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IDEXX Laboratories

Renal Disease Case Studies

Authors
Dennis DeNicola, DVM, PhD, DACVP Chief Veterinary Educator, Clinical Pathologist, IDEXX Laboratories Richard Goldstein, DVM, DACVIM, DECVIM-CA

Dr. DeNicola completed his DVM in 1978 and his PhD in 1981, both at Purdue University. For more than twenty years, he served as educator in clinical and surgical pathology. In addition, he directed the primary cytology and surgical pathology service at the veterinary school laboratory and ran a private pathology service for 15 years. A speaker at more than 100 national and international education symposia, Dr. DeNicola also has authored or co-authored more than 150 publications in various aspects of veterinary clinical pathology.

Assistant Professor, Small-Animal Medicine, Cornell University

Dr. Goldstein received his DVM from the Koret School of Veterinary Medicine, the Hebrew University of Jerusalem, Israel. He completed his residency in smallanimal internal medicine at the University of California, Davis. He is a diplomate of the American College of Veterinary 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.

Fred Metzger, DVM, DABVP Owner, Metzger Animal Hospital

Dr. Metzger is a 1986 graduate of the Purdue School of Veterinary Medicine and a diplomate of the American Board of Veterinary Practitioners, with specialties in canine and feline medicine. He is an adjunct professor at Pennsylvania State University and serves on the practitioner advisory boards of Veterinary Economics and Veterinary Medicine magazines. He recently 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 State College, Pennsylvania, that received the 1998 Veterinary Economics/Pzer Practice of Excellence award.

Roberta Relford, DVM, MS, PhD, DACVIM,


DACVP Divisional Vice President of Worldwide Pathology Coagulation, Cytology, Internal Medicine, IDEXX Laboratories

Pete Fernandes, DVM, DACVP Clinical Pathologist, IDEXX Laboratories

Dr. Relford received her DVM from Auburn University in 1982 and worked as a small-animal practitioner for four years before pursuing her advanced training. She started her residency training in clinical pathology and obtained an MS in pathology from Mississippi State University. She then transferred to Texas A&M, where she completed her pathology residency training and obtained a PhD in pathology. While completing her PhD, Dr. Relford pursued a residency in small-animal internal medicine. Dr. Relford is board-certified in internal medicine by the American College of Veterinary Internal Medicine and in clinical pathology by the American College of Veterinary Pathologists. She currently serves as Divisional Vice President of Worldwide Pathology for IDEXX Reference Laboratories. Dr. Relford has given numerous lectures on a wide variety of topics including clinical pathology, internal medicine, infectious diseases, cytology, platelet disorders, health maintenance programs and zoonotic diseases.

Dr. Fernandes completed his DVM at the University of Wisconsin-Madison, followed by an internship in smallanimal medicine and surgery at South Shore Animal Hospital in Boston. Dr. Fernandes residency was in clinical pathology at Texas A&M University and the University of Florida. He is a diplomate of the American College of Veterinary Pathologists.

Brian Poteet, DVM, DAVCR, DABSNM

Director, Gulf Coast Veterinary Diagnostic Imaging

Dr. Poteet received his DVM from Texas A&M University and completed his radiology residency at the University of Tennessee. In addition to being board-certied 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 medical associations, Vice President of the Veterinary Cancer Associates, and holds two adjunct faculty positions at Texas A&M University.

Case Study 1

Jake Douglas

Patient Three-year-old intact male Labrador retriever 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, generalized peripheral lymphadenopathy, uveitis, bilateral swollen hocks and right stifle

Case Study 1
Hematology
Hct Hgb RBC MCV MCH MCHC RDW % RETIC RETIC WBC NEU LYM MONO EOSIN BASO PLT = = = = = = = = = = = = = = = = 32.2 10.1 4.9 63.5 21.33 33.2 17.3 0.6 40,000 18,237 14,200 900 2,900 223 14 360 % g/dL L fL pg g/dl % % L L L L L L L K/L LOW LOW LOW 37 12.0 5.50 60.0 19.50 32.0 12.0 55 18.0 8.50 77.0 24.50 37.0 16.0

HIGH

HIGH HIGH LOW HIGH

5,500 2,000 1000 100 100 0 175

16,950 12,000 4,900 1,400 1,490 100 500

Biochemical profile
Alk Phos ALT (SGPT) Albumin Total Protein Globulin Total Bilirubin BUN Creatinine Glucose Calcium Phosphorus Sodium Potassium Chloride = = = = = = = = = = = = = = 899 201 1.6 8.1 6.5 0.2 37 2.2 99 10.3 9.0 150 5.1 111 U/L U/L g/dL g/dL g/dL mg/dL mg/dL mg/dL mg/dL mg/dL mg/dL mEq/L mEq/L mEq/L HIGH HIGH LOW HIGH HIGH HIGH 23 10 2.2 5.2 2.8 0.0 7 0.5 77 7.9 2.5 144 3.5 109 212 100 3.9 8.2 4.5 0.4 27 1.8 125 12.0 6.8 160 5.8 12

HIGH

Complete Urinalysis: Cystocentesis


Dipstick Tests Color Transparency Specific Gravity Protein Glucose Bilirubin Blood pH Yellow Clear 1.013 3+ Negative Trace Negative 6.5 Urine Sediment Examination WBCs/hpf 0 RBCs/hpf 0 Epithelial cells/hpf 0 Casts/hpf 5 to 7, granular Crystals 0 Bacteria 0 UPC Ratio 5.1

Case Study 1
Serology
Leptospirosis SNAP 3Dx Test Heartworm antigen E. canis antibody Lyme C6 antibody Rocky Mountain spotted fever negative negative negative positive negative Lyme-positive SNAP 3Dx Test

Cytology
Arthrocentesis (hock and stifle): suppurative inflammatory joint fluid Lymph node FNA (inguinal & popliteal): lymphoid hyperplasia, consistent with reactive lymph nodes

Cytology: ne-needle aspirate

Renal biopsy 10x

Renal biopsy 60x

Case Study 1
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 inammatory condition. The thrombon/platelets are within normal limits

Diagnosis
The clinical diagnosis is Lyme nephritis.

Biochemical prole
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 specic gravity 1.013 indicates some, yet inadequate, concentrating ability, and hypoalbuminemia may be masked somewhat by dehydration. Signicant hypoalbuminemia is caused by protein-losing glomerulopathy and worsened by systemic vasculitis, severe hepatic insufciency 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 inammation or infection and ischemia.

Treatment/Plan
Blood was sent to a reference laboratory for quantitative C6 antibody testing. The patient was treated with doxycycline, intravenous uid 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 in our 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.

Urinalysis
Urine specic gravity shows inappropriate concentrating ability caused by glomerular and tubular dysfunction. Observation of granular casts can conrm 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 immunemediated glomerular disease, decreased perfusion and hypoxia, and the toxic effects of severe proteinuria are most likely responsible.

Additional testing
Serology 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 specic for Borrelia burgdorferi infection. Dogs with leptospirosis, Rocky Mountain spotted fever, babesiosis, ehrlichiosis and heartworm disease do not have antibodies to C6, nor are antibodies to C6 produced in response to immunization with currently available canine Lyme vaccines.

Case Study 2

Muriel Jones

Patient Nine-year-old DSH female cat Presenting Complaints Mild PU/PD, intermittent vomiting sometimes containing hair, weight loss Physical Exam Moderate dental tartar, unkempt coat, evidence of diarrhea on tail, tachycardia, dehydration and palpable thyroid nodule

Case Study 2
Hematology
Hct Hgb RBC MCV MCH MCHC RDW % RETIC RETIC WBC NEU LYM MONO EOSIN BASO PLT = = = = = = = = = = = = = = = = 47 10 10.97 49 15 33 19 0.2 15.3 18,025 16,680 1,000 230 115 0 220 % g/dL L fL pg g/dl % K/L L L L L L L K/L HIGH HIGH 30 0.0 5.0 41.0 12.50 29.0 17.3 0.0 5,500 2,000 900 100 100 0 175 45 15.1 10.0 58.0 17.60 36.0 22.0

HIGH

60 19,500 12,500 7,000 790 790 100 600

Biochemical profile
Alk Phos ALT (SGPT) Albumin Total Protein Globulin Total Bilirubin BUN Creatinine Cholesterol Glucose Calcium Phosphorus Sodium Chloride Potassium Total T4 = = = = = = = = = = = = = = = = 86 80 2.6 6.8 4.2 0.2 39 2.7 145 148 9.3 5.9 152 116 3.8 7.9 IU/L IU/L g/dL g/dL g/dL mg/dL mg/dL mg/dL mg/dL mg/dL mg/dL mg/dL mEq/L mEq/L mEq/L ug/dL HIGH HIGH 0 28 2.3 5.9 3.6 0.0 15 0.8 82 70 8.2 3.0 145 111 3.9 0.7 62 76 3.3 8.5 5.2 0.4 34 2.3 218 150 11.8 7.0 156 125 5.8 5.2

HIGH HIGH

LOW HIGH

Complete Urinalysis: Cystocentesis


Dipstick Tests Color Transparency Specific Gravity Protein Glucose Bilirubin Blood pH Yellow Clear 1.045 Negative Negative Negative Negative 6.7 Urine Sediment Examination WBCs/hpf 0 RBCs/hpf 0 Epithelial cells/hpf 0 Casts/hpf 0 Crystals 0 Bacteria 0 UPC Ratio 2.7

Case Study 2

SNAP T4 Test

Nuclear scintigraphy

Thoracic radiograph: lateral

Thoracic radiograph: DV

Case Study 2
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 lm) with lymphopenia suggests a stress leukogram.

Diagnosis
The clinical diagnosis is hyperthyroidism with likely concurrent chronic renal disease.

Biochemical prole
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 difcult 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 renal disease. 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.

Treatment/Plan
Hyperthyroidism can increase cardiac output, decrease peripheral vascular resistance, increase renal blood ow and increase GFR. This chain of events cannot only decrease BUN and creatinine, but also perhaps lead to glomerular hypertension and hyperltration, thereby potentially inducing or worsening concurrent renal disease. Systemic hypertension can be associated with hyperthyroidism, and supervision of some patient therapy may benet 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.

Urinalysis
Urine specic 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 less common than a bilateral lesion in feline hyperthyroidism.

Additional testing
Blood pressure Systolic 180 mm/Hgif repeatable, consistent with mild hypertension

Case Study 3

Spike James

Patient One-year-old castrated male poodle-mix Presenting Complaints Stumbling and vomiting History 12 hours of lethargy, vomiting, ataxia Physical Exam Dehydration, slow menace bilaterally

Case Study 3
Hematology
Hgb Hgb RBC MCV MCH MCHC RDW % RETIC RETIC WBC NEU LYM MONO EOSIN BASO PLT MPV PDW PCT = = = = = = = = = = = = = = = = = = = 45.3 13.6 5.92 76.5 22.97 30.02 14.5 0.3 17.8 21,620 16,830 1,680 1,790 0 0 280 12.36 13.2 0.3 g/dL g/dL L fL pg g/dl % % K/L L L L L L L K/L fL % % 37 12.0 5.5 60.0 19.5 32.0 12.0 55 18.0 8.5 77.0 24.5 37.0 16.0

LOW

HIGH HIGH HIGH

5,500 2,000 700 100 100 0 175

16,900 12,000 4,900 1,400 1,490 .1 500

Biochemical profile
BUN Creatinine Phosphorus Calcium Total Protein Albumin Globulin ALT Alk Phos Total Bilirubin Glucose Cholesterol Sodium Potassium Chloride Bicarbonate Anion Gap = = = = = = = = = = = = = = = = = 33 2.6 8.4 10.2 8.4 2.3 6.1 84 68 0.1 85 289 158 4.1 114 15 33 mg/dL mg/dL mg/dL mg/dL g/dL g/dL g/dL U/L U/L mg/dL mg/dL mg/dL mEq/L mEq/L mEq/L mEq/L mEq/L HIGH HIGH HIGH HIGH HIGH 7 0.5 2.5 7.9 5.2 2.2 2.5 10 23 0.0 77 110 144 3.5 109 15 13 27 1.8 6.8 12.0 8.2 3.9 4.5 100 212 0.9 125 320 160 5.8 122 25 25

HIGH

Complete Urinalysis
Dipstick Tests Color Transparency Specific Gravity Protein Glucose Bilirubin Blood pH Yellow Clear 1.011 Trace Trace Negative Trace 5.0 Urine Sediment Examination WBCs/hpf 520 RBCs/hpf <5 Epithelial cells/hpf None seen Casts/hpf Granular Crystals Calcium oxalate Bacteria None seen UPC Ratio 0.4

Case Study 3

Blood lm

Renal ultrasound

Renal biopsy: H&E

Renal biopsy: polarized

Urine sediment

Case Study 3
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 lm. Changes are most consistent with mild inammation. No signicant abnormalities are observed in the erythron, and platelet numbers are adequate.

Diagnosis
Ethylene glycol toxicity

Biochemical prole
There is a mild azotemia (increased BUN and creatinine) supporting decreased glomerular ltration (GFR). The nding of a nonconcentrated urine specic gravity supports the presence of renal azotemia (renal insufciency). 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 nding 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 signicant 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 inammation.

Treatment/Plan
Blood gas analysis Osmolality and osmolar gap
evaluation

Abdominal ultrasound Ethylene glycol assay Initiate therapy for suspected


ethylene glycol toxicity (uids, electrolytes, acid base therapy, maintain adequate urine volumes)

4-methylpyrazole (4MP) Consider dialysis if available

Urinalysis
The nding 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 signicant abnormalities are noted within the microscopic portion of the urinalysis. The nding of monohydrate calcium oxalate crystals is strongly supportive of ethylene glycol toxicity. The presence of granular casts suggests the presence of signicant tubular injury. The presence of white blood cells (WBC) in the urine sediment indicates the presence of inammation; however, localization of the inammation is not possible since the sample is a free-catch specimen. A trace protein content is difcult to accurately assess in a urine sample that has a xed specic gravity (no concentration); however, the urine protein to urine creatinine (UPC) ratio suggests that signicant proteinuria is not present. Even if there were a slight signicant increase in the UPC ratio, accurate interpretation would be difcult since the urine sediment is active (WBC and granular casts present). Any slight protein present may be associated with mild inammation or tubular injury.

Case Study 4

Fezzie Smith

Patient Eight-year old spayed female Shetland sheepdog Presenting Complaints Vomiting, diarrhea, lethargy, anorexia, edema History Five-day history of lethargy, anorexia, vomiting and diarrhea Physical Exam Increased respiratory rate; bilateral facial, ventral and peripheral edema

Case Study 4
Hematology
Hct Hgb RBC MCV MCH MCHC RDW % RETIC RETIC WBC NEU LYM MONO EOSIN BASO PLT = = = = = = = = = = = = = = = = 36 11.1 5.1 69 22 31 12.4 1 51 18,800 16,300 900 1,600 0 0 468 g/dL g/dL L fL pg g/dl % % K/L L L L L L L K/L LOW LOW LOW 37 12.0 5.5 60.0 19.5 32.0 12.0 55 18.0 8.5 77.0 24.5 37.0 16.0

LOW

HIGH HIGH LOW HIGH

5,500 2,000 1,000 100 100 0 175

16,950 12,000 4,900 1,400 1,490 100 500

Biochemical profile
Alk Phos ALT (SGPT) Albumin Globulin Total Protein Total Bilirubin BUN Creatinine Cholesterol Glucose Calcium Sodium Potassium Chloride Bicarbonate Anion Gap = = = = = = = = = = = = = = = = 97 4 1.7 4.2 5.8 0.2 96 5.5 443 99 10.1 151 4.8 121 14 21 U/L U/L g/dL g/dL g/dL mg/dL mg/dL mg/dL mg/dL mg/dL mg/dL mEq/L mEq/L mEq/L mEq/L mEq/L LOW LOW HIGH HIGH HIGH HIGH 23 10 2.2 3.0 5.2 0.0 7 0.5 110 77 7.9 144 3.5 109 15 13 212 100 3.9 4.3 8.2 0.9 27 1.8 320 125 12.0 160 5.8 122 25 25

LOW

Complete Urinalysis: Cystocentesis


Dipstick Tests Color Transparency Specific Gravity Protein Glucose Bilirubin Blood pH Yellow Clear 1.009 3+ Negative Negative Negative 6.5 Urine Sediment Examination WBCs/hpf <5 RBCs/hpf <5 Epithelial cells/hpf None seen Casts/hpf 0 Crystals 0 Bacteria 0 Culture Pending UPC Ratio 18.6

Case Study 4

Blood lm 10x

Blood lm 40x

Renal ultrasound

Renal ultrasound

Renal biopsy

Case Study 4
Interpretive Summary
Hematology
Modest leukocytosis composed of mature neutrophilia and monocytosis with concurrent lymphopenia is a stressed leukogram. This is typically consistent with inammation, infection or increased cortisol concentrations from exogenous use or hyperadrenocorticism.

Diagnosis
The clinical diagnosis is amyloidosis.

Biochemical prole
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 insufciency), making liver insufciency 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.

Treatment/Plan
Thoracic radiographs blood gas analysis Urine culture Nonspecic therapy for proteinuria and hypertension Will not likely benet from immunosuppression. Consider: DMSO, MSM

Urinalysis
A very high UPC of 18.6 was identied 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 other abnormalities are seen. The hyperechoic cortex is a nonspecic nding seen in both acute and chronic renal disease. Amyloidosis can also cause hyperechoic renal cortices. The mild pyelectasia is suggestive of recent uid administration.

Additional testing
Renal Biopsy Severe glomerulopathy with amorphous pink material consistent with amyloid.

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