Urinary Flashcards
causes of hemoglobinuria - equine
RBC breakdown (intravascular)
red maple toxicity
infectious disease of hemaotpoeitic system
immune mediated disease
causes of myoglobinuria - quine
muscle damage/necrosis
rhabomylolysis
sycamore toxicity
stypical myopathy
trauma
polysaccharide storage myopathy
idiopathic
causes of hematuria - equine
blood from urinary, renal, bladder, repro
oak toxicity
urethral rents
urethritis
bacterial cystitis
urolithiasis
pyelonephritis
idiopathic
verminous nephritis
renal and vesicular neoplasia
discoloured urine - false
oxidation after exposure to air
darked after contact with snow
plant derived pigment - white clover
drug induced
- bright orange/red - rifampin/phenothiazine/nitazoxinade
- dark brown/black - doxycycline
urinalysis - red urine
dipstick - haem
spin - clear serum –> hameturia
ammonium sulphate 80% - hemaglobin will precipitate, myoglobin won’t
microscopy - cell types, crystals
endoscopy - neoplasia in bladder (Transitional cell carcinoma)
US - stones, bladder wall thickness
renal biopsy - indicated when azotemia in otherwise young healthy horse with acute renal failure
ddx PUPD - equine
PPID
Diabetes mellitus
Diabetes insipidus
kidney disease/renal failure
drug induced - alpha 2s, steroids, antibiotics, pychogenic polydipsia (bored)
polydipsia in horses - quantity
> 100ml/kg/day (>10% bodyweight)
polyuria in horses - quantity
> 50ml/kg/day
testing in PUPD - equine
watch to quantify/confirm PD - >70ml/kg/day
hematology - anemia, neutrophilia, ACTH/TRH stim
biochem - azotemia, glucose, calcium, liver parameters
urinalysis - USG (low not consistent with PUPD and suggests renal concentrating issue, medium consistant with chronic renal failure, high not consistent with PUPD and kidneys fine), glycosuria
water restriction trial - differentiate between diabetes insipidus and psychogenic
causes PUPD - dog
physiological - activity, weather, diet change
renal - CKD, pyelonephritis, AKI, fanconis
hepatic
cushings
diabetes
hypercalcemia
pyo
iatrogenic
psychogenic dolydipsia
causes PUPD - cat
physiological - diet change, activity, increased grooming, playing with water
renal - CKD, AKI, post obstructive diureses
diabetes
iatrogenic
hyperthyroidism
causes of PUPD - ferrets
renal
cushings
diabetes
causes of PUPD - rabbits
diet change - hay to grass in spring
renal - CKD
hepatic
pyo
metabolic
pregnancy toxemia
pain
causes of PUPD - birds
during egg laying
renal
hepatic
toxins
pituitary adenoma
stress/fear
clinical exam in PUPD
Neuro -
altered mentation - hepatic encephalopathy
hyperactivity - primary polydipsia or result of hyperthyroidism
ocular -
icterus - hepatic
cataracts - diabetes mellitus
retinal changes - hypertension secondary to CKD, AKI, hyperthyroidism
cervical palpation -
goitre - hyperthyroidism
oral -
mm -
icterus - heaptic
congested - systemic inflammatory
pale - anemia of chronic disease (CKD, neoplasia)
lingual ulceration/halitosis - advanced CKD
thoracic -
tahcycardia - hyperthryoidism, pheochromocytoma, sepsis
bradycardia - addisons
painting - cushings
tachypnoea - pulmonary neoplasai/mets
derm -
cushings - skin thinning, hair loss, pigment change
hepatocutaneous syndrome
repro -
egg laying - physiological polydipsia
pregnancy - toxemia, gestational diabetes
discharge - open pyo
plantigrade stance/struggling to jump - diabetic peripheral neuropathy
urinalysis - PUPD
USG - renal
dipstick -
glucose - diabetes or fanconis (or stress)
ketones - diabetes mellitus
blood - renal, pyo, contamination from repro
protein - renal, UTI, cushings
sediment -
protein:creatinine - renal, cushings
active sediment - pyo or UTI
culture - UTI, pyo, contaminated sample
blood testing - PUPD
renal -
increased urea and creatinine
+/- phosphate
non-regenerative anema
hepatic -
increased liver enzymes
decreased albumin
diabetes mellitus -
increased glucose
increased ALP, bilirubin and cholesterol
hypokalemia
cushings -
increased cholesterol, ALP and bile acids
decreased urea
stress leukogram
hyperthyroidism -
increased RBC
stress leukogram
increased glucose, renal enzymes, phosphate
decreased creatinine
hypercalcemia -
increased total and ionised calcium
pyo -
neutrophilia
mild anemia
increased globulins , liver and kidney enzymes
decreased glucose
targeted disease testing - PUPD
SDMA - renal
bile acid stim - hepatic
fructosamine - diabetes mellitus
ACTH stim/low dose dexmethasone suppression - cushings
total/free T4 - hyperthyroidism
pre renal AKI
before kidney - vasculature
decrease in perfusion to kidneys
reduction in GFR –> increase in SDMA/urea/creatinine
reduced perfusion due to hypotension, hypovolemia, shock
–> ishemia
efferent venous drainage issues - cirrhotic liver disease, right sided heart failure, fluid overload
usually milder increases in creatinine than other types of SKI
can lead to intrinsic AKI if not treated
AKI vs CKD
AKI can return to normal if treated
AKI on CKD - can only return to previous CKD state, usually to a worse state than before teh AKI
CKD - at least 3 months
intrinsic AKI
primary - AKI is the main presenting sign
secondary - AKI secondary to larger constellation of conditions
non specific signs -
lethargy
hypo/anorexia
nausea/vomiting/diarrhoea
PUPD
uremic breath
post renal AKI
urine not able to leave kidneys properly
obstruction of urinary tract
back up of urine –> increased tubular pressure –> reduction in GFR –> increase SDMA/creatinine/urea
urethral or ureteral obstructions or urinary tract rupture
mroe likely to be hyperkalemic - look for obstructions if see this
causes of AKI requiring immediate treatment (within hours)
infectious - pyelonephritis, pyelonephrosis
obstructive - rethral or ureteral
addisons (dogs)
causes of AKI requiring immediate treatment (within days)
neoplasia - usually present as CKD
glomerulanephritis
infectious AKI
pyelonephritis - infection of kidneys - usually e coli
pyelonephrosis - dilation of renal pelvis with pus
more common in acute on chronic
risk factors -
obstruction
diabetes
renal and non renal neoplasia
signs -
pyrexia
neutrophilia
renal pain
renal pelvic/uretal dilation or free fluid on ultrasound
diagnosis - cystocentesis - culture
treatment -
antibiotics with good renal perfusion
lepto - doxy or amoxyclav
sepsis - amoyclav
surgical drainage
AKI - addisons in dogs
hypovolemia and distrubutive shock –> marked pre renal azotemia
hyperkalemia and hyperphosphatemia
looks like AKI - check basal cortisol to rule out addisonian crisis
if high suspicion then ACTH stim and treat preemptively
treatment AKI
supportive care
maintain hydration
maintain calorie intake
assessing and treating systemic hypertension
address electrolyte and acid base imbalance
discontinue nephrotoxic drugs
supportive care for AKI
fluids
electrolytes
feeding tube/assisted feeding
maintaining hydration in AKI
stages of fluid therapy -
resuscitation - replacing intravascular deficits, only needed if signs of shock
optimisation - rehydration of total body deficits - based on % dehydration signs and monitored
stabilisation - maintenance water requirements - if not able to do themselves, consider ins and outs
evacutation - de escalation - reduce until drinking on its own with regular hydration assessments
lactated ringers
potassium supplementation if needed
creatinine will go up when stop - removing dilution effect
note oliguria and anuria - ins and outs approach
maintaining calorie intake AKI
uremia –> nausea –> anorexia
oral ulceration - pain
medications - anti nausea (maropitant), appetite stimulants
if can’t eat 75% required intake by 48 hours - tube
treating hypertension in AKI
lots of animals with AKI get hypertension
some antihypertensive medications are nephrotoxic
amlopidine
RAAS inhibitors can worsen AKI, can use in CKD so when reclassified at 3 months can reevaluate
addressing acid base and electrolyte imbalances in AKI
hyperkalemia - in obstructive AKI - IV or oral supplements
hyperphosphatemia - always present in AKI
hypernatremia - usually resolves with rehydration
renal amyloidosis
rare
synthesis and deposition of misfolded proteins in tissues
profuse diarrhoea - fibrin deposition in intestinal mucosa
enlarged kidney - palpable per rectum
subcutaneous oedema
weight loss
protein losing nephropathy - foamy urine
amyloid deposition in renal glomeruli
euthanasia, condemned at slaughter
pyelonephritis
cattle and pigs
bacterial infection - renal pelvis
actinobacterium suis or e coli in pigs
range of bacteria in cattle
pus in ureters at pm
actinobacterium suis - pyelonephritis
pigs
in prepuce and preputial diverticulum of boars
infection through natural service
pus
abscesses
cystitis - common reason for culling
pain (hunched back)
anorexia
polydipsia
loss of condition
vulval discharge
hematuria
may die suddenly
urine test - bacteriology
treatment - antibiotics (success dependent on stage of infection)
e coli - pyelonephritis
pyelonephritis in sows that are AI’d
ascending infection from fecal contamination of vulva
predisposed by restricted water (not flushing out enougyh)
cystitis
pyelonephritis
increased urine frequency - little and often
pus/blood in urine
treatment - antibiotics, renal damage may be permanent if pyelonephritis set in
prevention - hygiene and unrestricted water access
pyelonephritis - cattle
more in older beef cattle
range of bacteria
acute - pain, dullness, frequent urination, coloured urine, pyrexia, enlarged kidney
chronic - loss of condition, drop in yield, urination little and often
treatment - antibiotics probably won’t work
condemnation of carcass at salughter if systemic infection
acute tubular necrosis
ruminants
nephrotoxins - oak, oxalates, heavy metals, aminoglycosides, tetracyclines
renal ischemia - caused by mastitis, metritis, abomasal torsion, salmonellosis
depression
inappetance
mild bloat
diarrhoea
treatment, supportive care, remove toxin
nephrosis
lambs up to 4 months
dull
anorexia
weight loss
death
swollen pale kidneys at PM
usually following coccicia, menatodirus or crypto infection
black disease
Clostridium Novyi B
necrotic liver damage
blackleg
Clostridium chauvoei
muscle tissue damage
botulism
clostridium botulinum
nervous, flaccid paralysis
tetanus
clostridium tetani
nervous, after open wounds, rigidity
pulpy kidney
clostridium perfringens D
4-10 week old lambs - unvaccinated dam
older weaned lambs that aren’t vaccinated
often triggered by move onto better pasture or supplemental feeding
sudden death
enterotexmia - from clostridial toxins, not from kidney disease
convulsion
pulmonary oedema
friable kidneys at PM
prevent - vaccinate pregnant ewes, vaccinate lambs twice before weaning
leptospirosis
zoonosis - abortion material and urine splash high risk for humans
abortion, still birth, weak calves, infertility
milk drop
colonises renal tubules and intermittently excreted in urine - infected waterways
serology for diagnosis
vaccination available
redwater fever (babesiosis)
coffee coloured hematuria
ixodes ricinus - heather, fern, tall grass, hilly regions - peak in spring and autumn
zoonosis - rare but serious
signs -
dullness
inappetence
pyrexia
loud heart sounds
hematuria
pipe stem feces –> constipation
young animals usually have no signs
early exposure - immunity in endemic areas
prevention - tick control
treatment - imidocarb (long withdrawal), blood transfusion, symptomatic treatment (laxative for constipation)
AKI - horse - signs
NB often due to predisposing disease, common in hospitalised horses
uremia –> anorexia
colic signs
uremic encephalopathy - nervous signs
attempting to urinate and showing discomfort (obstruction)
pyrexia - acute septic nephritis (rare)
signs often masked by primary condition
AKI - horse - diagnosis
history, signs
azotemia
isosthenuria
electrolyte abnormalities -
variable potassium (reduced excretion but diet can compensate)
serum magnesium - high in renal or pre renal
calcium - elevated in Chronic renal failure
minimal proteinuria
bacteremia rare
USG - differentiate pre ranl azotemia from kidney disease
AKI - horse - treatment
treat underlying disease
correct dehydration and hypertension
avoid nephrotoxic drugs
surgery - remove obstructions
chronic renal failure - horse
irreversible
greater than 3 months
less common than acute
chonic renal failure - horse - signs
non specific
wight loss
dull
PUPD
peripheral oedema
dull coat
anemia
inappetence
change in mentation
mild diarrhoea
uremic encephalopathy
chronic renal failure - horse - test
azotemia
mild anemia
low albumin
hyperkalemia - distinct feature
urinalysis - renal casts, WBCs, proteinuria (more often in AKI)
Ultrasound - more useful in chronic than acute
biopsy - not that useful, can cause haemorrhage
chronic renal failure - horse - treatment
progressive and irreversible
symptomatic treatment
steroids
avoid dehydration
avoid nephrotpxic drugs
vegetable oil - increase calorie intake
high energy low calcium diet
stone removal - probably won’t bother
poor prognosis long term
azotemia
increase in creatinine and/or urea
uremia
clinical signs associated with azotemia
mechanisms of CKD
normal - gradual inflammation and destruction of kidney functional units, 2/3 gone to signs
acute kidney insult - causing long lasting inflammation and damage –> follows normal pattern
acute on chronic - acute attack with existing CKD, once acute attack over then return to CKD state, usually worse off
neoplasia - grows and reduces function
degenerative (eg polycystic kidney disease) - cysts spread in increase in size –> reduced function
juvenile onset CKD - start reducing function, over time clinical
glomerular disease - marked proteinuria, excess protein, reduction in function
tubulo-interstitial nephritis most common cause
markers of GFR
Creatinine -
produced in muscles
filtered by kidneys
main parameter
no increase until 75% loss
also affected by muscle mass, hydration state and hyper thryoidism
urea -
produced by liver
filtered by kidneys
more variable than creatinine
less reliable
SDMA -
produced by most cells
filtered by kidneys
less affected by external factors
earlier diagnosis
not affected by muscle mass
less good for monitoring progression -m normal day to day variation
USG -
urine concentrating ability
phosphates -
disurption of phosphate calcium vitamin D cycle
higher may mean more discomfort
anemia -
anemia of chronic disease
reduced erythropoietin production
pH -
metabolic acidemia in very advanced CKD
FGF-23 -
novel biomarker for CKD
only in cats currently
early indication of phosphate increases
CKD signs
uremia - weight loss, halitosis, dullness, anorexia, nausea, mouth ulcers, muscle and condition loss
signs relating to underlying cause
different sized kidneys
signs vary a lot with degree of azotemia
management of nutrition and hydration - CKD
renal diet - adequate calorie, digestible, good quality protein, supplements
slow transition onto new diet
assisted feeding
appetite stimulants - metazopine, capromorelin
anti nausea - ondansetron, metazpoine
(don’t use metazopine and ondansetron together)
gastroprotectants - omeprazole (only if ulceration)
readily available water, water falvour enhancer
early renal diets - low phosphate and restricted protein
fluids
management of hyperphosphatemia - CKD
target lower than range interval
dietary restriction
phosphate binders - given with foodm calcium or aluminium based
monitor with FGF-23
management of proteinuria - CKD
protein restricted diet
monitor
RAAS inhibitors - dogs angiotension receptor blocks, cats ace inhibitors
management anemia - CKD
treat at PCV <0.2
erythropoeitin and iron supplements
may need transfusion
management of hypertension - CKD
can lead to issues with other organs and seizures
reliable BP measurements
dogs - ace inhibitor
cat - amlodipine or angiotension receptor blocker
other management considerations - CKD
nephrotoxic drugs - NSAIDs - discontinue
positive urine cultures - treat as pyelpnephritis
hypokalemia - seen in advanced cases, lethary anorexia and muscle weakness, supplement oral potassium
hypercalcemia - complicated
acidemia - muscle wastage and anorexia, can supplement potassium cirtate or sodium bicarbonate but can put them off food
monitoring CKD
iris 1 - every 6 months
iris 2 - 3-6 months
iris 3 - 1-3 months
iris 4 - 1-2 months
starved sample - blood/urine
BCS
muscle condition
hydration
creatinine (and urea but not as important)
phosphates
urine protein:creatinine
BP - doppler
PCV - anemia of chronic disease
optional - acid:base, ionised calcium, FGF-23
cysto centesis - if suspicious of pyelonephritis
SDMA
glomerular filtration marker
increases earlier in damage
still affected by pre- and post-renal causes
day-to-day variation so not as good for tracking progress as creatinine
not affected by muscle mass
will definitely be up if creatinine already increased
FGF-23
only in cats
indicator of phosphate levels - assessment of whether phosphate restriction working
assess need for early renal diet in early stages
