CHAPTER 10
Case Studies

CASE EXAMPLE: Urinalysis Case Number: 1

Signalment: Two‐year‐old spayed female Weimaraner dog.

History and Physical Examination: She has had pinkish‐to‐brown urine observed by the owners for at least six months. She is normal in every other respect, as is her physical examination. She has had no clinical urinary tract signs.

Interpretation of Urinalysis: The brown color to the urine is often due to the presence of hemoglobin oxidation products or myoglobin in the urine. Since there are TNTC RBC, the color is attributed to RBC and oxidation of hemoglobin. The urine is well concentrated at 1.039 USG. The pH of 7.0 could be in part accounted for by the amount of bleeding into the urine (plasma pH of 7.4). The 2+ protein on the dipstrip is likely from the proteins in the numerous RBC and plasma entering the urine. The rare granular cast per LPF is considered normal in the face of the 1.039 USG. The mild increase in WBC is most likely from the entry of blood into the urine; less likely it is from inflammation. The squamous epithelial cells are not of concern as they are almost always contaminants from the lower urogenital tract especially in samples collected during voiding or catheterization.

Hematuria is the most important finding in this urinalysis. There is a high amount of occult blood on dipstrip and RBC during microscopy. The origin of the RBC cannot be determined on findings from the urinalysis alone.

Further Diagnostics and Assessment: The finding of painless hematuria usually indicates upper urinary tract disease (kidneys, ureters). Differential diagnosis for painless hematuria should include renal neoplasia, nephrolithiasis, renal pelvic blood clot from trauma, and benign essential renal hematuria. Neoplasia is unlikely in a well dog with hematuria of this duration. Benign essential renal hematuria is the most likely consideration at this point.

A hemogram was normal with the exception of a mild microcytic anemia attribute to the chronic blood loss. Routine serum biochemistry was normal. Urine culture on a sample obtained by cystocentesis was negative.

Urinary tract imaging with radiographs and ultrasonography was normal. Urethrocystoscopy revealed no anatomical abnormalities, but bright red blood was seen from a urine jet emanating from the left ureteral orifice.

No treatment to interrupt the renal bleeding was provided. Iron supplementation over the next six months resulted in resolution of the microcytic anemia.

Final Diagnosis: Benign essential renal hematuria.

CASE EXAMPLE: Urinalysis Case Number: 2

Signalment: Three‐year‐old spayed female Domestic Shorthair cat.

History and Physical Examination: The current owner complaint is pollakiuria, stranguria, and hematuria for the past four days. This cat does not always use the litterbox for urinations during the past year. The cat is otherwise normal. Abdominal palpation is normal with the exception of some discomfort during palpation of the bladder; no masses were detected.

Interpretation of Urinalysis: The occult blood positive reaction on the dipstrip and the increased numbers of RBC are the main abnormalities to be observed from this urinalysis. Some of the RBC may have been added by the cystocentesis method of urine collection. Sometimes during cystocentesis, the needle more readily adds RBC to the urine when there is an underlying inflammatory process in the bladder wall. There is no pyuria but there were a few extra free non squamous epithelial cells observed. Desquamation of urothelial cells can occur during urinary tract neoplasia and inflammation during cystitis or urolithiasis. A few struvite crystals were observed in urine that is well concentrated and with a pH of 6.5.

Moderate numbers of cocci that are reported are not aligned with an increase in the number of WBC, so there is suspicion that these bacteria may not be “real.” Caution must be used in the interpretation of reported bacteria because many artifacts in urine can be misinterpreted as bacteria, especially in cats. Brownian motion of small particles in urine sometimes leads to the interpretation of these particles as bacteria. Small crystals, lipid droplets, cellular debris, mucus threads, and precipitated stain can all resemble bacteria.

Further Diagnostics and Assessment: Urinary tract imaging with abdominal radiographs and ultrasonography were normal, excluding the presence of urolithiasis. Urinary sediment cytology was negative for bacteria, and quantitative urine culture was negative for bacterial growth. The cocci described in the urinary sediment apparently were artifacts. Reports of bacteria on urine sediment examination that are not substantiated by bacterial culture of urine are common.

Crystalluria need not be present to diagnose idiopathic/interstitial cystitis, and most cats with this disorder have few or no crystals in their urine sediment, especially when consuming diets designed to promote urinary acidification.

Final Diagnosis: Idiopathic/interstitial cystitis.

CASE EXAMPLE: Urinalysis Case Number: 3

Signalment: Nine‐year‐old spayed female German Shepherd Dog.

History and Physical Examination: This dog had increased frequency and straining to urinate over the past three days with occasional urinary spotting “accidents” in the house. Some red discoloration was observed by the owners in the dog’s urine, and an unusually strong odor was noticed. There was no change in water consumption or daily urine volume output. This dog had normal appetite, bowel movements, and attitude. A urine sample was collected by the owner from a small puddle on thee floor.

The dog is bright, alert, and hydration assessed as normal based on skin turgor. Mild mucopurulent vaginal discharge is noted. The bladder is small and possibly thickened on abdominal palpation; the dog is very uncomfortable during the palpation of the bladder.

Interpretation of Urinalysis: Urinalysis results are from a post‐voided sample; it was aspirated from a urine puddle in the house by the owner. Since she has a vulvar discharge, it is likely that some inflammatory elements will be picked up as the urine passes through the vestibule and vulva as a form of extra‐urinary contamination.

Brown cloudy urine is abnormal and likely due to the inflammatory elements identified during urine microscopy. The USG of 1.024 shows at least modest urine concentrating capacity. Any consideration for a urinary concentrating defect cannot be made at this time as we do not know the time of the day and relationship to when the dog ate and drank as to when the sample was collected. Bacterial urinary infection can impair urine concentration at times.

The high urine pH (8.0) is compatible with infection by a urease‐producing organism (e.g. Staphylococcus aureus, Proteus spp.). In this setting, urea is hydrolyzed to ammonium and carbonate ions. The carbonate ions bind hydrogen ions and remove them from solution resulting in more alkaline urine. Infection by cocci is suspected based on the appearance of the bacterial organisms in the urine sediment. The presumptive diagnosis is bacterial urinary tract infection, suspect for S. aureus.

The 2+ proteinuria on the dipstrip is attributed to postrenal contamination with proteins associated with the active urinary sediment.

The predominant element identified during urine microscopy was the WBC (20–30/HPF). Lesser numbers of RBC (10–20/HPF) accompany the WBC as part of an inflammatory process. Clumping of leukocytes in the urine often adds support for an underlying bacterial etiology. Contamination from the genital tract also must be considered because the sample was voided, and the dog had a mucopurulent vaginal discharge. The report of “few cocci” is likely to be real and not an artifact given the inflammatory response (WBC, RBC, and +2 protein). Increased numbers of squamous epithelial cells are likely from genital tract contamination from the voided sample. Increased numbers of nonsquamous epithelial cells (urothelial) are likely from desquamation association with the inflammatory process.

Further Diagnostics and Assessment: Based on the uncertainty for the origin of the elements in the active sediment on the voided urine sample, another sample was obtained by cystocentesis. All the urinalysis results were very similar, except that squamous epithelial cells were no longer identified. Culture of the sample collected by cystocentesis grew a pure culture of S. aureus at >30 000 cfu/mL that was susceptible to all the routine urinary antimicrobials.

Another option while awaiting urine culture results to return could have been to perform a urine cytology to confirm the presence of cocci.

Since Staphylococcus species are associated with initiation and growth of struvite stones in the dog, an abdominal radiograph was taken to exclude the presence of radiodense urinary calculi. None were found.

The dog’s clinical signs resolved within three days of starting a 10‐day course of oral amoxicillin. Given the age of the dog, if long‐term response to treatment is poor, the clinician should consider additional diagnostic testing (e.g. contrast radiography, ultrasonography, and urine cytology) to rule out urinary tract neoplasia or other structural abnormality.

Final Diagnosis: Bacterial UTI due to S. aureus.

CASE EXAMPLE: Urinalysis Case Number: 4

Signalment: Three‐year‐old intact male Great Dane.

History and Physical Examination: Vomiting and anorexia of one‐week duration were noted. The owner reports red to dark urine over the past few days without any urinary distress (no stranguria, pollakiuria, or dysuria). Daily urine volume is about the same as usual, and there is no increased thirst. There is no history of trauma and no exposure to rodenticides.

The dog was painful on abdominal palpation and the spleen was markedly enlarged. The mucous membranes were slightly pale.

Interpretation of Urinalysis: Dark brown turbid urine is attributed to the +3‐occult blood reaction that is mostly from free hemoglobin in the urine (positive for hemolyzed blood but not for intact RBC). There were only minor increases in the WBC and intact RBC during urine microscopy. Increased transitional epithelial cells are attributed to urinary catheterization used to collect the urine sample.

The urine is moderately concentrated with a USG of 1.025. The strong occult blood reaction is mostly due to the presence of free hemoglobin in the urine (very few RBC were identified in the sediment and the occult blood was negative for intact RBC). Based on later laboratory data, the positive protein reaction on the dipstrip is attributed to prerenal delivery of free hemoglobin from hemolysis into the urine.

The presence of granular cast cylindruria identified during urine microscopy is of concern for the possibility of AKI and accelerated renal tubular degeneration. Alternatively, granules within the casts could result from precipitates of hemoglobin into the cast matrix protein following systemic hemolysis.

Precipitated hemoglobin in the urine sediment can sometimes be confused with red blood cells; therefore, the sediment should be reviewed to confirm that the reported red blood cells do not represent precipitated hemoglobin (hemoglobin pigmenturia versus hematuria). In this particular case, numerous precipitates of hemoglobin were initially identified as intact RBC in error, but upon closer inspection, these globules varied widely in size, unlike for RBC.

Hemoglobinuria following systemic hemolysis can be associated with several conditions in dogs, including transfusion reaction, disseminated intravascular coagulation, postcaval dirofilariasis syndrome, heat stroke, zinc toxicity, severe hypophosphatemia, red cell enzyme deficiencies, and autoimmune hemolytic anemia. The young age of the dog and the presence of splenomegaly on physical examination led to the suspicion of splenic torsion.

The presumptive diagnosis was splenic torsion with hemoglobinuria and possible hemoglobinuric nephrosis.

Further Diagnostics and Assessment: The hemogram disclosed moderate anemia (PCV 27%) with target cells, polychromasia, and red cell fragmentation supporting the finding of a hemolytic process. The platelet count was 78 000 μlL. A biochemical profile was normal except for a mild increase in alkaline phosphatase (178 IU/L). The heartworm and Coombs’ tests were negative, but fibrin degradation products were detected in serum.

Abdominal radiographs confirmed marked splenomegaly and ultrasonography showed diffuse enlargement of the spleen with uniform echogenicity. Exploratory laparotomy revealed splenic torsion and splenectomy was performed.

The mechanism of hemolysis and hemoglobinuria in splenic torsion is unknown but may be due to microangiopathy and damage to red cells by intraluminal fibrin strands. This is supported by the presence of red cell fragments on the hemogram. The presence of thrombocytopenia and fibrin degradation products support a diagnosis of concurrent disseminated intravascular coagulation. Renal damage as indicated by the presence of granular casts was subclinical, and azotemia did not develop in this dog.

Final Diagnosis: Splenic torsion with systemic hemolysis and DIC; probable hemoglobinuric nephrosis; prerenal proteinuria.

CASE EXAMPLE: Urinalysis Case Number: 5

Signalment: Seven‐year‐old spayed female Domestic Shorthair cat.

History and Physical Examination: This cat stopped eating during the past week and is less active; the owners are unsure of water consumption and urine output. They have noted an increased volume/weight of clumping litter in the litter box in recent times. The owners also suspect mild weight loss over the past several months.

The cat was thin and had reduced skin turgor. We do not have a previous weight with which to compare today’s weight. The kidneys were small and irregular, and the cat resisted palpation that was interpreted to be pain. A small thyroid nodule on the left side was suspected on palpation of the neck. The bladder was moderately full. The cat had a grade II/VI right sternal border systolic murmur. Systolic blood pressure was 175 mmHg on repeated measurements.

Interpretation of Urinalysis: The slightly cloudy appearance to the urine sample is attributed to the active urine sediment findings. The 1.019 USG is far less than should occur in a cat with dehydration based on skin turgor changes and anorexia. The 2+ dipstrip proteinuria is abnormal, especially in urine that is minimally concentrated and is likely associated with the inflammatory findings in the urine sediment. The protein could be renal or postrenal in origin. The 1+ occult blood for intact RBC matches up with the 10–15 RBC per HPF seen on urine microscopy. The RBC are likely originating from the same process adding WBC to the urine, but some RBC could have been added from the trauma of cystocentesis.

The finding of 30–40 WBC per HPF, 10–15 RBC per HPF, 5–7 free transitional cells per HPF, and few rod bacteria on urine microscopy from a sample collected by cystocentesis supports the presence of an inflammatory process caused by bacterial urinary infection. The report of rods in the urine is more convincing than the finding of cocci in general. Clumping of WBC often indicates that organisms are between the WBC causing the clumping. The site of the infection as upper or lower urinary tract cannot be determined.

The presence of small and irregular kidneys with pain upon palpation suggests the possibility of pyelonephritis superimposed on CKD. The possibility for hyperthyroidism exists, but this diagnosis is difficult to make with certainty in the face of nonthyroidal illness.

Further Diagnostics and Assessment: The hemogram disclosed leukocytosis (41 000/μL) due to neutrophilia (37 000/μL) and a left shift (2000 bands/μL). The PCV (28%) and plasma proteins (7.6 g/dL) were normal. The biochemical profile disclosed azotemia (BUN 68 mg/dL, creatinine 4.1 mg/dL), hyperphosphatemia (8.5 mg/dL), decreased serum bicarbonate (10 mEq/L), and mild hypokalemia (3.2 mEq/L). Serum thyroxine concentration was 2.1 μg/dL, well within the reference range.

Abdominal ultrasonography showed that the kidneys were smaller than normal and had increased medullary echogenicity. Mild pelvic dilatation also was noted.

Bacterial culture of the urine grew a pure culture of >30 000 cfu/mL of Escherichia coli that was susceptible to most of the common urinary antimicrobials.

The cat was treated with intravenous fluids and intravenous sodium cephalothin. There was improvement in the cat’s attitude and appetite over the next four days. The cat was treated with cephalexin for two weeks.

At re‐evaluation, the cat was doing well and had a good appetite. A hemogram showed resolution of the leukocytosis, but the PCV was now mildly decreased (21%). The biochemical profile showed improvement in azotemia (BUN 43 mg/dL, creatinine 2.6 mg/dL) and resolution of hypokalemia, metabolic acidosis, and hyperphosphatemia. Urinalysis on a urine sample collected by cystocentesis showed resolution of pyuria and no bacteria were observed. Urine specific gravity was 1.017. The protein on the dipstrip had declined to trace positive at this time.

Final Diagnosis: Azotemic CKD, E. coli bacterial UTI, pyelonephritis; hyperthyroidism is likely.

CASE EXAMPLE: Urinalysis Case Number: 6

Signalment: Five‐year‐old intact male German Shepherd Dog.

History and Physical Examination: Presented to the emergency service for the evaluation of acute onset of vomiting and severe lethargy. The owner reports rapid breathing and possible exposure to antifreeze containing ethylene glycol.

Temperature was 100.1 F, respiratory rate was 60, and heart rate was 170. Pulses were weak. The dog was lethargic and estimated to be 8% dehydrated based on skin turgor and dryness of mucous membranes. Heart sounds were muffled, and lung sounds were normal. The dog became progressively weaker and collapsed during the exam.

Interpretation of Urinalysis: The initial urine sample was collected before any treatments were started. The USG of 1.010 in the face of dehydration indicates impaired urine concentration that could be caused by a number of different disorders, including ethylene glycol ingestion. An osmotic diuresis happens shortly after the ingestion of ethylene glycol and its renal excretion before it is metabolized. AKI of any other cause is also under consideration as the cause for isosthenuria.

A biased examination of the urine sediment was performed to see if there were any calcium oxalate dihydrate or monohydrate crystals that could support the diagnosis of ethylene glycol intoxication, but none were found. However, absence of oxalate crystalluria does not exclude a diagnosis of ethylene glycol intoxication. Some animals with ethylene glycol intoxication have oxalate crystalluria within six hours of toxin ingestion; the number of crystals observed will depend on the amount consumed, the degree of metabolism, and the timing of the urine sample.

The presence of a large number of free small epithelial cells and renal tubular epithelial cell casts indicate that the kidneys are being actively damaged by some disease process (e.g. nephrotoxins, ischemia, or nephritis).

Further Diagnostics and Assessment: Thoracic radiographs disclosed an enlarged cardiac silhouette. Gas‐filled bowel loops were observed in the pericardial sac resulting in a diagnosis of pericardial diaphragmatic hernia.

Serum creatinine concentration was 3.7 mg/dL and BUN was 120 mg/dL. Azotemia in combination with a 1.010 USG immediately incriminates primary renal disease. The hematocrit was 54% and total protein concentration was 8.1 g/dL. A rapid point‐of‐care test for Leptospirosis was negative. Abdominal ultrasonography showed kidneys of normal size and a mild increase in echogenicity.

Dehydration was rapidly corrected, and the extracellular fluid volume expanded by intravenous administration of lactated Ringer’s solution to improve renal perfusion. Surgery was performed to decompress the hernia. The BUN and serum creatinine concentrations returned to normal within 72 hours after surgery and the hematocrit and total protein concentrations also returned to normal 24 hours after beginning fluid therapy.

The original identification of free renal tubular epithelial cells and epithelial cell casts in the urine sediment are attributed to ischemic AKI, secondary to reduced renal perfusion from the pericardial hernia and ECF volume contraction.

The initial azotemia is considered to be partly prerenal because it resolved with fluid therapy, but some of the azotemia is attributed to AKI since the USG was isosthenuric. Prerenal azotemia alone should result in elaboration of a USG >1.030.

Final Diagnosis: Prerenal and primary‐renal azotemia; ischemic AKI; pericardial diaphragmatic hernia.

CASE EXAMPLE: Urinalysis Case Number: 7

Signalment: 10‐year‐old spayed female mixed‐breed dog.

History and Physical Examination: This dog has been taking a longer time to urinate over the past several months. Stranguria has been noted over the past few weeks, and a small amount of red color has been observed in the urine on the ground. She has been licking her vulvar area more than usual during this time. Appetite and attitude are normal.

The dog was bright and alert and in good body condition. Moderately severe dental tartar and lenticular sclerosis in both eyes were noted. No abnormalities were detected on abdominal palpation and thoracic auscultation. Rectal palpation revealed a firm irregular thickening (approximately 1.5‐cm diameter) of the urethra along the pelvic floor; no pelvic lymphadenopathy was palpated.

Prominent urethral thickening can be caused by urothelial neoplasia (TCC) most commonly, or proliferative urethritis. UTI is not likely to account for this degree of urethral change by itself.

Interpretation of Urinalysis: UA results are from a mid‐stream voided urine collection. Voided urine, compared to cystocentesis, can provide more diagnostic material at times when the disease is mostly within the urethra.

Cloudy urine is accounted for by the active sediment findings (RBC, WBC, epithelial cells). The 1.031 USG shows adequate concentrating ability. The 7.5 pH on dipstrip can indicate the presence of a urease positive bacterial UTI or could represent a protracted post‐prandial alkaline tide (we do not know the timing of the urine collection in relationship to fasting or feeding). The 2+ protein is likely associated with the active urinary sediment findings. The 2+ occult blood aligns with the microscopic reports of RBC in the urinary sediment. The dipstrip showed both intact RBC and free hemoglobin on the dipstrip. The free hemoglobin is attributed to lysed RBC in the urine.

The predominant findings during microscopy were the increased RBC (20–30 per HPF), increased free and clumped transitional epithelial cells (10–15 per HPF), and a modest increase in WBC (5–10 per HPF). No bacteria were identified. These findings indicate the presence of inflammation, desquamation of epithelial cells, and hemorrhage. The pyuria could be the result of a bacterial UTI despite absence of identified bacteria. “Rafts” or clumps of urothelial cells are always of concern that they could arise from urinary tract neoplasia, but they sometimes arise during UTI and urolithiasis. There was no comment as to the morphology of the free or clumped epithelial cells, unfortunately.

The two differentials that need to be distinguished are TCC (UCC) of the urethra and proliferative urethritis.

Further Diagnostics and Assessment: CBC, serum biochemistry, thoracic radiographs, and abdominal radiographs were normal. Ultrasonography of the bladder was not performed since urethrocystoscopy was planned instead.

Unstained urine sediment from a voided urine collection was smeared on glass slides and submitted for standard dry mount cytology. Alternatively, urine could be submitted to the laboratory to then prepare the slides for cytology. Urine was not collected by cystocentesis since the process seemed to predominantly involve the urethra. Alternatively, aspiration biopsy of the urethra could have been performed during the passage of a urethral urinary catheter. Urine cytology from the voided urine sample revealed anaplastic transitional cells, some of which were binucleated.

A urinary catheter was passed into the urethra during the use of a handheld vaginoscope. The catheter was advanced with some resistance approximately 3–4 cm into the urethra. A sample of catheterized urine was submitted for bacterial culture and sensitivity and returned with >10 000 cfu/mL Escherichia coli. This level of quantitative bacterial growth of rods usually aligns with bacteria reported in the urinalysis, but that was not true in this case.

Urinary endoscopy showed a roughened and irregular distal and mid‐urethral mucosa. The proximal urethra, bladder neck, and bladder appeared normal except for focal hemorrhages. Projections of tissue into the urethral lumen that are attached on both ends that are typical of proliferative urethritis were not observed. Biopsy material retrieved using forceps resulted in the histopathologic diagnosis transitional cell carcinoma (UCC).

The dog was treated with amoxicillin for the bacterial urinary tract infection and with piroxicam for its palliative effects in dogs with transitional cell carcinoma. The dog improved considerably within the first month after beginning treatment but still had some difficulty urinating. The dog did reasonably well for approximately nine months after which time she began to lose weight, had a reduced appetite, and increased difficulty urinating. At that time, the owner elected euthanasia.

Final Diagnosis: Transitional cell carcinoma (urothelial cell carcinoma) of the urethra; bacterial UTI.

CASE EXAMPLE: Urinalysis Case Number: 8

Signalment: Eight‐year‐old spayed female Scottish Terrier dog.

History and Physical Examination: The owner reports the recent observation of blood in the dog’s urine. The dog’s urine during voiding is initially yellow but blood is observed toward the end of urination. There is also an increased frequency in urination. The dog seems systemically well with a good appetite and attitude. The dog was alert and in good body condition. There was moderately severe dental tartar. The bladder was thickened on abdominal palpation but without pain. No masses were palpated within the bladder wall or within the bladder lumen. Palpation of the kidneys was normal. Rectal examination was normal.

The history and physical examination findings in this dog are compatible with bladder neoplasia, cystic calculi, or a bacterial urinary tract infection. Scottish Terriers have the greatest risk for any dog breed to develop urothelial neoplasia (TCC or UC), so it is essential to rule this diagnosis in or out.

Interpretation of Urinalysis: Cloudy urine is attributed to the active urinary sediment (RBC, WBC, and epithelial cells). A USG of 1.033 shows good concentrating capacity. A highly alkaline urinary pH of 8.0 often develops in the presence of a urease‐producing bacterial UTI (Staphylococcus, Proteus, mycoplasma spp). The 2+ proteinuria on dipstrip is attributed to postrenal origin from the inflammatory/hemorrhagic increases in RBC and WBC observed during urine microscopy. The 2+ occult blood color reaction on the dipstrip was only for intact RBC, which matches up with the 15–20 RBC per HPF identified during microscopy. Pyuria at 10–15 WBC per HPF in association with some cocci in urinary sediment supports the presence of a bacterial UTI. Pyuria could also be secondary to inflammation arising from a bladder tumor or urinary stones. The finding of rare squamous epithelial cells is not clinically relevant as they sometimes enter normal urine that is collected by voiding. The 10–15 free transitional cells per HPF are clinically relevant, but no further details about their appearance was provided. Desquamation of transitional cells of this magnitude into urine is most common with urothelial neoplasia, but reactive desquamation from urolithiasis or UTI is still possible. Epithelialcyturia in a Scottish Terrier is worrisome for the diagnosis of urothelial neoplasia.

Further Diagnostics and Assessment: A hemogram and biochemical profile were within normal limits. Thoracic radiographs were normal. An end‐urination voided urine sample was collected and submitted for cytology. Results of urine cytology showed increased numbers of transitional cells with some atypical cytological features. Some of these cells were binucleate but differentiating neoplastic from reactive epithelial cells was not possible.

A focal mass involving the cranioventral aspect of the bladder was identified on both contrast cystography and bladder ultrasonography. Portions of the mass projected into the bladder lumen, but not in a way typical for polypoid cystitis. A urethrogram was normal. There were no lesions at the trigone, the location where about two‐third of TCC develop. No urinary stones were identified.

A sample of catheterized urine was submitted for bacterial culture and sensitivity and returned with >30 000 cfu/mL Staphylococcus aureus. The dog was treated with cefadroxil for the bacterial urinary tract infection.

At exploratory cystotomy, a 3‐cm mass was identified and was removed from the bladder by partial cranial cystectomy. Histopathology revealed the mass to be a transitional cell carcinoma. This diagnosis could have been achieved following cystoscopy, but surgery was chosen instead in order to remove what appeared to be a focal cranial bladder mass.

The dog improved considerably after surgery and did well for approximately 21 months while treated with piroxicam for its palliative effects on TCC. At 21 months, there was a recurrence of clinical signs and imaging studies disclosed multiple masses within the bladder. The owner elected euthanasia.

If the diagnosis had been in question earlier and the owners were unwilling to go further to get a tissue diagnosis, submission of a test to detect the BRAF mutation in epithelial cells shed into urine might have secured the diagnosis of TCC or UCC. The BRAF mutation exists in about 85% of dogs with this tumor.

Final Diagnosis: TCC of bladder apex. Staphylococcus UTI.

CASE EXAMPLE: Urinalysis Case Number: 9

Signalment: Six‐year‐old spayed female mixed‐breed dog.

History and Physical Examination: Decreased appetite, weight loss, and a bloated appearance of the abdomen were noted by the owners over the past month. The dog was thin and had a dry haircoat. The abdomen was distended, and a fluid wave was balloted. Hydration based on skin turgor was assessed as normal.

Interpretation of Urinalysis: The USG of 1.019 shows minimally concentrated urine, but it is not possible to tell if this is physiological or pathological by itself. The clear appearance to the urine aligns with a mostly inactive urinary sediment (only hyaline casts were seen during microscopy). Despite collection by cystocentesis, there was no increase in RBC in urinary sediment or occult blood dipstrip reaction. The most striking finding from the urinalysis is the 4+ dipstrip proteinuria. Remember that the urinary chemistry dipstrip for protein is most sensitive for the detection of urinary albumin. The hallmark of glomerular origin proteinuria is the finding of proteinuria associated with an inactive urinary sediment, as in this case. The observation of 2–4 hyaline casts per LPF is attributed to glomerular proteinuria, which favors the precipitation of the THP matrix protein. The presumptive diagnosis was glomerular disease (glomerulonephritis or amyloidosis). The marked proteinuria and the ballotable fluid wave in the abdomens provide suspicion for the presence of the nephrotic syndrome (NS).

Further Diagnostics and Assessment: The UPC was very high at 17.0, which confirms renal proteinuria, most of which is likely albumin. Dogs with advanced glomerular amyloidosis often have values above 10.0, but those with glomerulonephritis may have values that can range up to 40.0. GN and renal amyloidosis can have widely differing prognoses, so a renal biopsy is necessary to distinguish these two diseases. Amyloidosis is generally considered to be a relentlessly progressive disease.

A hemogram was normal except for low plasma proteins (5.0 g/dL; normal = 6.0–8.0 g/dL). On serum biochemistry, the dog was nonazotemic but had hypercholesterolemia (436 mg/dL), hypoalbuminemia (1.2 g/dL), and low serum proteins (4.5 g/dL). A sample of fluid obtained by abdominocentesis was interpreted as a pure transudate, attributed to the low oncotic pressure from the low circulating albumin.

The combination of severe glomerular proteinuria, hypoalbuminemia, hypercholesterolemia, and varying amounts of edema or body cavity effusions defines nephrotic syndrome (NS). NS can also be associated with accelerated clotting.

Ultrasound‐guided renal biopsy was performed after assessment of buccal mucosal bleeding time (1 minute; normal = <2 minutes) and systolic blood pressure by Doppler technique (110 mmHg; normal = 100–140 mmHg). Results of routine histopathology and immunofluorescence microscopy resulted in a diagnosis of membranous glomerulonephritis associated with immune complexes.

When possible, an antigen hunt (HW, SLE, vector‐borne titers, and leptospirosis) is undertaken in an effort to find an antigen that could be eliminated from the dog’s body with treatment. Often, the offending antigen is not determined no matter how extensive the antigen search. An extensive panel of possible antigens is costly and this owner did not allow the attending DVM to submit such tests.

A sodium‐restricted diet, furosemide, and the ACE‐I enalapril were prescribed for this dog. Re‐evaluation at four weeks showed stable laboratory results with continued proteinuria. Re‐evaluation at six months showed resolution of ascites, normal serum cholesterol concentration, and improvement in serum albumin concentration. The magnitude of the proteinuria had substantially declined (UPC of 2.9) and there still was no azotemia.

GN associated with immune complexes and NS are rarely observed to spontaneously go into remission. Perhaps the antigen provoking the development and deposition of immune complexes was no longer active. In many dogs with ICGN, persistent renal proteinuria and progression of intrarenal lesions continue unless aggressive immunosuppressive treatments are provided.

Final Diagnosis: Glomerulonephritis, nephrotic syndrome.

CASE EXAMPLE: Urinalysis Case Number: 10

Signalment: Eight‐month‐old spayed female Yorkshire Terrier dog.

History and Physical Examination: The puppy was bumping into walls and experienced an acute onset of generalized seizures over the past 24 hours. Prior to this time the dog appeared to be normal. The dog was very quiet on physical examination, but no specific abnormalities were detected.

The differential diagnosis included concerns for toxins, hepatoencephalopathy, other metabolic disorders, and structural brain disease (encephalitis and hydrocephalus).

Interpretation of Urinalysis: The urine sample was collected as a post‐void sample from the cage floor. The urine was described as cloudy, likely due to increased urinary sediment activity associated with free RTE and RTE casts. The low urine specific gravity (1.010) could have been the result of intravenous fluid therapy or due to renal tubular damage (see sediment activity). Unfortunately, there were no urinalysis results obtained before fluid therapy was initiated. 1+ protein on the chemistry dipstrip is likely indicative of renal proteinuria, especially in urine of low USG, but this was not further pursued with a UPC or MA test. The trace + reaction for occult blood occurred for free hemoglobin during the finding of 3–5 RBC per HPF; it is conceivable lysis of some RBC occurred in this instance. The occult blood reaction is more sensitive to free hemoglobin than to that in the intact RBC.

The most striking change during urine microscopy is the “shower” (5–10 per LPF) of cellular casts containing RTE. The 10–15 per HPF free epithelial cells were small. They had similar size and shape as those observed in the accompanying casts, suggesting common origin in the kidney (i.e. renal tubular epithelium). Some of the free epithelial cells had basal nuclei adding further credence to their identity as tubular in origin. Many of the RTE casts were tubular fragments, as entire contiguous tubular segments had sloughed into the urine rather than the addition of sporadic cells to a matrix protein.

Cellular casts are not found in normal urine. The finding of excessive numbers of renal tubular epithelial cells and epithelial cell casts/tubular fragments indicates marked damage to the renal tubular epithelium.

Further Diagnostics and Assessment: Examination of a blood smear on the CBC showed basophilic stippling and nucleated RBC in the absence of anemia. Based on these findings and the history, blood lead was submitted and returned with a concentration of >150 ug/dL (normal, <20 ug/dL) confirming the diagnosis of lead poisoning. Further questioning of the owners revealed that they lived in a very old house and were scraping paint from the interiors, the likely source for the puppy to ingest lead. BUN, serum creatinine, and serum phosphorus concentrations were initially normal and remained so throughout treatment. All other routine serum biochemical parameters were normal. Treatment consisted of IV calcium ethylene diamine tetraacetate (EDTA), intravenous fluids, and anticonvulsants as needed. The dog responded well to therapy.

Even though this dog remained nonazotemic, an episode of AKI can predict a future diagnosis of CKD associated with the initial nephron drop out in some animals. Consequently, routine twice yearly evaluation of serum biochemistry and urinalysis was recommended.

Final Diagnosis: Nonazotemic AKI due to nephrotoxic agents (lead and calcium EDTA).

CASE EXAMPLE: Urinalysis Case Number: 11

Signalment: Six‐year‐old spayed female Doberman Pinscher dog.

History and Physical Examination: Sudden onset of severe polyuria and polydipsia that was ongoing for one week. The dog is otherwise well. There were no abnormal findings on physical examination.

Interpretation of Urinalysis: The isosthenuric USG of 1.014 supports the historical complaint of PU/PD. The trace protein reaction on the dipstrip could indicate pathological proteinuria in a urine sample that is not concentrated, but this was not pursued further with UPC or MA testing.

The observation of cellular casts in urine is always abnormal and indicates some active process in the kidneys. White blood cell casts (0–1 per LPF) are associated with renal inflammation that is most commonly caused by bacterial infection (i.e. pyelonephritis). An occasional granular cast can be normal in concentrated urine. In the presence of a low USG and cellular casts, the presence of granular casts indicates renal tubular injury. Granules can form in casts as cells degenerate. The presence of WBC casts was likely detected in this case because of how quickly urine microscopy was performed after urine was collected. WBC casts are known to break up quickly, so they are infrequently identified during microscopy at later times.

The finding of only a few free white blood cells and no bacteria observed in the urine sediment does not support the diagnosis of a bacterial UTI. However, pyuria and bacteriuria can be intermittent and are not always observed in animals with upper urinary tract infection.

The presumptive diagnosis was bacterial pyelonephritis.

Further Diagnostics and Assessment: A routine serum biochemistry profile and hemogram were performed to evaluate renal function and any potential systemic response to the suspected renal infection – results were normal. Renal function is often normal in acute pyelonephritis in animals that are well hydrated. Neutrophilia and left shift can be observed in dogs with acute pyelonephritis, but often it is an early and transient finding. Bacterial urine culture returned with no growth of bacteria.

The dog was treated with a cephalosporin antibiotic for four weeks on the suspicion of upper urinary tract infection despite the negative culture. Polyuria and polydipsia resolved within four days and the dog appeared to be normal two years later. Urine specific gravity values greater than 1.025 were observed on numerous subsequent urinalyses.

Final Diagnosis: Pyelonephritis, bacterial.

CASE EXAMPLE: Urinalysis Case Number: 12

Signalment: Five‐year‐old castrated male Border Collie dog.

History and Physical Examination: The owner reports that the dog has urinated in the house and was observed to be lethargic while being watched by a friend when the owner was out of town; the owner believes the dog is producing a larger urine volume and drinking quite a bit more water for the past 7–10 days. He is well house‐trained and has not urinated in the house since he was a puppy. The dog seems to be “off” to the owners and is not as eager to finish his meals. He has free range of their farm for a few hours each day. Normal temperature, pulse, and respiration were found at presentation. Hydration based on skin turgor was assessed as normal. The dog was alert but very quiet during physical examination. No abnormalities were detected.

Interpretation of Urinalysis: The presence of a low USG at 1.008 supports the historical concern for polyuria and polydipsia. A 2+ protein dipstrip reaction usually indicates pathological proteinuria especially in urine that is not concentrated. The 1+ positive occult blood reaction for free hemoglobin on the dipstrip reagent pad may reflect lysis of erythrocytes despite limited numbers of erythrocytes in the urinary sediment. The proteinuria and mild pyuria (5–10 free WBC per HPF) could result from a bacterial urinary tract infection or nonbacterial inflammation; no bacteria were identified in the urinary sediment. The proteinuria with a low USG and minimal sediment abnormalities warrants follow‐up with a UPC and or MA. The three to five finely and coarsely granular casts per LPF in the face of 1.008 USG point to an intrarenal process with accelerated cellular degeneration in order to form these granular casts. Alternatively, some of the granular casts could represent precipitates of filtered proteins.

The presumptive diagnosis was renal disease of unknown cause to account for the dilute urine, proteinuria, and cylindruria.

Further Diagnostics and Assessment: The hemogram disclosed mild thrombocytopenia (72 000/μL) and hyperproteinemia (8.1 g/dL) with a normal leukogram. The biochemical profile disclosed azotemia (BUN 70 mg/dL and creatinine 7.1 mg/dL), hyperphosphatemia (8.4 mg/dL), hyponatremia (134 mEq/L), hypochloremia (106 mEq/L), and hypokalemia (3.0 mEq/L). A clotting profile was within normal limits except for mild thrombocytopenia.

Radiographs and abdominal ultrasonography revealed enlarged kidneys (9–9.5 cm long) with poor corticomedullary distinction on ultrasonography.

Urine culture yielded no growth and the urine protein‐to‐creatinine ratio was 4.0. The high UPC can indicate tubular and or glomerular origin in those with leptospirosis (see serology below).

The dog’s azotemia and hyperphosphatemia became progressively worse over the next few days (serum creatinine 9.3 mg/dL, BUN 101 mg/dL, and serum phosphorus 9.5 mg/dL) and the dog became oliguric. An exploratory laparotomy was performed to place a peritoneal dialysis catheter and a renal biopsy was taken. The surgeon remarked that the kidneys were very swollen, and that the renal parenchyma bulged from the incision that was made in the renal capsule. Histopathology disclosed acute interstitial nephritis characterized by infiltration of neutrophils, lymphoplasmacytes, and severe edema. The dog was treated with ampicillin and aluminum hydroxide and underwent peritoneal dialysis for approximately two weeks.

Serology for leptospirosis was performed twice over a 10‐day interval. A fourfold increase in titer was found for serovars pomona and bratislava and a twofold increase for grippotyphosa. At the time of release from the hospital, the dog’s serum creatinine concentration was 2.4 mg/dL and BUN was 40 mg/dL. After the amoxicillin treatment, doxycycline was given to the dog in order to help clear leptospiral organisms from the kidneys. The dog eventually made a full recovery.

Final Diagnosis: Azotemic AKI due to leptospirosis.

CASE EXAMPLE: Urinalysis Case Number: 13

Signalment: Four‐year‐old castrated male Domestic Longhair cat.

History and Physical Examination: The cat had experienced four episodes of urethral obstruction over the past six months. During each episode, the cat was treated by use of an indwelling urinary catheter for at least 24 hours, antibiotics, and glucocorticoids. The cat has had signs of lower urinary tract irritation between episodes of urethral obstruction (e.g. stranguria and pollakiuria). Perineal urethrostomy was performed to prevent future episodes of obstruction and the surgical procedure went well. A region of urethral stricture was observed and corrected during surgery. Urine flow through the urethrostomy site was excellent. The cat had a poor appetite postoperatively and was lethargic. Body temperature was 103.0 °F; normal auscultation of heart and lungs, hydration based on skin turgor, and abdominal palpation were found on physical examination. The bladder was small and nonpainful, and the kidneys were normal to mildly enlarged, but not painful.

Interpretation of Urinalysis: This urine sample was collected from the surface of the exam table two days after surgery. It is not possible to assess urinary concentrating capacity since the USG of 1.008 was measured while the cat was on IV fluids; no presurgical or prefluids USG was determined. The cylindruria (see later on microscopy) and low USG could indicate the presence of primary renal disease. The 2+ proteinuria and the 2+ occult blood along with the 10–15 RBC per HPF are attributed to the underlying inflammation and hemorrhage from the urethral obstructions, intervening cystourethritis, and surgical trauma. Pyuria is not present, but the cat is being treated with antibiotics and this could reduce pyuria even in the presence of infection. Also, one to three WBCs per HPF in dilute urine may be more clinically relevant than a similar number in concentrated urine. Lastly, treatment with glucocorticoids may have suppressed WBC diapedesis into urine. The few cocci‐like bacteria are difficult to interpret because the sample was collected from a cleaned litter pan.

Most alarming in this urinalysis is the degree and type of cylindruria. The finding of granular casts at two to four per LPF in urine that is not concentrated likely indicates renal tubular cell degeneration. The one to two hyaline casts per LPF were surprising to find as it is more difficult for these casts to form in urine that is this dilute. The presence of broad casts (hyaline and granular) suggests dilatation of some portions of the nephron. The finding of waxy casts is of concern as this implies substantial intrarenal stasis. The presence of waxy casts suggests some chronicity since waxy casts take the longest time to be formed in the kidney.

At this point, the presumptive diagnosis was chronic pyelonephritis.

Further Diagnostics and Assessment: Mild leukocytosis with a left shift was observed on the hemogram; it was not present two days before surgery. Renal function as evaluated by BUN and serum creatinine concentrations was normal before and after surgery. Ultrasound examination after surgery showed bilateral dilatation of the renal pelves and diverticulae. These findings provide support for a diagnosis of pyelonephritis. Pyelonephritis could have been caused by bacterial infection that was not documented and/or by multiple episodes of urethral obstruction affecting the kidneys.

After surgery, bacterial culture of a midstream voided sample of urine returned with no bacterial growth at a time when the cat was being treated with antibiotics. Several days after changing antibiotics, the cat’s fever abated, and he began to eat. He was treated with antibiotics for six weeks. Serial urinalysis showed resolution of the cylindruria, but the USG at 1.020–1.025 remained lower than expected for normal cats (≥1.035 USG) on several urine samples. He had no further episodes of urethral obstruction or signs of lower urinary tract inflammation during the next year. Surveillance of renal function was suggested based on our suspicion for early CKD.

Final Diagnosis: Pyelonephritis.

CASE EXAMPLE: Urinalysis Case Number: 14

Signalment: Eight‐year‐old intact male Basset Hound dog.

History and Physical Examination: Poor appetite for the past few weeks and vomiting two to three times a day for the past week have been observed. Prior to this time, the dog had no known prior health problems. On physical examination, the dog had a dry haircoat and was slightly thin. The dog’s skin turgor was decreased suggesting moderate dehydration. The prostate was moderately enlarged with some loss of the median raphe, but not painful. Fundic examination revealed partial retinal detachment in the left eye and several retinal hemorrhages in the right eye. Systolic blood pressure measured by Doppler was 190 mmHg (normal = 110–140 mmHg).

Interpretation of Urinalysis: The 1.016 USG during dehydration shows impaired urinary concentrating capacity as the USG at these times should be much higher (>1.040 USG). The dog had not received any drugs (e.g. corticosteroids, furosemide) that might have interfered with concentrating ability.

The presence of heavy proteinuria (500 mg/dL) based on urinary dipstrip with low urine specific gravity and mostly inactive urinary sediment suggests the presence of underlying glomerular disease (glomerulonephritis, glomerular amyloidosis, or glomerulosclerosis).

The mild increase in leukocytes (five to seven free WBC) in the urine sediment may reflect underlying prostatic disease, a bacterial urinary tract infection, nonspecific change during inflammatory renal disease, or may be clinically insignificant. There were no bacteria identified during urine microscopy to further indicate bacterial urinary infection.

The presumptive diagnosis at this point was glomerular disease (glomerulonephritis, amyloidosis, and glomerulosclerosis).

Further Diagnostics and Assessment: A nonregenerative anemia (PCV 34%) and lymphopenia (500/μL) were noted on the CBC. A serum biochemical panel revealed increases in BUN of 145 mg/dL, creatinine of 8.4 mg/dL, phosphorus of 9.2 mg/dL, cholesterol of 402 mg/dL, and a CK of 875 IU/L. Decreased serum bicarbonate at 11 mEq/L, albumin at 1.8 g/dL, and total proteins at 5.3 g/dL were also observed.

Abdominal radiographs were performed to evaluate renal size and showed the kidneys to be at the upper limit of normal in size. Prostatomegaly and mild splenomegaly were also noted. Quantitative urine culture was negative for bacterial growth.

The dog was treated with intravenous lactated Ringer’s solution, famotidine, aluminum hydroxide, and amlodipine. After two days of fluid therapy, azotemia was improved but not resolved (BUN 85 mg/dL and creatinine 6.1 mg/dL). Serum phosphorus and bicarbonate concentrations had returned to normal. The nonregenerative anemia was more severe with a PCV of 30%. These changes were attributed to rehydration and resolution of prerenal azotemia. Blood pressure gradually returned to normal during escalating doses of amlodopine.

The owner elected to have ultrasound‐guided renal biopsy performed despite a guarded prognosis. On light microscopy, glomeruli were hypocellular with presence of amorphous pink material on H&E‐stained sections. This material demonstrated green birefringence when stained with Congo red and examined by polarization microscopy. Moderately severe interstitial fibrosis and infiltration of lymphocytes and plasma cells also were observed. Tubular atrophy and focal tubular dilatation were also noted.

The UPC was initially 6.4 and declined to 2.8 when high systemic blood pressure was controlled. Addition of an ACE‐I or ARB to further reduce glomerular proteinuria was considered but not implemented. The reason that renal amyloidosis develops is often elusive, but chronic infectious, inflammatory, and neoplastic diseases are found at times. It is possible that prostatic disease contributed to the development of renal amyloidosis in this case, but the prostate was not further evaluated.

Final Diagnosis: CKD; Glomerular amyloidosis with secondary chronic tubulointerstitial nephritis.

Only gold members can continue reading. Log In or Register to continue

Stay updated, free articles. Join our Telegram channel

Tags: Urinalysis in the Dog and Cat

Apr 18, 2023 | Posted by admin in SMALL ANIMAL | Comments Off

Veterian Key

Fastest Veterinary Medicine Insight Engine

10: Case Studies

CHAPTER 10
Case Studies

Full access? Get Clinical Tree