Laboratory testing of renal function Flashcards
(133 cards)
1
Q
What tests are usually used to diagnose renal disease?
A
Serum urea and creatinine levels
AND
Urinalysis
2
Q
At what point does the kidney lose the ability to concentrate urine?
A
Once 66-75% of renal mass has been lost
3
Q
At what point does the kidney lose the ability to excrete nitrogenous waste - leading to azotaemia?
A
Once >75% of the nephrons are non-functional
4
Q
Azotaemia
A
elevated blood concentrations of non-protein nitrogenous wastes (urea and creatinine) in the blood
5
Q
What % of urea is reabsorbed in the kidney?
A
About 40%
6
Q
Why does hypovolaemia/hypoperfusion lead to azotaemia?
A
Reduced GFR
7
Q
Which marker is more markedly increased in pre-renal azotaemia?
A
Urea
Tubular flow rate will also be decreased, which will in turn cause increased water (and urea) reabsorption in the kidney.
serum urea concentration can underestimate renal function in dehydrated animals
8
Q
When are serum urea concentrations increased?
A
Reduced renal excretion
○ hypovolaemia/reduced perfusion
○ renal disease
Gastrointestinal bleeding
High dietary protein content
○ Should stave animals for 12 hours prior to taking bloods and urine
High rate of endogenous protein catabolism
○ e.g. hyperthyroidism, prolonged starvation, pyrexia
9
Q
When are serum urea concentrations decreased?
A
Portosystemic shunt
Marked hepatocellular dysfunction/failure (70-80%)
Low protein diet
Glucosuria
Diabetes insipidus (central or nephrogenic)
10
Q
Creatinine production
A
Mainly derived from breakdown of creatine in skeletal muscle.
In addition, a small amount of ingested creatinine contributes to the serum creatinine concentration (hence the need to starve animals prior to sampling).
Creatinine production is constant and is related to the amount of skeletal muscle mass.
11
Q
When might serum creatinine levels be decreased?
A
Animals with low muscle mass - emaciated
12
Q
Removal and metabolism of creatinine
A
In the circulation, creatinine is not protein bound and is freely filtered by the glomerulus.
Unlike urea, there is minimal tubular reabsorption or secretion of creatinine (in domestic species), although some creatinine can be removed and metabolised by bacteria in the gut in severe renal disease.
13
Q
Which parameter is a better marker of of GFR?
A
Serum creatinine is less influenced by hydration status than serum urea, and so is a better marker of GFR, in general (provided that muscle mass is normal).
14
Q
Urea vs creatinine
A
Urea is more influenced by non-renal factors (particularly dehydration) than creatinine
Serum creatinine concentrations are a more reliable marker of GFR/renal function than serum urea concentrations provided muscle mass is normal
Serum creatinine concentration is best, commonly used marker of renal function in animals
15
Q
What does SDMA stand for?
A
Symmetric dimethylarginine
16
Q
What can serum SDMA levels tell you?
A
Produced in the nucleus of all nucleated cells at a constant rate.
Released into the blood where it is freely filtered at the glomerulus and excreted into the urine.
Inversely correlated with GFR, similar to serum creatinine concentrations.
However, because SDMA is produced by all cells (unlike creatinine which is only produced by muscle cells), it should be less affected by the reduced muscle mass which can occur in animals with chronic diseases like CKD.
Therefore it has been suggested that it might be a better marker of GFR in animals with reduced muscle mass.
17
Q
Testing SDMA levels
A
Expensive relative to serum creatinine and urea so should be reserved for non-azotaemic animals with marked loss of muscle mass where you suspect
18
Q
Serum urea and creatinine in hyperthyroidism
A
An increased GFR, even in animals with concurrent renal disease, which will contribute to reduced serum urea and creatinine concentrations.
Hyperthyroid cats also have reduced body muscle mass (due to muscle catabolism) which will reduce serum creatinine concentrations.
The increased muscle catabolism will increase serum urea concentrations and the polyphagia will also increase dietary protein intake which can also contribute to an increased serum urea concentration.
19
Q
Serum urea and creatinine in hypothyroidism
A
decreased GFR, even in animals without renal disease, which will increase the serum urea and creatinine concentrations.
20
Q
Pre-renal causes of azotaemia
A
Decreased renal perfusion
o Dehydration
o Hypovolaemia/blood loss
o Heart failure (failure to perfuse kidney effectively – cardiorenal syndrome)
Increased production of nitrogenous wastes (mainly increasing urea)
o High protein diet
o Gastrointestinal haemorrhage
o Increased protein catabolism (e.g. hyperthyroidism)
21
Q
Causes of renal azotaemia
A
Intrinsic renal disease and can be due to either an acute kidney injury (AKI, often known as acute renal failure or ARF) or chronic kidney disease (CKD or often called chronic renal failure, CRF).
22
Q
Causes of post renal azotaemia
A
Conditions of the lower urinary tract which prevent nitrogenous wastes from being removed from the body.
This would include urethral obstruction (e.g. in cats) and urinary tract rupture/uroperitoneum.
23
Q
Expected USG in pre-renal azotaemia
A
> 1.030 dog
1.035 cat
1.025 horse
24
Q
Serum potassium concentration in pre-renal azotaemia
A
Usually normal (increased with hypoadrenocorticism)
25
PCV/plasma in pre-renal azotaemia
Both may be increased
26
History/clin exam expected in pre-renal azotaemia
Dehydration, shock, blood loss, decreased cardiac output
27
Response of azotaemia to IV fluids in pre-renal azotaemia
Complete resolution
28
Expected USG in renal azotaemia
AKI - variable
CKD - 1.007-1.029 (dog)
CKD - 1.007 - 1.034 (cat)
29
Serum potassium concentration in renal azotaemia
AKI - normal or increased
CKD - normal or decreased
30
PCV/plasma proteins in renal azotaemia
PCV may be decreased (CKD)
Plasma protein is normal
31
History/clinical exam expected in renal azotaemia
Sudden onset (AKI)
PUPD (CKD)
32
Response of renal azotaemia to IV fluids
Initial improvement if some pre-renal component
33
Expected USG in post-renal azotaemia
Variable
34
Serum potassium concentration in post renal azotaemia
Usually increased
35
PCV/plasma protein in post-renal azotaemia
Normal
36
Expected history/clin exam in post renal azotaemia
Dysuria
Enlarged/ruptured bladder
Uroabdomen
37
Response of post-renal azotaemia to IV fluids
Minimal imporvement if obstruction/rupture not resolved
38
What is the main distinguishing criteria between Pre-renal and renal azotaemia?
Urine specific gravity
39
Parameteres useful for determining if azotaemia is pre-renal or renal?
USG
PCV
Serum TP
Clinical history
40
What can falsely increase USG?
Lots of glucose or protein in the urine
Heavily haemocontaminated or haemoglobinuric samples
41
Is low USG a specific marker of renal disease?
No
However if urine is concentrated (so high USG) then unlikely to have renal disease
42
USG >1.030 (dog) or >1.035 (cat)
Normal renal concentrating ability
43
USG 1.013-1.029 (dog) or 1.013-1.034 (cat)
Suboptimally concentrated urine
44
USG 1.007-1.013
Isosthenuric
45
USG <1.007
Hyposthenuric
46
USG in prerenal azotaemia
Kidney trying to conserve as much water as possible so normal range of USG
47
USG in renal azotaemia
suboptimally concentrated (early disease and residual tubular function) or isosthenuric urine (USG 1.007-1.013).
48
What is normal USG in non-azotaemic animals?
Concentrated as well as hyposthenuria, isosthenuria or suboptimal urine concentration may be normal.
49
Hyposthenuria
USG <1.007 and indicates that the urine concentration (osmolality) is below that of urine ultrafiltrate within the Bowman’s capsule (which corresponds to the plasma osmolality).
Actively diluted so the tubules have to still be functional, and therefore not typically seen in animals with renal disease and renal tubular dysfunction.
Usually caused by a lack of ADH production (central diabetes insipidus) or ADH activity in the collecting duct (nephrogenic diabetes insipidus, e.g. hypercalcaemia or hyperadrenocorticism).
Could be normal in a dog without a history of polydipsia and polyuria.
50
When would you suspect post-renal azotaemia?
Post renal azotaemia cannot be distinguished from either pre-renal or renal azotaemia using USG.
Post renal azotaemia can be suspected based on the combination of azotaemia and:
· Compatible clinical signs and history (e.g. large bladder, abdominal fluid, history of dysuria)
· Elevated serum potassium concentration
(However this can also be elevated in acute kidney injury or secondary to artefactual changes such as delayed serum separation or EDTA contamination)
51
Potassium handling by the kidney
Excess dietary potassium or potassium released from cells is excreted from the body by the kidneys through the urine.
Renal excretion relies on maintenance of a favourable concentrating gradient for potassium movement from tubular epithelial cells into the urine by continued urine flow.
52
What happens to potassium in AKI?
Animals with acute kidney injury (oliguric or anuric) can develop hyperkalaemia due to reduced urine flow rate through the nephron which diminishes the concentration gradient for potassium excretion in the distal tubule.
53
What happens to potasssium in pst-renal azotaemia?
hyperkalaemic due to leakage of urine (which is rich in potassium) back into the body.
54
What happens to potassium in cats with CKD?
Hypokalemic because of polyuria and increased urinary flow rate, which enhances the concentration gradient for potassium excretion and thus increased potassium losses in the urine.
55
What happens to potassium in pre-renal azotaemia?
Secondary to dehydration/hypovolaemia is not associated with hyperkalaemia, because ADH (which is increased in hypovolaemic states) will itself stimulate renal potassium excretion.
56
When might hyperphosphataemia occur with azoataemia?
Occurs in any condition associated with decreased GFR, therefore phosphate can be increased in all forms of azotaemia (pre-renal, renal, post-renal).
Early renal disease PTH secretion stimulates reduced phosphate resorption so hyperphosphataemia only in progressed renal disease.
57
What increases serum phosphate levels
Reduced GFR
Tissue necrosis
Low PTH
Young age
58
What reduces serum phosphate levels?
High PTH
Phosphate restricted diets
Phosphate binders
Rapid insulin action
59
What happens to calcium levels in renal disease?
May be increased, normal, or decreased
60
Why might animals with renal disease develop ionised hypocalcaemia?
calcium precipitates as calcium phosphate under influence of high phosphorus
bones acquire resistance to PTH induced calcium mobilization
reduced calcitriol synthesis in the kidneys reduces GI calcium uptake
61
Why might animals develop total and ionised hypercalcaemia in renal disease?
more calcium complexes with phosphates and other ions, increasing total calcium concentrations
the parathyroid glands hypertrophy and reset their trigger point at which to respond to hypercalcaemia, causing increases in total and ionized levels (tertiary hyperparathyroidism)
62
What happens to amylase and lipase in azotaemia?
any reduction in GFR (pre-renal, renal, post-renal azotaemia) will cause a retention of amylase and lipase and increased serum amylase and lipase activity, despite the pancreas being normal
63
What heppens to PCV in azotaemia?
Since the kidney produces erythropoietin, animals with CKD may have a non-regenerative anaemia.
Sometimes treatment with erythropoietin (or analogues like darbopoietin) can be indicated in anaemic animals with CKD in which anaemia is adversely affecting their quality of life.
Animals with pre-renal azotaemia may have increased PCV if they are dehydrated or hypovolaemic.
64
What happens to serum sodium levels in azotaemia?
Sodium concentrations are usually very tightly controlled by renal regulation of excretion and reabsorption.
Plasma sodium is generally held at normal levels until the very terminal stages of renal disease when they can either increase or decrease.
65
What is involved in a complete urinalysis?
USG, dipstick analysis, sediment analysis
66
When should you get a urine sample?
First thing in the morning is the best time to assess concentrating ability
If also taking bloods then best to get both samples at the same time
ALWAYS before they are put on lfuids
67
Methods for obtaining a urine sample
Free catch
Catheterised samples
Cystocentesis
68
Free catch urine sample
Mid-stream
Clean container
Don't touch animal
Limited use for urine culture
69
Catheterised urine sample
Easiest in male dogs > male cats > female dogs - v hard in female cats
Need at least two people, chemical restraint needed in most cats
Easy to introduce infection so ensure sterility where possible
Not ideal for urine culture
70
Cystocentesis urine sample
Needle through abdo wall - blind or with US
Sterile sample
May contain small amounts of blood (iatrogenic contamination)
71
What pot to put a urine sample in
Plain pots
Boric acid can reduce liklihood of a postive urine culture
72
When to look at a urine sample
ASAP
Degereative changes after 30mins
Out in fridge for a max of 6-12hrs
73
What degeerative changes can occur in urine that has been left for too long?
Casts will disintegrate
pH may increase
Bacteria will grow - hard to know if genuine or contaminants
Struvite crystals will form
74
Gross assessment of urine sample
Assess your sample for colour, turbidity, sediment.
Urine is generally pale yellow to straw coloured.
Normal rabbit urine can have variable colour and be quite turbid. Horse urine can also turn red or brown during storage or on exposure to snow.
75
USG measurement
Always use a refractometer for this, and interpret your results in conjunction with the history, clinical examination, dipstick analysis and ideally with bloods to look at renal function if that is the reason for sample collection.
Large amounts of blood, glucose or protein in the urine may also increase the USG (usually not more than 0.005-0.01 units).
When checking a USG, it is preferable to centrifuge the sample first and analyse the supernatant.
76
Dipstick examination of urine
First check that:
This is a very easy examination to perform IF:
· Sticks are in date and have been stored as instructed
· Fresh urine is used, which has been in plain tubes, not boric acid.
· Samples are brought to room temperature and protected from direct sunlight prior to analysis
· The instructions are followed – pads have different times at which they should be examined and the colour changes are accurately read.
Several dipstick types are available, and some just look at glucose and ketone levels.
Some parameters are not useful in animals: leukocytes and USG.
77
Normal urine pH
The pH of normal carnivore urine is 6.0-7.5, and for herbivores is 7.5-8.5.
78
Causes of increased urine pH
Urease bacteria/UTI
Old sample
Transient alkalinuria after a meal
Metabolic alkalosis
79
Causes of decreased urine pH
Metabolic acidosis
Renal tubular acidosis
Hypokalemia
80
Common causes of error in dipstick pH estimation
Leaching from protein pad onto pH pad (as protein pad contains alkaline substances)
Pigmenturia (e.g. marked haematuria or haemoglobinuria)
81
Measurement of urine protein by dipstick
Small amounts of protein on a dipstick may be normal, though again this should be interpreted in light of the USG – a trace of protein is fine if urine is concentrated, but if the urine is dilute, this is more of a concern.
The urine dipstick only detects albumin, not globulins or Bence Jones proteins.
82
Common causes of error in dipstick protein estimation
False positives are common in cats due to the presence of the protein cauxin in the urine
Highly alkaline urine (pH >8.0)
Gross haematuria and pigmenturia
Chlorhexidine
Some disinfectants
83
Sulphosalicylic acid turbidity test (SSA)
semi-quantitative test or proteinuria. It is better for detection of Bence Jones proteins than the dipstick.
84
Urine protein:creatinine (UPC) ratio
The quantity of protein present is compared to the creatinine, used as a measure of GFR to counteract the USG variations.
UPC will not be reliable if there is any urinary tract inflammation.
85
Normal UPC
<0.5 for dogs and < 0.2 for cats
86
What can artificially increase the UPC?
Marked blood contamination (>200 RBCs/hpf) will increase UPC.
87
Protein handling by the kidney
The normal urine of animals contains only a small amount albumin and other proteins because the glomerulus is selectively permeable which minimises protein filtration and excretion.
Most proteins that are filtered and which enter the urine are reabsorbed in the proximal convoluted tubules by pinocytosis.
88
Transient proteinuria
secondary to exercise, pyrexia or seizures (physiological proteinuria)
89
Categories of pathological proteinuria
Post renal
Renal glomerular
Renal tubular
Pre-renal
90
Post-renal proteinuria
Most common cause
excretion of protein from the urinary tract in response to inflammation and/or infection.
proteinuria of any magnitude.
UPC up to 40.8 possible with UTI (in dogs).
important to check the urine sediment and dipstick to rule out urinary tract inflammation which might falsely increase the UPC.
Blood alone (without inflammation) should not increase the UPC unless the urine is grossly haematuric.
91
Renal glomerular proteinuria
caused by reduced selectivity of the glomerular barrier.
Usually associated with marked proteinuria with UPC >2. E.g. glomerulonephritis, amyloidosis.
92
Renal tubular proteinuria
caused by reduced reabsorption of proteins in tubules, therefore associated with lower magnitude of proteinuria.
e.g. renal tubular disease (feline CKD), hypertension, hyperthyroidism, hyperadrenocorticism, steroid therapy, systemic inflammation.
93
Pre-renal proteinuria
caused by increased serum concentrations of small proteins (e.g. myoglobin or paraproteins) which can pass through the glomerular barrier.
Amounts of these proteins exceed the capacity of the tubules to reabsorb them.
Relatively uncommon cause of proteinuria.
94
UPC persistently elevated and active sediment/grossly haematuric sample
Probably post renal proteinuria
95
UPC persistently elevated and evidence of intravascular haemolysis, myopathy, myeloma (increased globulins)
Consider pre-renal proteinuria (uncommon)
96
UPC persistently elevated >2, no active sediment or grossly haematuric sample
Probably renal glomerular proteinuria
97
UPC persistently elevated, but <2, no active sediment or grossly haematuric sample
Possible renal tubular proteinuria
98
Urine glucose
Glucose is freely filtered at the glomerulus and normally fully reabsorbed in the tubules, leaving no glucose in the final excreted urine sample of normal animals.
Glucose concentration in urine can be determined by urine dipstick examination.
99
Categories of the causes of glucosuria
Hyperglycaemia glucosuria
Normoglycaemic glucosuria
100
When is renal tubular transport of glucose exceeded (too much glucose in blood for kidneys to deal with)
cats – 16 mmol/L,
dogs – 10-12 mmol/L,
horses and cattle – 8 mmol/L
101
Common causes of hyperglycaemic glucosuria
Stress (especially in cats)
Diabetes mellitus
Insulin resistance (e.g. hyperadrenocorticism)
102
Causes of normoglycaemic glucosuria
occurs due to marked renal tubular injury which reduces transport maximum,
e.g. Leptospirosis, very end stage CKD, congenital or acquired Fanconi syndrome
103
Common causes of false positives in dipstick urine glucose estimation
Chlorine bleach (e.g. contaminants from floor)
Cephalosporins
Enrofloxacin
104
Common causes of false negatives in dipstick urine glucose estimation
Cold samples – therefore ensure samples come to room temperature before analysis
Marked bilirubinuria
105
Measurement of urine ketones
Can be measured by urine dipsticks
Urine dipsticks will detect acetone and acetoacetate, however they do not detect beta-hydroxybutyrate (the first and most abundant ketone produced when in NEB), therefore it is possible that an animal can be ketonaemic without a positive dipstick ketone result (i.e. low sensitivity for ketosis).
106
What is ketonuria a reflection of?
Ketonaemia which occurs when there is a shift in energy production from carbohydrates to lipids, usually as a consequence of negative energy balance.
107
What biochemistry changes can accompany ketonuria?
Hyponatraemia and hypokalaemia due to urinary losses of cations
108
Causes of ketonuria
Diabetic ketosis/ketoacidosis
Ketosis in cows (lactational)
Severe starvation
109
Common cause of error in dipstick ketone estimation
Pigmentiuria (false positives)
110
How to determine haematuria/haemaglobinuria/myoglobinuria
Urine dipsticks give an estimate of amount of haem/blood, however the pad cannot distinguish haematuria, haemoglobinuria and myoglobinuria.
Haematuria can be distinguished from haemoglobinuria/myoglobinuria by sediment examination.
If red cells are present, they should be present in the urine sediment.
111
How to distinguish haemoglobinuria from myoglobinuria
Haemoglobinuria – might see anaemia, possible evidence of regeneration (if not pre-regenerative), possibly Coombs test positive (if caused by IMHA) or evidence of red cell injury on smear (Heinz bodies, acanthocytes, schistocytes)
Myoglobinuria – usually expect to see markedly increased serum CK activity (provided sample is not haemolysed!)
112
Common causes of error in dipstick haem estimation
Chlorine bleach (false positive)
Bacterial and leukocyte peroxidases (false positive)
113
Urine bilirubin
Bilirubinuria can be detected on dipstick and mild bilirubinuria (1+ or 2+) can be a normal finding in dogs.
Bilirubinuria is not a normal finding in cats.
114
Causes of pathological bilirubinuria
Reflects hyperbilirubinaemia which is caused by:
· Haemolytic disease (pre-hepatic hyperbilirubinaemia)
· Hepatocellular dysfunction (hepatic hyperbilirubinaemia)
· Cholestasis (post-hepatic hyperbilirubinaemia)
115
Common causes of error in dipstick bilirubin estimation
Prolonged sunlight exposure (false negative)
Pigmenturia (false positive)
116
Urine sediment analysis
Use about 5ml urine, and spin it down at 1000rpm for about 5 minutes.
Decant off the supernatant, and use the few drops remaining to resuspend the sediment, use 1 drop of sediment to place on a microscope slide with a cover slip.
117
Crystals that can be found in urine
Struvites
Calcium oxalate dehydrate
Calcium oxalate monohydrate
Calcium carbonate
Ammonium biturate/uric acid
Calcium phosphate
Cysteine
118
Struvites
Sort of roof shaped (rectangular). Have a coffin lid appearance and are quite variable in size.
Magnesium ammonium phosphate
Can be present in low numbers in normal dogs and cats, form in alkaline urine and in the presence of urease producing bacteria.
Consider urine culture if they are present.
Not a reliable indicator of struvite urolithiasis.
119
Calcium oxalate dehydrate
Have a maltese cross structure.
Can also be present in low numbers in normal dogs and cats.
May lead to formation of calcium oxalate uroliths and can be associated with hypercalcaemia or rarely ethylene glycol toxicity.
120
Calcium oxalate monohydrate
These crystals have a needle like shape in dogs and in cats can have rounded ends or a dumbbell shape. Sort of pad-like in appearance
Rarely seen in normal urine of dogs and cats.
Tend to be pathological in origin and associated with:
○ Ethylene glycol toxicity
○ Hypercalcaemia
121
Calcium carbonate
Roundish with darker outline.
Common and normal in urine of horses and cows.
122
Ammonium biturate/uric acid crystals
Have a thorn apple or mite like appearance - its giving coronavirus a little.
Associated with hepatic disease, especially portosystemic shunts.
Dalmatians have a metabolic defect leading to the formation of ammonium biurates.
123
Calcium phosphate
Small, needle like clusters
May be seen in normal dogs, but most commonly associated with hypercalcemia, may be associated with urolithiasis
124
Cysteine crystals
Form in acid urine, found as a familial tubular resorption defect in Bulldogs, Dachsunds and Chihuahuas
125
Cells in urine
Red and white cells in low numbers (<5/hpf) may be normal, as are small numbers of transitional epithelial cells from the bladder lining.
Increased white cell levels reflect infection or inflammation.
Red cells may be present as iatrogenic contaminants if the sample was taken by cystocentesis, or could reflect other causes of haematuria.
126
What can sometimes be mistaken for red cells in urinalysis?
Lipid droplets
127
Bacteria on urine smear
Can be seen on dry smear, both with or without pyuria or haematuria.
Sometimes lipid droplets or other debris can imitate bacteria.
If you suspect bacteria are present, then air dry the preparation and stain with Diff Quik in order to visualise them and confirm.
128
Casts on urinary smear
Casts are formed in the renal tubules from mucoprotein secreted by the renal tubular epithelial cells.
These condense to form hyaline casts, which may acquire cellular debris to become granular casts, or lipid droplets to become fatty casts.
These then deteriorate to become waxy casts with age.
Normal urine contains very few hyaline or granular casts, but increased numbers reflect tubular damage.
129
Indications for cytology of the urinery bladder
when a mass is visualised on ultrasound or cystoscopy
130
How to obtain samples for cytology of the urinary bladder
suction biopsy technique is preferential to performing urine cytology because cells in the urine quickly develop morphological artefacts that make interpretation very difficult.
It is advisable to avoid fine needle aspiration of bladder masses due to the risk of seeding the tumour cells into the abdominal cavity.
131
How can you diagnose urothelial carcinoma?
If the epithelial cells from the bladder wall obtained by suction biopsy show marked criteria of malignancy in the absence of inflammation.
However if there is concurrent inflammation (e.g. a urinary tract infection), then differentiating between epithelial cell dysplasia and neoplasia is very difficult on cytology alone, and a biopsy for histopathology is likely to be needed to confirm the diagnosis.
132
Diagnosis of prostatitis
Prostatitis can be diagnosed if there is neutrophilic inflammation present within the sample (suction biopsy), and bacteria may also often be seen.
Culture should be performed on the samples to confirm bacterial involvement and antibiotic sensitivity.
133
Prostatic wash samples from dogs with BPH vs prostatic carcinoma
BPH will yield sheets of monomorphic epithelial cells that show minimal or no criteria of malignancy, whereas samples from dogs with prostatic carcinoma will contain epithelial cells with marked criteria of malignancy.
However a diagnosis of carcinoma cannot often be confidently made on cytology alone if there is concurrent inflammation.
