urinary Flashcards
renal disease
-A functional or morphological impairment in one
or both kidneys; regardless of the extent of disease
-Disease may regress, remain stable or progress May or may not lead to renal insufficiency or failure
- Morphologic abnormalities:
Anomalies, UTI, neoplasia, infarct, etc. - Functional abnormalities:
Nephrogenic diabetes insipidus, cystinuria,
renal insufficiency
- Existence of impaired renal function due to disease
- Any one of a # of renal functions may be impaired
- If urine concentrating ability is affected this implies that 2/3 of the functional nephrons are damaged
renal failure
- Clinical syndrome that occurs when the kidneys are no longer able to maintain their regulatory, excretory and endocrine functions
-Implies ¾ of nephrons nonfunctional or lost - Clinically you see:
- Azotemia: retention of nitrogenous wastes results
- Derangements in fluid, electrolyte, and acid base balance
evaluating a patient with suspected urinary tract problem
-use information from your minimum data base:
Relevant information from the signalment, history and physical examination, as well as from basic
laboratory findings -complete blood count (CBC), serum biochemistry and a urinalysis.
- In some cases, additional problem specific diagnostic testing will also be important
- Make a problem list, list of ranked DDx, a diagnostic +/- therapeutic plan
questions to as for EVERY case
-What is the nature of the problem -is it a functional or morphologic problem of the urinary tract?
* Where in the urinary tract would you localize the problem and what is the extent of the disease?
* Is the disease acute or chronic? Is it likely to be progressive (i.e., is it curable or just managable?
* What nonurinary complications can be anticipated and should be evaluated for?
* What is the short and long-term plan for treatment/management and how will you monitor the effectiveness of your therapeutic plan?
* Finally, is there a way to determine an accurate prognosis to convey this to the owner?
signalment for urinary patients
- Breed – familial or congenital renal disease has been
recognized in many breeds.
-Age – chronic renal failure and most neoplasms are more prevalent in older animals.
- Gender – female dogs are more prone to UTI
-Environment - Animals that roam free have a greater risk of exposure to toxins
-Diet - may influence formation of some uroliths, or lead to tubular disease or AKI in rare cases
determine the presenting complaint and get complete history
-General attitude and activity level - non-specific clinical signs such as lethargy, anorexia, weight loss, dehydration
- Diet history
- Ask questions regarding current and past drug therapy administered and response to therapies
-Environment/Husbandry: ask about access to the outdoors and travel history to other areas of Canada or globally to assess risk of exposure to toxins and infectious diseases
urinary tract specific history
- Changes in the pet’s pattern or frequency of urination - need to differentiate between pollakiuria,
incontinence and polyuria
-* Has there been any changes in drinking habits and the volume of urine produced? polydipsia or polyuria
Pollakiuria vs incontinence
- Pollakiuria: frequent voiding of small volumes of urine. Suggests cystitis, urethritis, and urolithiasis.
- Incontinence: loss of voluntary control of micturition vs urge incontinence
-Ask about voiding posture, frequency of urination
* Changes in the pet’s volume of urination - differentiate polyuria from oliguria from anuria
-ask about urine appearance and smell
- Ask about any difficulty or pain during urination (dysuria/stranguria): suggests a problem causing inflammation in the lower urinary tract
- Ask about previous therapies for urinary disorders and response to these therapies
- Ask about previous urinary tract or pelvic trauma or surgery
differentiate polyuria from oliguria from anuria
Polyuria: normal to increased frequency with large volumes of urine. Does the animal need to urinate during
the night (nocturia)? This can suggest many different disease processes.
Anuria: need to differentiate lack of urine production (acute renal failure) from the inability to urinate
(urolithiasis, traumatic bladder rupture).
Oliguria: decreased urine production. Suggests renal failure or inability to completely urinate (partial urinary
obstruction, reflex dyssynergia).
polydipsia vs polyuria
Polydipsia: increased water intake (> 100 ml/kg/day in dogs & > 45 ml/kg/day in cats) may be noticed
before polyuria especially if pet urinates outdoors and is unobserved
- Polyuria: increased volume of urination > 2 ml/kg/hr ; may see nocturia – excessive urination at night
- Reduced urine production states / reduced drinking (hypodipsia and adipsia)
- Anuria – absence or lack of urine production –
- Oliguria – decreased urine production 1-2 ml/kg/ hr
urine appearance
-red:
Hematuria –blood in the urine
Pigmenturia – hemoglobinuria or myoglobinuria
Pseudohematuria/pigmenturia
- Deep yellow to orange urine: highly concentrated urine, bilirubinuria.
- Brown/ port wine colored urine: methemoglobinuria, myoglobinuria but
can be hemoglobinuria with bilirubin - Colorless or pale yellow: dilute urine – lacks urochrome pigments
urine smell
- Foul smelling urine suggests a urinary tract infection (UTI); alkaline
urine can be more pungent; ketonuria – patient’s breath may have a
slight sweet smell
physical exam
-Do a complete physical examination, including fundic examination
- Look for signs consistent with uremia if systemically sick
- Look for/ observe for signs of lower urinary inflammation
- Palpate the kidneys for pain or changes in renal size
- Palpate the bladder for tone, size, and position; do a rectal to palpate the trigone region as well as the pelvic urethra and sublumbar nodes
- Palpate after urinating for any uroliths or a thickened bladder wall
- Performing a complete neurologic exam is very important for patients with micturition disorders
palpate kidneys findings
Painful kidneys – pyelonephritis, acute glomerulonephritis, obstructive uropathy, renoliths
- Small kidneys - chronic renal insufficiency or failure
- Large kidneys = renomegaly – neoplasia, renal cysts, hydronephrosis, acute renal failure (AKF), acute
glomerulonephritis, granulomatous disease (FIP), obstructive uropathy,
signs of uremia
- Poor body condition – muscle wasting
- Dehydration
- Oral ulceration, tongue tip necrosis, halitosis
- Hypothermia
- Bony changes associated with renal
secondary hyperparathyroidism - Pale mucus membranes from anemia
Paraneoplastic Syndromes From
Urological Malignancies
Paraneoplastic hypercalcemia – PTHrP or localized osteoclastic effects – urothelial carcinoma
-Syndrome of in appropriate growth factor production
* insulin or IGF-2 secretion with renal tumors causing hypoglycemia
GFR determination
-tests renal function
-GFR = volume of glomerular filtrate produced per unit time
indications:
* To evaluate for suspected renal insufficiency.
* To assess the function of each kidney if nephrectomy of one kidney is indicated.
* To establish baseline measurements prior to use of a potentially nephrotoxic drug
normal values: 2 ml/kg/hr
methods:
evaluate azotemia, creatinine clearance tests, nuclear scintigraphy, iohexol clearance. PLASMA Clearance and IMAGING methods
renal clearance
- Clearance of sub X = GFR only if substance X is
freely filtered, there is no tubular reabsorption
or secretion and if substance X is not
synthesized or metabolized in the body
-rate of which a substance is cleared from the plasma.
-insulin is gold standard
GFR Determination - Clinical Surrogate
-Typically we have to rely on detection and trending of azotemia
* Localization of azotemia – very important to understand
Prerenal, Renal and Postrenal or a combination of these
* Use your history, physical examination, USG and knowledge of
hydration status of the patient to determine
* Always try to get a urine sample
azotemia
- Elevated concentrations of nitrogenous waste products (BUN and creatinine) in the blood
assess patients hydration status and do USG then–> catagorize
3 types:
Prerenal
Renal
Postrenal
-can see all three types in the same patient
uremia definition
Uremia is a clinical syndrome
* Polysystemic toxic syndrome that results from the inability to form and excrete urine adequately
-Uremia may or may not be
caused by renal disease
May be secondary to postrenal
obstruction
*ALL uremic animals are
azotemic but NOT all azotemic
animals are uremic
urea = BUN= serum urea nitrogen
- Nitrogenous waste product formed from ammonia
- Synthesized in the liver from NH3
- Diffuses throughout all fluid compartments
- Kidneys are the main route of excretion
- Urea recycling is very important for helping to maintain the medullary concentrating gradient
Any abnormality that decreases GFR will increase BUN
BUN =urea causes of increases and decreases
-crude measurement of GFR due to urea not excreting at constant rate and there is some reabsorption.
increases: dehydration, high protein, bleed into GI tract
decreases: low protein, liver insufficiency
creatinine
- Kidneys are the major route of excretion
- Crude index of GFR but better than BUN in most cases because it produced at constant rate, fewer non renal factors, non reabsorbable
- When is it not a good indicator of GFR, with muscle wasting or necrosis.
prerenal azotemia
- Usually a consequence of reduced renal perfusion, or GI hemmorage, high prot
- Kidney function is normal if exists alone or with just postrenal component; but can be superimposed on renal and postrenal azotemia
KEY FEATURE : azotemic mild but USG > 1.030 dog, > 1.035 cat, > 1.025 horse/cow
renal azotemia
- Azotemia resulting from renal failure or disease
- Implies > 75 % of nephrons are nonfunctional
- KEY FEATURE: azotemia with dilute urine specific gravity < 1.030 dogs, < 1.035 cats
and < 1.025 horses/cows
-Patients with other long-standing causes of PU/PD leading to medullary washout and some cats with CKD that maintain urine concentration abilities while in IRIS stage I / II
postrenal azotemia
-Azotemia resulting from either an obstruction in the excretory outflow tract or from a uroabdomen (tear in excretory pathway)
- Key feature: degree of azotemia and urine specific gravity are variable but clinical findings are suggestive (distended bladder, stranguria, fluid filled abdomen)
SDMA
- Relies primarily on renal elimination for excretion (>90%) so circulating concentrations are
primarily affected by changes in GFR and therefore correlate to kidney function - Not affected by muscle mass like creatinine, better test than creatnine for GFR
- Reference Intervals: adult dogs and cats < 14 ug/dl and < 16 ug/dl in puppies and kittens
- Values expected with early kidney disease between 15 and 20 mg/dL ; > 20 mg/dlwith more
advanced disease
acute renal failure
- Definition: azotemia caused by renal parenchymal disease or injury that occurs over hours to days
- Potentially reversible
- Clinically:
- Acute onset
- Oliguria/anuria or polyuric AKF states
- Azotemia and not concentrating their urine if producing urine
- Generally not anemic and in good body condition
- Nephrotoxins, infectious causes, and ischemia are the most common
causes
chronic renal failure
- Azotemia caused by renal disease or injury that
has occurred over a prolonged duration (months
to years) - Irreversible and progressive
- Clinically:
- Slow Insidious clinical onset unless acute on
chronic crisis; IRIS stages I-V - PU/PD – not concentrating their urine
- Progressive azotemia and eventual uremia
- Anemia, poor body condition
- Small and irregular kidney
- Commonly see diminished urine concentrating
ability - Isosthenuria or hypersthenuric
renal secondary hyperparathyroidims
- Subclinical or clinical syndrome
- Pathogenesis is controversial
- Involves:
Hyperphosphatemia – decreased excretion
Low circulating levels of vitamin D due to
loss of nephrons that activate precursor
± Reduced serum ionized [Ca 2+]
Skeletal resistance to PTH
urinalysis physical analysis
- Color
Red – Hemoglobin, myoglobin, RBCs
Orange – bilirubin
Other – drugs, dyes, foods - Clarity
- Smell
-USG
-urine osmolariy: # of particles in urine
urine specific gravity
Refractometer typically used
Urine concentration varies with many nonrenal
factors (diet, water intake, extrarenal diseases)
Remember there is no true normal** urine specific gravity, must assess
* Assess hydration status
* Use your history
Is there evidence of fluid losses
urinalysis chemical dipstick analysis
- Urine pH – careful not to overinterpret
acidic urine: meat-based diet, systemic acidosis, alkaline urine: old sample, UTI - Glucose – relevance varies with plasma
glucose
Hyperglycemia = diabetes glucosuria expected
Normoglycemia/hypoglycemia – tubular disorder - Ketones – should be negative
Positive with DKA, starvation - Protein
only detect albumin above a 30 mg/dl threshold
always be interpreted in view of the urine sediment
examination and the USG; small amount of protein may be normal
bilirubin on chemical dipstick analysis
-results from prehepatic (RBC hemolysis) or from hepatic or posthepatic diseases
-measure only unconjugated bilirubin
-maybe seen prior to detection of hyperbilirubinemia
-Trace to 1+ bilirubin can be normal in canine urine
(especially males) but ANY bilirubin in feline urine is
abnormal
chemical dipstick analysis red urine
- Red urine
RBCs, Hemoglobin
Myoglobin, methemoglobin - have to Occult blood:
-Intact RBCs, hemoglobin, and myoglobin all produce positive results
-Differentiation depends on sediment analysis and examination of plasma (red with hemoglobinuria, normal with myoglobinuria)
-method of collection my influence RBC if cysto
To differentiate these:
* PCV/TP
* Serum analysis
* Urine sediment analysis
urine sediment analysis
- Microscopic examination of gently resuspended sediment of centrifuged urine – can evaluate
stained (Sedi-Stain®) and unstained slides (wet mount)
-method of collection will influence results
look for:
RBC
WBC
Squamous cells
transitional cells
sperm
-microbes can also be seen, bacteria, fungal elements (shouldnt see with cysto as its sterile)
casts on urine sediment analysis
- Absence does not rule out tubular injury (e.g., anuric AKI)
- Cylindruria (casts in the urine) localizes disease to the kidneys; can provide the
earliest indication of tubular injury when administering a nephrotoxic drug - Cylindrical molds of the renal tubules composed of protein and/or cells. Low numbers of casts (1-2 /lpf) in very concentrated urine are normal. Look for them at low power
different types of casts seen in sedimentation
Hyaline: Tamm-Horsfall mucoproteins. Small numbers may be seen with fever, dehydration or heavy exercise. Mos common
type of cast. Increased # with pathological proteinuria.
Cellular: epithelial, RBCs or WBCs and are always abnormal. Epithelial cell casts signify severe tubular disease from toxins or hypoxia. RBC casts indicate hemorrhage. WBC casts suggest
inflammation.
Granular casts: degeneration of either cellular or hyaline casts; low numbers < 2 p/lpf normal – exercise, tubular dz may increase
Waxy casts: final stage of degeneration of granular casts; highly refractile and result from extreme urine stasis
Fatty casts: seen in patients with nephrotic syndrome and diabetes mellitus. Can be normal in cats
other things seen on sediment
- Lipiduria – common in cat urine and normal
- Amphorphous debris – common – cells, crystals
- Contaminants: plant grains or pollens
-parasite life stages
Urinalysis Sediment Findings Crystalluria
- Crystallization occurs when urine composition (pH, SG, mineral composition) favors
oversaturation of certain minerals; - Visualization also depends on pH, solubility of the crystals, and temperature of the urine
Crystals more likely to form in concentrated urine - Significance depends on the type of crystal and other clinical findings – some types such as
struvite and calcium oxalate can be normal or clinical importance and some are always of
clinically significant
Evaluation of Proteinuria
Proteinuria can result from:
Prerenal:
* Bence-Jones withmultiple myeloma,
* IMHA, platelet problem
Renal: disorders of the glomeruli
* neoplasia,
* Glomerulonephritis
* Amyloidosis
Postrenal:
* Neoplasia, UTI, urolithiasis
- Interpret in light of:
The USG and the urine sediment exam
The method of collection in some patients
Trace or 1+ may be normal if urine concentrate
Quantification of proteinuria with inactive sediment
- Urine protein creatinine ratio
normal < 0.4 cat; < 0.5 dog - 24 hour urine collection
- Microalbuminuria can be used to detect dz early in predisposed breeds such as Whaeton Terrier
proteinuria imaging
-kidneys may be normal sized if acute
-with chronic glomerulonephritis kidneys are irregular and small
renal biopsy: only way to differentiate glomerulonephritis from amyloidosis
evaluation of tubular function
- Assessment of urine concentrating ability – USG and osmolality
- Remember no “normal” urine specific gravity since concentrating ability is affected by
non-renal factors such as diet, water intake, - Provocative testing of urine concentrating ability through a Modified Water Deprivation
Test – more on how to perform this and indications in the lecture on PU/PD
assessment of Tubular Reabsorption of Electrolytes, other solutes
Hyposthenuria:
USG is < 1.008
❑ This does NOT suggest renal failure; production of dilute urine
is an active process performed by the renal tubules
isosthenuria
USG is fixed and between 1.008-1.015
Hypersthenuria/baruria
these terms are rarely used; baruria urine that is very concentrated - > 1.030 dog, > 1.035 cat;
hypersthenuria refers to urine of higher total solute concentration than glomerular filtrate (USG >1.015, Uosm> 300 mOsm/kg) but is not highly concentrated.
evaluation of tubular function indications
Detection of aminoaciduria, glucose, increased HCO3, etc.
* Fractional excretion of electrolytes
- Indications
- Differentiating prerenal from renal azotemia
- Monitor tubular function when nephrotoxic drug given
- Investigating renal tubular acidosis or Fanconi syndrome
- Provocative Testing for determination of the type of renal tubular acidosis
Urine Culture and Sensitivity
Get a cystocentesis sample unless contraindicated
* For best results culture within 6 hours of collection
* False negatives can occur if urine is refrigeration is prolonged
* Quantitative vs qualitative cultures
medical imaging for urinary system kidneys
Plain radiographs – assess size on a
V/D and symmetry
* Dog 2.5-3.5 L2
* Cat 2.0-3.0 L2 (smaller if neutered)
Normal kidneys have a smooth outline
Renomegaly- AKI, obstruction, hydronephrosis,
PSS, acromegaly, amyloidosis, compensatory
renal hypertrophy, neoplasia,
urinary bladder rads
-Assess size and for displacement
Nonvisual – empty, ruptured, displaced due to
a hernia or mass (sublumbar
lymphadenopathy, colonic impaction,
prostatomegaly)
Enlarged – normal, urine retention, urethral
obstruction
Small bladder – normal, anuria, tear
Abnormal shape – diverticula
Radiopaque calculi
Dystrophic mineralization
normal urethra not visible
hematuria history questions
- can range from yellow (microscopic hematuria or abnormal red to brown (macroscopic hematuria)
-history:
reproductive status
trauma
straining to defecate in male dogs
systemic illness
-need to do tests to rule out pigmenturia and bilirubinuria
hematuria physical exam
- Physical examination
-look for coagulopathy - Any evidence of petechia and or ecchymosis
- Examine for mucus membrane pallor,
epistaxis, hematochezia, swollen joints,
bleeding from venipuncture sites - Do a rectal, examine the genitalia do a specific urogenital examination, digital vaginal exam
- Careful palpation of the bladder and the
kidneys and examination of the genitalia
Observe Micturition for hematuria
-Observing the patient during voiding to verify hematuria and confirm or detect abnormalities such as dysuria / stranguria that could localize the source
* The stage of micturition at which blood appears:
-start of urination: urethral source
-end of urination: urinary bladder origin
-blood throughout = kidney or ureteral origin maybe bladder
prerenal proteinuria
Physiologic/Benign Proteinuria
* Strenuous exercise
* Seizures
* Fever
- Pathologic
- Paraproteinemias
- Multiple myeloma
- Lymphomosarcoma
Post Renal Proteinuria
- Postrenal proteinuria results from
inflammation or hemorrhage in the
LUT - Common causes: cystitis, metritis,
prostatitis, or neoplasia
Proteinuria: Renal
- Disorders of the Glomeruli
-albumin is lost - Disorders of the renal tubules or interstitium
-low molecular wt - The hallmark of glomerular disease is proteinuria in the face of an “inactive”
urine sediment
-can lead to: chronic renal failure, nephrotic syndrome
Nephrotic Syndrome has 4 components:
- Proteinuria
- Hypoalbuminemia
- Hypercholesterolemia
- SC edema or body cavity effusions
Proteinuria: UPCR normal ranges (on exam) and test
- Urine protein creatinine ratio: this test is used to quantify the magnitude of protein loss
- This test should only be done once the results of a complete UA have been evaluated
Normal ranges for dogs and cats** (will be on exam)
* UP/C ratio <0.2 is normal for dogs and cats
* Grey Zone UP/C ratio ≥ 0.2 to 0.5(dogs) and ≥ 0.2 to 0.4(cats)
* Abnormal UP/C ratio is ≥ 0.5 and ≥ 0.4 for dogs and cats
- Can perform on a single random sample of urine or pooled samples
- The UPC ratio CANNOT be used to differentiate patients with glomerulonephritis from
renal amyloidosis
protenuria clinical signs
-azotemia
hypoalbuminemia
-hypercoagulability (decrease in antithrombin III) and increase platelet aggregation
hematuria type
-Hematuria refers to blood in urine – hematuria may be macroscopic (visible with the naked eye with pink, red, or dark brown urine +/- contain blood clots) or microscopic (only visible with
microscope examination of the urine sediment
-Hematuria can be classified as benign (damaged mucosa of bladder) or pathologic (inflammation, neoplasia)
-These pathologic disorders can be classified as prerenal, renal and postrenal
lower urinary tract signs
– typically see pollakiuria, stranguria and dysuria.
upper urinary tract signs
may see signs of systemic disease
steps to determine cause of hematuria
1: good history and physical exam
2: confirm the hematuria and eliminate other causes of red urine (pigments
such as hemoglobin, myoglobin and bilirubin). This will require a urinalysis to begin with.
-. Perform Dipstick Occult Blood Test
-USG
-observe micturition
-urethral catheterization
Pseudohematuria
- if the dipstick and sediment of a second urine sample remains negative
for RBCs/ bilirubin but the urine is still discolored, consider pseudohematuria—urine
discoloration from pigments derived from drugs, food dyes, toxins
Bilirubinuria
- the clinical significance of bilirubinuria depends on the patient’s
species, sex and urine specific gravity.
a. Any bilirubinuria in a cat is significant. In dog urine trace or 1+ bilirubinuria is
acceptable with a USG > 1.020 but if the urine is very dilute 1this maybe
Intermittent Hematuria
-depending on the scenario consider microscopic hematuria of unknown
cause or intermittent hematuria
quantification of proteinuria
-the magnitude of the proteinuria will help determine if renal proteinuria is
glomerular or tubulointerstitial in origin. Magnitude is assessed using a quantitative test for urine protein
-Why is persistent renal proteinuria significant? Proteinuria is a negative
prognostic indicator for chronic kidney disease. It leads to interstitial fibrosis as well as tubular degeneration and atroph
Glomerular Proteinuria - Clinical Evaluation
-results can be falsely elevated with
alkaline urine, pigmented urine, or with highly concentrated urine. Acidic urine can cause false negative results
-SSA test - a semi-quantitative test is able to detect proteinuria at values > 5 mg/dl and detects albumin and other proteins such as globulins, Tamm-Horsfall and Bence Jones proteins, although it often underestimates them. False positive results occur with the presence of radiographic contrast agents, some drugs (e.g., cephalosporins, penicillin).
There are fewer false negatives compared to the dipstick test
normal water homeostasis relies on
a) Normal secretion of the hormone ADH
b) Normal responsiveness of the renal tubules to ADH and vasopressin
c) The maintenance of a high osmolarity renal medullary interstitium; this medullary concentrating
gradient is largely the result of Na, Cl and urea reabsorption
d) intact thirst centre
polyuria
increased volume of urination > 2 mls/kg/hr or > 50 mls/kg/day
polydipsia
increased drinking > 100 mls/kg/day (dogs) and > 45 mls/kg/day (cats)
For PU/PD to be considered a true problem, two criteria need to be meet:
a) The owner reports or documents sustained increased water intake or urine output.
b) The USG for the animal is found to be persistently low** except DM
A one time low USG is not meaningful in an otherwise
healthy animal or an animal without clinical signs of PU/PD
◼ Need to take into account the age of the animal, the species, the diet when evaluating the significance of a USG
◼ Medication history is important
Aldosterone and Thirst
◼ Thirst center in hypothalamus
❑ Stimulated by a decline in plasma volume 10-15%, Via baroreceptors and ang II
◼ Aldosterone - principal function is to sustain extracellular
fluid volume by conserving body sodium
❑ Also important for regulating plasma K+
◼ Produced by the adrenal cortex –RAAS activation
Pu/PD causes types
◼ Causes of PU/PD can be either divided into two broad categories:
❑ Primary polydipsia with compensatory polyuria
◼ Primary or secondary
❑ Primary polyuria with compensatory polydipsia – most common**
❑ ** some patients have both
-Differentiation of the PU/PD disorders is important since treatment will differ and the wrong treatment can have
deleterious consequences
Primary polydipsia
compensatory polyuria causes
❑ Primary (idiopathic) psychogenic polydipsia
❑ Secondary polydipsia –
fever, pain, overactive thirst
center
-could be:
-lack of production of ADH
-renal insensitive to ADH
❑ Osmotic diuresis
❑ Disorders associated with renal
medullary washout – ALWAYS RULE
OUT FIRST
mechanisms of PU/PD**
acronym for PU/PD causes
◼ CLAMPED RIBS
❑ C alcium
❑ L iver insufficiency/disease
❑ A drenal disease
❑ M etabolic – including electrolytes (low K or Na, high Na)
❑ P sychogenic, polycythemia, pyelonephritis, pyometra
❑ E ndocrine – hyperadrenocorticism, acromegaly…
❑ D rugs, diabetes mellitus, diabetes insipidus
❑ R enal insufficiency/failure
❑ I nfection
❑ B rain
❑ S alty treats, salty diets
Causes of PU/PD resulting from a lack of production or secretion of ADH (also termed central
diabetes insipidus or neurogenic diabetes insipidus
❑ Primary or metastatic CNS disease
❑ Infection - sepsis
❑ Idiopathic**- this is the most common cause
❑ Granulomatous disease
❑ Trauma
❑ Iatrogenic
❑ High set osmoreceptors
Causes of renal tubule insensitivity or resistance to ADH (also termed nephrogenic diabetes
insipidus) include
Primary = congenital NDI – rare
◼ Secondary = acquired
HyperPTH
◼ Secondary = acquired Osteomyelitis
HOG IN YARD
H yper PTH
O steomyelitis
G ranulatamous disease
I diopathic -cats
N eoplasia
Y outh. spurious
A ddisons**
R enal disease
D vit D toxicosis
Causes of renal medullary washout include:
a) This may be a component of many causes of PU/PD because loss of medullary hypertonicity will occur with any cause of prolonged polyuria.
◼ CRF – not enough nephrons left
◼ Diabetes mellitus * USG not that low in cats
◼ Diuretic therapy
◼ Post obstructive diuresis
-diet
Causes of primary polydipsia
-with compensatory polyuria can be caused by fever, pain, CNS, GI and liver disease
neoplasia or encephalopathies, or may be idiopathic
most common causes of PU/PD cats and dogs
❑ Dogs: CRF, hyperadrenocorticism, diabetes
mellitus, pyometra
❑ Cats: CRF, hyperthyroidism, and diabetes
mellitus
◼ But Beware of being trampled by the zebra or
by the unicorn
❑ Kitten with head trauma that develops central diabetes
insipidus
pu/pd diagnostic approach
-singlement gives you a clue to it
-complete history and physical exam
-rule out pharmalogiacl causes
-PU/PD animal produces large volumes of urine with no stranguria or dysuria. Nocturia or
inappropriate urination may be seen
-look at your minimun data base of tests
-rule out endocrine
-urine culture
-imaging
-if still unknown -have owner measure water intake for 5-7 days to get baseline, perform water deprivation test
Pollakiuric
-animals typically produce only very small volumes and will show evidence of stranguria, hematuria or dysuria
true incontinent
- animal do not posture to urinate normally, and may show other neurologic deficits
What if you still do not have a definitive diagnosis for
PU/PD in a patient after such an initial work-up to rule out
the usual suspects?
-Need to differentiate Diabetes Insipidus from Psychogenic Polydipsia
-If the underlying cause is still unknown and no clear contraindications exist, the next step is to either
measure GFR or to perform a modified water deprivation test (MWDT)
Miscellaneous disorders with complex or unknown mechanisms causing PU/PD
a) Hyperthyroidism
b) Cushing’s
c) Hypoadrenocorticism
d) Liver disease
MWDT (water deprevation test)
◼ Used to distinguish primary polydipsia from diabetes
insipidus (central and nephrogenic)
❑ Typically do last when you have failed to find a cause with more practical diagnostic tests
◼ Response to injectable administration of vasopressin in stage III
may allow differentiation of nephrogenic diabetes insipidus from
central diabetes insipidus
◼ CDI – expect a response – USG will increase
◼ NDI – expect no response – USG will not increase
modified water deprivation test contraindications and indications
Contraindications for a MWDT
1. Documented renal disease – azotemia with dilute USG, etc.
2. Dehydration – clinically detected or detection of azotemia.
3. Hypercalcemia
◼ Only perform when all the common causes ruled out
3.The test is preformed in three stages: gradual water restriction, followed by abrupt water restriction, and if necessary, an ADH response test
Diabetes Insipidus characteristics
a) Diabetes insipidus (DI) results from either a complete or partial deficiency of ADH (central or
partial central DI) or resistance to ADH at the level of the distal renal tubules and the collecting
ducts (primary and secondary nephrogenic DI).
◼ Characterized by PUPD and hyposthenuria (USG < 1.008)
Onset of c/s may be insidious, but more commonly is abrupt
❑ Nocturia and incontinence secondary to PU may be seen
❑ Weight loss
Treatment of Diabetes Insipidus
◼ Central DI (idiopathic) can be treated with a long acting ADH analogue
DDAVP (desmopressin) $$$
◼ Nephrogenic Diabetes Insipidus – whenever possible you need to
identify and treat the underlying disease
❑ Continuous supply of water
-if no underlying cause can treat with thiazide dieretic
Psychogenic Polydipsia
◼ Compulsive Drinking
◼ Boredom in young large breed dogs
◼ Tx options are limited – behavioral modification, behavioral medications and
water restriction with BW monitoring ideally
