because cats can have renal azotemia with relatively concentrated
urine. Moreover, the urine of hyperthyroid cats can be nonconcentrated
as a direct result of the hyperthyroidism without any secondary renaldisease. Hypokalemia is present and can occur with many feline diseases
including CRF (chronic renal failure) and hyperthyroidism. Total T4
in
markedly elevated and hyperthyroidism is likely, especially considering the
associated polycythemia, azotemia and elevated liver enzymes.
Urinalysis
Urine specific gravity is concentrated and the urine protein ratio is
moderately elevated, especially for an azotemic patient.
Radiography
Mild cardiomegaly is present, characterized by biatrial enlargement. This is
recognized on the VD view (valentine heart).
Nuclear scintigraphy shows a right-sided, unilateral lesion, which is lesscommon than a bilateral lesion in feline hyperthyroidism.
Additional testing
Blood pressure
Systolic 180 mm/Hgif repeatable, consistent with mild hypertension
DiagnosisThe clinical diagnosis is
hyperthyroidism with likely concurrent
chronic renal disease.
Treatment/Plan
Hyperthyroidism can increase cardiac
output, decrease peripheral vascular
resistance, increase renal blood flow
and increase GFR. This chain of
events cannot only decrease BUN
and creatinine, but also perhapslead to glomerular hypertension and
hyperfiltration, thereby potentially
inducing or worsening concurrent
renal disease.
Systemic hypertension can be
associated with hyperthyroidism, and
supervision of some patient therapy
may benefit from regular monitoring
of UPC with a UPC less than 0.5 as a
target for treatment. With successful
Rx of hyperthyroidism (radioactive
iodine, methimizole, thyroidectomy),
the UPC may return to normal or
may worsen if CRF is progressive.
Careful monitoring of this patient is
recommended.
Case Study 2
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Patient
One-year-old castrated male poodle-mix
Presenting Complaints
Stumbling and vomiting
History12 hours of lethargy, vomiting, ataxia
Physical Exam
Dehydration, slow menace bilaterally
Spike James
Case Study 3
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Case Study 3
HematologyHgb = 45.3 g/dL 37 55
Hgb = 13.6 g/dL 12.0 18.0
RBC = 5.92 L 5.5 8.5
MCV = 76.5 fL 60.0 77.0
MCH = 22.97 pg 19.5 24.5
MCHC = 30.02 g/dl LOW 32.0 37.0
RDW = 14.5 % 12.0 16.0
% RETIC = 0.3 %
RETIC = 17.8 K/L
WBC = 21,620 L HIGH 5,500 16,900
NEU = 16,830 L HIGH 2,000 12,000
LYM = 1,680 L 700 4,900
MONO = 1,790 L HIGH 100 1,400
EOSIN = 0 L 100 1,490
BASO = 0 L 0 .1
PLT = 280 K/L 175 500
MPV = 12.36 fL
PDW = 13.2 %
PCT = 0.3 %
Biochemical profileBUN = 33 mg/dL HIGH 7 27
Creatinine = 2.6 mg/dL HIGH 0.5 1.8
Phosphorus = 8.4 mg/dL HIGH 2.5 6.8
Calcium = 10.2 mg/dL 7.9 12.0
Total Protein = 8.4 g/dL HIGH 5.2 8.2
Albumin = 2.3 g/dL 2.2 3.9
Globulin = 6.1 g/dL HIGH 2.5 4.5
ALT = 84 U/L 10 100
Alk Phos = 68 U/L 23 212Total Bilirubin = 0.1 mg/dL 0.0 0.9
Glucose = 85 mg/dL 77 125
Cholesterol = 289 mg/dL 110 320
Sodium = 158 mEq/L 144 160
Potassium = 4.1 mEq/L 3.5 5.8
Chloride = 114 mEq/L 109 122
Bicarbonate = 15 mEq/L 15 25
Anion Gap = 33 mEq/L HIGH 13 25
Complete UrinalysisDipstick Tests Urine Sediment Examination
Color Yellow WBCs/hpf 520
Transparency Clear RBCs/hpf
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Case Study 3
Blood film Renal ultrasound
Renal biopsy: H&E Renal biopsy: polarized
Urine sediment
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Interpretive Summary
Hematology
There is a mild leukocytosis characterized by a mild neutrophilia, a minimal
left shift, a mild monocytosis and eosinopenia observed on microscopic
examination of the blood film. Changes are most consistent with mild
inflammation. No significant abnormalities are observed in the erythron, and
platelet numbers are adequate.
Biochemical profile
There is a mild azotemia (increased BUN and creatinine) supporting
decreased glomerular filtration (GFR). The finding of a nonconcentrated
urine specific gravity supports the presence of renal azotemia (renal
insufficiency). There is a mild hypernatremia, which correlates with the
clinically noted dehydration and decreased water balance; however, the
chloride is relatively low compared to the sodium, suggesting loss or
sequestration of chloride. The clinical finding of vomiting suggests loss of
HCl-rich gastric contents is most likely and a metabolic alkalosis is present.The moderately increased anion gap indicates the presence of significant
amounts of unmeasured anions, such as phosphates and sulfates due
to the decreased GFR. This is supportive of the presence of a titrational
metabolic acidosis; however, the degree of azotemia and increased anion
gap appear discordant, and the presence of other unmeasured anions,
such as ethylene glycol, must be considered.
The within-reference-range TCO2
is due to the negating effects of the
typical increased TCO2
with metabolic alkalosis and the typical decreased
TCO2
with titrational acidosis. Blood gas analysis to determine the
degree of acidemia or alkalemia is warranted. The hyperphosphatemia
is most likely due to the decreased GFR and retention of phosphorus.
The slight hypokalemia may be due to decreased intake. There is a slight
hyperproteinemia characterized by a low-normal albumin and a mild
hyperglobulinemia. This protein pattern is most supportive of inflammation.
Urinalysis
The finding of an acidic urine in the face of a metabolic alkalosis and acidosis
suggests the acidosis condition is more severe and acidemia may be
present. Evaluation of the blood gas data to determine if there is acidemia
or alkalemia and the severity of the disorder is warranted. Multiple significant
abnormalities are noted within the microscopic portion of the urinalysis. The
finding of monohydrate calcium oxalate crystals is strongly supportive of
ethylene glycol toxicity. The presence of granular casts suggests the presence
of significant tubular injury. The presence of white blood cells (WBC) in the
urine sediment indicates the presence of inflammation; however, localization
of the inflammation is not possible since the sample is a free-catch specimen.
A trace protein content is difficult to accurately assess in a urine sample that
has a fixed specific gravity (no concentration); however, the urine protein to
urine creatinine (UPC) ratio suggests that significant proteinuria is not present.
Even if there were a slight significant increase in the UPC ratio, accurate
interpretation would be difficult since the urine sediment is active (WBC and
granular casts present). Any slight protein present may be associated with
mild inflammation or tubular injury.
DiagnosisEthylene glycol toxicity
Treatment/Plan
Blood gas analysis
Osmolality and osmolar gap
evaluation
Abdominal ultrasound
Ethylene glycol assay
Initiate therapy for suspectedethylene glycol toxicity (fluids,
electrolytes, acid base therapy,
maintain adequate urine volumes)
4-methylpyrazole (4MP)
Consider dialysis if available
Case Study 3
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Case Study 4
Patient
Eight-year old spayed female Shetland shee
Presenting Complaints
Vomiting, diarrhea, lethargy, anorexia, edem
HistoryFive-day history of lethargy, anorexia, vomiti
and diarrhea
Physical Exam
Increased respiratory rate; bilateral facial, ve
and peripheral edema
Fezzie Smith
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Case Study 4
HematologyHct = 36 g/dL LOW 37 55
Hgb = 11.1 g/dL LOW 12.0 18.0
RBC = 5.1 L LOW 5.5 8.5
MCV = 69 fL 60.0 77.0
MCH = 22 pg 19.5 24.5
MCHC = 31 g/dl LOW 32.0 37.0
RDW = 12.4 % 12.0 16.0
% RETIC = 1 %
RETIC = 51 K/L
WBC = 18,800 L HIGH 5,500 16,950
NEU = 16,300 L HIGH 2,000 12,000
LYM = 900 L LOW 1,000 4,900
MONO = 1,600 L HIGH 100 1,400
EOSIN = 0 L 100 1,490
BASO = 0 L 0 100
PLT = 468 K/L 175 500
Biochemical profileAlk Phos = 97 U/L 23 212
ALT (SGPT) = 4 U/L LOW 10 100
Albumin = 1.7 g/dL LOW 2.2 3.9
Globulin = 4.2 g/dL 3.0 4.3
Total Protein = 5.8 g/dL HIGH 5.2 8.2
Total Bilirubin = 0.2 mg/dL 0.0 0.9
BUN = 96 mg/dL HIGH 7 27
Creatinine = 5.5 mg/dL HIGH 0.5 1.8
Cholesterol = 443 mg/dL HIGH 110 320Glucose = 99 mg/dL 77 125
Calcium = 10.1 mg/dL 7.9 12.0
Sodium = 151 mEq/L 144 160
Potassium = 4.8 mEq/L 3.5 5.8
Chloride = 121 mEq/L 109 122
Bicarbonate = 14 mEq/L LOW 15 25
Anion Gap = 21 mEq/L 13 25
Complete Urinalysis: CystocentesisDipstick Tests Urine Sediment Examination
Color Yellow WBCs/hpf
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Case Study 4
Blood film 10x Blood film 40x
Renal ultrasound Renal ultrasound
Renal biopsy
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Interpretive Summary
Hematology
Modest leukocytosis composed of mature neutrophilia and monocytosis with
concurrent lymphopenia is a stressed leukogram. This is typically consistentwith inflammation, infection or increased cortisol concentrations from
exogenous use or hyperadrenocorticism.
Biochemical profile
This dog is suffering from severe hypoalbuminemia. Because the serum
globulin concentration is high-normal, this is likely a result of liver disease, renal
loss or vasculitis. All other parameters assessing liver function (cholesterol,
glucose, and bilirubin) are within normal limits (the cholesterol is actually high
and not low as in liver insufficiency), making liver insufficiency much less likely.
Therefore, renal loss and vasculitis become the two likely possibilities. The
facial edema evident on presentation may be a result of the hypoalbuminemia,
with or without a degree of vasculitis.
UrinalysisA very high UPC of 18.6 was identified in this dog. This degree of proteinuria
is very likely to be glomerular in origin and is enough to explain the severe
hypoalbuminemia. This dog, therefore, has all four criteria for nephrotic
syndrome: proteinuria, hypoalbuminemia, hypercholesterolemia and edema.
Aggressive diagnostic and therapy are necessary in cases of nephrotic
syndrome in an attempt to reverse the cause. Likely causes include
glomerulonephritis and amyloidosis.
Radiology
Abdominal ultrasound report
The renal cortices appear to be mildly hyperechoic being isoechoic with
the adjacent spleen. There is mild dilatation of the renal pelvices. No otherabnormalities are seen. The hyperechoic cortex is a nonspecific finding seen in
both acute and chronic renal disease. Amyloidosis can also cause hyperechoic
renal cortices. The mild pyelectasia is suggestive of recent fluid administration.
Additional testing
Renal Biopsy
Severe glomerulopathy with amorphous pink material consistent with amyloid.
Diagnosis
The clinical diagnosis isamyloidosis.
Treatment/Plan
Thoracic radiographs blood
gas analysis
Urine culture
Nonspecific therapy for
proteinuria and hypertension
Will not likely benefit from
immunosuppression.
Consider: DMSO, MSM
Case Study 4
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