Canine Flash Notes - Renal Physiology Flashcards
what is azotemia? what are the different types & why is it important to characterize?
increase in BUN and/or creatinine
pre-renal, renal, & post-renal
important for accurate diagnosis, treatment, & prognosis
what is uremia?
clinical syndrome resulting from the accumulation of metabolic waste products due to renal failure
what is pre-renal azotemia? what is seen on lab values?
reduced renal perfusion - often caused by dehydration
increased BUN, creatinine, & USG over 1.030
what is renal azotemia? what is seen on lab values?
loss of 75% of nephrons
increased BUN, creatinine, & USG < 1.017
what is post-renal azotemia? what is seen on lab values?
blockage of urine outflow
increased BUN & creatinine, oliguria or anuria, & hyperkalemia
what is the pathophysiology of pre-renal azotemia? what happens if it remains uncorrected? sequela?
decreased renal perfusion causing a decrease in glomerular filtration of metabolites which results in an increase in BUN & creatinine while urine concentrating ability remains normal (normal tubular function)
renal ischemia & kidney destruction - renal disease or renal failure
what is the pathophysiology of renal azotemia?
GFR decreases due to loss of at least 75% of nephrons - renal disease results in azotemia, which eventually causes renal failure
acute renal failure - reversible or irreversible
chronic renal failure - irreversible
how do you treat pre-renal azotemia?
restore circulating fluid volume & renal perfusion, correct electrolyte abnormalities, & treat cause (dehydration, shock, addison’s, etc)
what is the prognosis of pre-renal azotemia?
usually, kidneys will resume normal function when re-perfusion is re-established if there is not prolonged ischemia
what are the 4 main causes of pre-renal azotemia?
- dehydration
- shock
- hypoadrenocorticism
- heart failure
what is the pathophysiology of post-renal azotemia?
blockage of urinary outflow & hyperkalemia develops as it can’t be eliminated
life threatening effects - cardiac conduction (bradycardia & death)
initially kidneys resume normal function if corrected, but too much time with obstruction can result in acute renal lesion (hydronephrosis)
what is the classic case presentation of a dog with renal azotemia? what lab changes are seen?
acute - anuric/oliguric, occasionally polyuric
chronic - pu/pd, gi signs (vomiting/diarrhea), & oral ulcers
increase in BUN/creatinine & low specific gravity
what are some causes of acute renal failure in dogs?
pre-renal ischemia from dehydration/hypovolemia, ethylene glycol toxicity, aminoglycoside toxicity, heavy metal toxicity, hypercalcemia, leptospirosis
chronic renal disease resulting in failure
how is renal azotemia treated?
acute - supportive care until it repairs itself (fluids, treat hyperkalemia, treat acidosis)
chronic - no cure, palliative care, fluids, & diet restricted proteins & phosphorus (hill’s k/d)
what is the classic presentation of an animal with post-renal azotemia? sequela?
oliguria, straining to urinate, abdominal discomfort
heart failure from hyperkalemia & hydronephrosis
what are the main causes of post-renal azotemia?
obstruction - calculi in renal pelvis/ureter/urethra, tumor block, entrapment of urinary tract from a hernia, trauma, stricture, or iatrogenic from surgery or catheterization
ruptured urinary tract
how is a diagnosis of post-renal azotemia made based off of lab changes?
increased BUN/creatinine, ECG shows bradycardia, spiked t waves, absent p waves
check creatinine of abdominal fluid if rupture is suspected
how is post-renal azotemia treated?
hyperkalemia addressed first!!!
unblock the animal - cystocentesis if you can’t immediately unblock
fluids - sodium bicarb 0.5-1.0 mmol/kg slow IV over 15 minutes, 20% dextrose 0.5-1.0 g/kg IV with </= 1 unit of regular insulin per 3 grams of dextrose, or 10% calcium gluconate up to 0.5-1.0 g/kg IV
what values designate an animal as being polyuric/polydipsic?
urine production > 25ml/lb/day (more than 50 ml/kg/day)
water consumption > 50 ml/lb/day (more than 100 ml/kg/day)
T/F: pu/pd is a manifestation of a disease & not a diagnosis
true
what is the mechanism of polydipsia?
low plasma osmolality stimulates chemoreceptors in the thirst center - posterior pituitary gland releases ADH
renal response to ADH is to concentrate urine requiring 1/3 functioning nephrons & a hypertonic renal medullary interstitium (2/3 non-functional nephrons for kidney not to concentrate urine causing polyuria)
what is the common presentation of an animal that is pu/pd?
nocturia, inappropriate urination, incontinence, pollakiuria, & polydipsia
what urine production metabolism rate is used for a caged animal?
urine volume 25-45 ml/kg/24 hours
if a pu/pd dog has a usg of 1.040, what do you think? what if it is less than 1.007? what if it is 1.025 or higher with pu/pd?
1.040 - unlikely to be polyuria
1.007 - hyposthenuria, tentative diagnosis of central diabetes insipidus, nephrogenic diabetes insipidus, or pituitary diabetes insipidus
1.025 - suggests hypoadrenocorticism, diabetes mellitus, or renal glucosuria
how is a water deprivation test used to diagnose disease in a pu/pd dog with no other signs of systemic disease?
if USG is over 1.025, suspect psychogenic polydipsia or cushing’s
if under 1.025, proceed with an ADH test
what tests are used to differentiate normal psychogenic polydipsia, hyperadrenocorticism, pituitary diabetes insipidus, nephrogenic diabetes insipidus, or medullary washout?
water deprivation tests, ADH test, gradual H2O test, & ADH + gradual H2O deprivation tests
how are results of an ADH test interpreted for an animal with pu/pd?
if USG is over 1.025 - pituitary diabetes insipidus, no ADH
if USG less than 1.025 - proceed with gradual H2O deprivation test
what is the point of doing a gradual H2O test on a pu/pd dog?
correct possible medullary wash out
how are results of an gradual H2O test interpreted for an animal with pu/pd?
if USG is higher than 1.025 - suspect psychogenic polydipsia or cushing’s
if USG is lower than 1.025 - proceed with ADH test
how are results of an ADH + gradual H2O test interpreted for an animal with pu/pd?
if USG is less than 1.025 - kidney unresponsive to ADH
if USG is higher than 1.025 - pituitary diabetes insipidus
what are some differentials for a dog that is pu/pd?
diabetes mellitus, hypoadrenocorticism, primary renal disease, liver disease, pyometra, hypercalcemia, hyperparathyroidism, pituitary diabetes insipidus, & psychogenic polydipsia
what is isosthenuria?
USG of 1.008-1.012 - same as plasma
what is hyposthenuria?
USG < 1.007, inability to concentrate urine
what are the minimal concentration ranges of USG in dogs & cats?
dogs: 1.013-1.030
cats: 1.013-1.035
what is the point of doing a water deprivation test on a pu/pd animal? what are the contraindications to doing it?
determines if ADH is released in response to subclinical dehydration
if kidneys can respond to ADH & concentrate urine
contraindications - dehydration, azotemia (BUN, creatinine), or hypercalcemia
when do you terminate a water deprivation test?
urine concentration > 1.025, > 5% weight loss, azotemia develops, dehydration develops
what is the benefit of doing a gradual water deprivation test?
for animals with psychogenic polydipsia with medullary washout (animal can’t concentrate on abrupt test), so this allows the gradient to be re-established
how is a gradual water deprivation test done?
reduce water intake bt 5% daily
what is a negative result for a gradual water deprivation test?
animal fails to concentrate without renal disease or lab abnormalities - indicates neurogenic or nephrogenic diabetes insipidus
when is an ADH response test done?
done after abrupt or gradual water deprivation test if there is an inadequate concentration
tests renal tubular ability to concentrate urine
how is an ADH response test done? how are the results interpreted?
vasopressin is given IM & USG is measured at 30, 60, 90, & 120 minutes
negative water deprivation test + positive ADH concentration >1.025 - diagnostic for neurogenic diabetes insipidus
both negative water deprivation & ADH response tests - indicate nephrogenic diabetes insipidus or DDI if after abrupt H2O deprivation
what is a negative result of an abrupt H2O deprivation test?
failure to concentrate, USG < 1.025 without renal disease or other lab abnormalities - indicates neurogenic or nephrogenic diabetes insipidus and/or medullary washout
what are the 3 main types of diabetes insipidus & their basic pathophysiology?
- nephrogenic - partial or complete renal tubule insensitivity to ADH
- central - partial or complete primary deficiency of ADH
- dipsogenic/psychogenic - excessive water intake
what are the main causes of nephrogenic diabetes insipidus?
acquired secondary - renal & metabolic disorders affecting renal tubules’ ability to respond to ADH (most acquired forms are reversible following correction of the cause)
primary causes - acute renal failure, hydronephrosis, chronic pyelonephritis, fanconi’s syndrome
secondary causes - pyometra, DM, liver disease, lymphoma, cushing’s, addison’s, hyperthyroidism
what metabolic changes can result in nephrogenic diabetes insipidus?
hypercalcemia & hypokalemia
what drugs are implicated as causes of nephrogenic diabetes insipidus?
steroids, anticonvulsants, & diuretics
how is nephrogenic diabetes insipidus diagnosed?
negative H2O & ADH test - both tests have a USG result of < 1.025
how is acquired nephrogenic diabetes insipidus treated? what about congenital?
acquired - treat predisposing cause & provide unlimited water supply
congenital - unlimited water supply, low sodium/protein diet, & chlorothiazide diuretics to enhance proximal tubule reabsorption of Na, Cl, & H2O
what are the main causes of central/pituitary diabetes insipidus?
idiopathic - most common
CNS trauma/infection, neoplasia, parasitic migration
what is the pathophysiology of central diabetes insipidus?
ADH acts on the distal tubules & collecting ducts to increase reabsorption of water, but there is either a lack of ADH formation and/or release of ADH
so decreased ADH = water diuresis (polyuria)
how is central diabetes insipidus diagnosed?
negative H2O test & positive ADH test
persistent hypernatremia, H2O test USG < 1.025, ADH test positive
how is central diabetes insipidus treated?
unlimited water!!!!
desmopressin for ADH supplementation
for pituitary tumors - cobalt radiation
what is the cause of psychogenic diabetes insipidus?
disorder of thirst centers resulting in primary psychogenic DI - behavior problem or from drugs (salt, diuretics, glucocorticoids, fluids, anticonvulsants)
secondary polyuria to rid the body of excessive H2O - large breed dogs, kidneys are usually functional, but causes medullary washout
how is psychogenic DI diagnosed?
urinalysis shows a USG of 1.001-1.003
water deprivation test shows concentrated urine
abrupt water deprivation diagnoses about 2/3 of cases
gradual water deprivation done in other 3rd to eliminate medullary washout
how is psychogenic DI treated?
gradual water restriction to restore renal hypertonic medullary interstitium
behavior modification - diazepam
what is the number one urolith in dogs & cats?
struvite
what are the main causes of urolithiasis in dogs?
UTI - commonly present with urease producing bacteria, resulting in alkaline urine precipitates
metabolic disorders - PSS causing urate crystals
calcium phosphate - hyperparathyroidism
how do dietary factors influence the formation of uroliths?
high magnesium - alkalinizing diet, favors struvite formation
corn gluten or soybean hulls - silica
high calcium or phosphorus diets - calcium phosphate
what breeds are predisposed to struvite crystal/urolith formation?
females > males - mini schnauzers, welsh corgis, dachshunds, poodles, pugs, pekingese, beagles, & scottish terriers
what breeds are predisposed to oxalate crystal/urolith formation?
males!!
mini schnauzers, mini poodles, yorkies, lhasa apsos, shih tzus, & dalmatians
what breeds are predisposed to urate crystal/urolith formation?
dalmatian!!!! 60% of all urate uroliths!!!!!
portosystemic shunt dogs - mini schnauzers, yorkies, & pekingese
what breeds are predisposed to silica crystal/urolith formation?
german shepherds
what breeds are predisposed to cystine crystal/urolith formation?
males!!!
dachshund, basset hounds, english bulldogs, yorkies, irish terriers, & chihuahuas
how are struvite uroliths treated?
abx for 3-5 days for UTI/struvite
ampicillin if no culture or TMS
medical dissolution of stones will not work on what type of urolith?
calcium oxalate!!!!
what urolith types require surgical intervention?
oxalate, calcium-phosphate, & silica
obstructed animals
those that medical treatment doesn’t effect
what is the urine pH of animals with struvite stones?
alkaline - urease bacteria!!!!
what does FLUTD stand for?
feline lower urinary tract disease
what are predisposing factors of FIC/FLUTD?
bacterial/viral infection, dirty litter boxes, alkaline urine, dry»_space;> canned food
what is the number one blockage site in cats with urinary obstructions?
penile urethra!
why do an ecg on a blocked cat?
look for life threatening side effects from hyperkalemia - tall T waves & bradycardia
what is post-obstructive diuresis?
often occurs following relief of urinary obstruction
kidneys shut down because they finally get a break
what fluids should be used on a blocked cat with hyperkalemia & acidosis?
0.9% saline + unblocking will quickly drop potassium
if it doesn’t, glucose & insulin therapy
bicarbonate if acidotic (ph < 7.2) 1-2 mEq slowly IV
calcium gluconate if life threatening arrhythmia
how do you prevent a cat from becoming blocked again?
low magnesium diet
canned food
encourage exercise & free choice water
clean litter box often
T/F: if a cat blocks once, there is a 70% chance it will happen again
true
what surgical option is available for a cat that continuously blocks?
penile urethrostomy
what must you differentiate urinary incontinence from?
abnormal elimination due to behavior, inadequate house training, or other disease
what is enuresis?
urinary incontinence while animal is asleep
what are some non-neurogenic causes of incontinence?
hormone-responsive, stress incontinence, urethral incompetence, pelvic bladder, urachal remnant, ectopic ureters
what are some neurogenic causes of incontinence?
low motor neuron bladder (atonic), upper motor neuron bladder (automatic bladder), detrusal-urethral disorders, urge incontinence, detrusor hyperreflexia
what are the normal phases of micturition in a healthy bladder?
storage (filling) phase - sympathetic (ANS) relaxes bladder detrusor muscle & increases internal urethral sphincter tone
somatic - controls external urethral sphincter (urethralis muscle)
stretch of bladder wall - sensory fibers to reflex & brain
voiding (emptying phase) - parasympathetic (ANS), contraction of detrusor muscle & inhibition of sympathetic & somatic urethral sphincters
what are the differences in clinical signs between urinary incontinence & abnormal micturition?
incontinence - dribbling of urine, loss of voluntary control, & urine-scald dermatitis
abnormal micturition - inability to urinate, disruption of urine stream (dyssynergia), stranguria/dysuria, & abdominal pain/discomfort
what is the first & most important step in working to diagnose urinary incontinence?
history questions!!!!
what are important parts of your physical exam on a patient you suspect has urinary incontinence?
physical exam - look for urine scalding, palpate bladder before & after urination
distended bladder = increased urethral resistance or decreased bladder contractility
neuro exam - check sacral reflex arc (pudendal nerve - sensory & motor)
perineal reflex - pinch perineum & look for contraction of anal sphincter & ventroflexion of tail
bulbospongiosus reflex - squeeze distal penis/vulva & look for constriction of anus
what diagnostics should be done for an animal you’re working up for incontinence?
blood values - renal values
urinalysis & culture
radiographs - look for obvious abnormalities, excretory urogram, positive contrast vaginogram, or retrograde urethrography
how are ectopic ureters in dogs diagnosed?
vaginoscopy with or without new methylene blue dye to use visualization of contrast for ectopic ureters - also check for urachal diverticulum, bladder wall thickening, calculi, prostatic enlargement, urethral strictures, & pelvic bone abnormalities
how are urodynamic studies used for diagnosing micturition disorders?
cystometrogram - checks bladder tone & volume & detrusor reflex
urethral pressure profile - looks at intra-urethral resistance
what is the purpose of using electromyography in an animal you suspect is incontinent?
looks at coordination of detrusor & urethral sphincter by checking anal sphincter
if a female adult animal presents with suspected incontinence, has reflexes present, & a small bladder, what two things are you mainly considering as differentials?
hormone responsive urinary incontinence or urinary tract infection
if a female adult animal presents with suspected incontinence, has reflexes present, a small bladder, and signs of a UTI, how do you treat? what do you do if the animal doesn’t respond?
treat UTI or FIC - if it stops, it was urge incontinence from the UTI/FIC
if incontinence continues - need to rule out neoplasia, chronic cystitis, polyps, uroliths, or urachal remnant
if a young adult animal presents with suspected incontinence, has reflexes present, & a small bladder, what three things are you mainly considering as differentials? how would you diagnose?
patent urachus - physical exam, see urine coming from the umbilicus
ectopic ureter - contrast urogram
vaginal stricture - digital vaginal exam, vaginoscopy, & contrast vaginography
if an adult animal presents with suspected incontinence, has reflexes present, & a large bladder that is difficult to express, what three things are you mainly considering as differentials? how would you diagnosis it?
obstruction due to calculi - urogram
upper motor neuron bladder - physical exam finding of spastic paresis in hind limbs
reflex dyssynergia - clinical signs show animal stop/start during urine stream
if an adult animal presents with suspected incontinence, has reflexes present, & a large bladder that is easy to express, what three things are you mainly considering as differentials? how would you diagnosis it?
lower motor neuron bladder - physical exam shows flaccid paralysis in the hind limbs
what clinical signs are seen with reflex dyssynergia? how is it diagnosed? how is it treated?
start & abrupt stop of urination with stranguria that is voluntary
dx - clinical signs, perineal reflex intact, large, non-expressible bladder that is easily catheterized
tx - decrease alpha sympathetic tone with phenoxybenzamine or bethanechol
what clinical signs are seen with LMN atonic bladder? how is it diagnosed? how is it treated?
continuous involuntary dribbling of urine & hindlimb flaccid paralysis
dx - no perineal reflex & large expressible bladder
tx - no effective treatment, manually express three times a day, & may try bethanechol/abx
what clinical signs are seen with UMN automatic bladder? how is it diagnosed? how is it treated?
intermittent involuntary incontinence & hindlimb spastic paralysis
dx - hyperactive perineal reflex & large turgid non-expressible bladder
tx - intermittent catheterization
what animals are usually affected by hormone-responsive incontinence?
older, spayed females
what clinical signs are seen with hormone-responsive incontinence? how is it diagnosed? how is it treated?
voluntary control of urine with intermittent dribbling
dx - normal reflexes/bladder, & positive response to treatment
tx - diethylstilbestrol +/- phenylpropanolamine
what clinical signs are seen with urethral incompetence? how is it diagnosed? how is it treated?
voluntary control + stressful incontinence
dx - normal reflexes/bladder & positive response to treatment
tx - increase alpha sympathetic urethral tone, phenylpropanolamine
what clinical signs are seen with urge incontinence? how is it diagnosed? how is it treated?
frequent small urinations, urine spraying, stranguria
dx - UTI/VIC, hyperreflexive detrusor, normal bladder, & response to treatment
tx - treat UTI/FIC, inhibit detrusor with propantheline
what clinical signs are seen with bladder atony/overdistension? how is it diagnosed? how is it treated?
long continuous involuntary dribbling of urine
dx - large flaccid bladder with large residual volume, difficult catheterization
tx - remove obstruction, place an indwelling catheter, & start bethanechol
what clinical signs are seen with paradoxical incontinence? how is it diagnosed? how is it treated?
short continuous involuntary dribbling of urine
dx - large turgid bladder (non-expressible) with normal reflexes
tx - remove obstruction & place indwelling catheter
what clinical signs are seen with ectopic ureters? how is it diagnosed? how is it treated?
voluntary urination & continuous dribbling of urine
dx - clinical signs (young animal), normal bladder reflexes
tx - ureteral transposition + phenylpropanolamine
what is the hallmark sign of glomerulopathies? what is the main cause?
proteinuria in absence of urinary tract inflammation
immune complexes found in glomerulus in most - but most cases, the exact cause is unknown
what are some examples of infectious causes of glomerulopathies?
bacterial endocarditis, infectious canine hepatitis, brucellosis, pyometra, heart worms, FIP, FeLV, lyme disease, & ehrlichiosis
what are some examples of neoplastic causes of glomerulopathies?
lymphoma & mast cell
what are some examples of inflammatory/immune-mediated causes of glomerulopathies?
systemic lupus erythematous, chronic pancreatitis, chronic pyoderma, & polyarthritis
what are the main sequela of glomerulopathies that can be life threatening?
uremia if more than 75% of nephrons are affected
pulmonary thromboembolism - hypercoagulable state due to loss of antithrombin III
nephrotic syndrome - from prolonged proteinuria & hypoalbuminemia with edema & ascites
how are glomerulopathies diagnosed?
blood values - non-regenerative anemia, hypoalbuminemia
UA - persistent proteinuria, use UPC to assess magnitude (1-5 = chronic interstitial nephritis, 3-40 = glomerulonephritis, & 10-40 = amyloidosis)
what is the only diagnostic test that can differentiate between amyloidosis & glomerulonephritis?
renal biopsy
what is the pathophysiology of glomerulonephritis? what is the prognosis?
deposition of antigen-antibody complexes in glomeruli - these immune complexes change the permeability of glomerulus leading to proteinuria & hypoproteinemia
guarded
what is the pathophysiology of amyloidosis? what is the prognosis?
disposition of fibrillar glycoprotein in organs
dogs - disposition primarily in glomeruli resulting in PLN
cats - disposition primarily in renal medullary interstitium resulting in chronic renal failure
poor prognosis
what are the suggested causes of amyloidosis?
idiopathic
secondary to inflammation & neoplastic processes - tissue injuries stimulates liver amyloid precursors (liver, spleen, & kidney primarily affected) leading to progressive kidney dysfunction
familial form in shar pei, abyssinians, & beagles
T/F: nephrotic syndrome is a descriptive term & not a diagnosis
true
nephrotic syndrome means what things are present?
edema, ascites, proteinuria, hypoalbuminemia, hypercholesterolemia, & edema
proteinuria of sufficient magnitude to cause hypoalbuminemia (decreased oncotic pressure = edema)
hypercoagulability - loss of antithrombin III (thromboembolism & compromised immune system)
what causes nephrotic syndrome in dogs & cats?
glomerulonephritis & amyloidosis
most patients with glomerular disease don’t develop nephrotic syndrome
what treatment is used for glomerulonephritis & nephrotic syndrome?
treat underlying cause if found
diet - sodium/protein restricted diet
enalapril, anticoagulants
vitamin B & C, free choice water
what treatment is used for amyloidosis?
no specific treatment proven effective - most animals are terminal
