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Clinical Pathology > Intro to Urinary Evaluation > Flashcards

Intro to Urinary Evaluation Flashcards

1
Q

What are the functions of the kidney?

A
  • Clear metabolic wastes from blood
  • Conserve nutrients
    • Glucose
    • Protein
  • Maintain water, electrolyte, and A-B balance
  • Hormone production
    • Erythropoietin
    • Vitamin D
    • Renin
  • Hormone degradation and/or excretion
    • PTH, Growth Hormone, Secretin, Cholecystokinin, glucagon, gastrin, prolactin, insulin, thyrotropin and ADH
  • Enzyme degradation and/or excretion
    • amylase, lipase
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2
Q

What determines what through the glomerular filtration barrier when healthy?

A
  • size (mol wt > 68,000 not filtered)
  • Charge
    • Basement membrane - negative charge
    • Negatively charged molecules may be repelled
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3
Q

During health what stays in the blood and what passes through the barrier?

A
  • Stays:
    • Cells (WBC, RBC, Platelets)
    • Most plasma proteins ( Albumin & larger proteins)
  • Passes:
    • Water
    • Solutes
      • Electrolytes
      • Glucose
      • Urea
      • Small proteins (other)
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4
Q

What are the major physiologic processes of the nephron?

A
  • Glomerular filtration (passive)
    • Substances move from plasma to tubules
  • Tubular resorption (passive & active)
    • Substances move from tubules to plasma
  • Tubular secretion (passive & active)
    • Substances move from plasma to tubules
  • Water Regulation
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5
Q

What is the Glomerular Filtration Rate (GFR)?

A
  • Volume of plasma filtered from glomerular capillaries into Bowman’s space per unit of time
    • Measured by determining rate of clearance of a substance from plasma
  • GFR: rate substances are cleared from plasma via glomeruli
  • ⇣ GFR: substances cleared slower; stay in plasma longer
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6
Q

What does GFR depend on?

A
  • Renal blood flow
  • # of functional nephrons
  • Hydrostatic pressure in Bowman’s capsule
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7
Q

How can renal function be evaluated?

A
  • Glomerular filtration - look for protein in urine
  • Glomerular filtration rate - Look for accumulation of waste products in blood (UN, creatinine)
  • Ability to concentrate urine - urine specific gravity
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8
Q

What is osmolality?

A
  • Total solute concentration
    • Concentration of solutes per kg Water (mmol/kg H2O)
  • Urine Osmolality varies greatly -
    • H2O conservation
    • Solutes excreted
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9
Q

How can osmolality and USG be measured?

A
  • Osmometer (measures osmolality)
    • Freezing point assay, not convenient, more accurate
    • Measure depends on the number of particles in the volume of water
  • Refractometer (measures USG)
    • Convenient, less accurate
    • Depends on particle weight and how each particle bends light
      • Prone to interference - difference between how glucose, electrolytes, urea, proteins, lipids, and other substances refract light
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10
Q

How are Urine Osmolality and USG related?

A
  • Typically excellent correlation between osmolality & USG
    • As osmolality increases, USG increases by an approximate factor of 30
  • Both change with # of particles/volume
    • USG also changes with types of particle
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11
Q

How does the kidney handle water?

A
  • Kidneys receive ~25% of cardiac output
  • ~99% of water entering the tubules is resorbed
  • Healthy person (70 kg)
    • ~180L of water enters the kidney
    • ~1-2 L of urine excreted daily
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12
Q

What is Antidiuretic hormone (ADH)?

A
  • Synonym = vasopressin
  • Synthesized in the hypothalamus
  • Secreted from the posterior pituitary gland (neurohypophysis)
  • Interacts with receptors on the cells of the distal tubules and collecting ducts
    • Opens water channels via aquaporin proteins (minutes)
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13
Q

What re the stimuli for ADH secretion?

A
  • Plasma hyperosmolality
    • Osmoreceptors (hypothalamus)
  • ⇣ cardiovascular pressure (hypovolemia)
    • Baroreceptors
  • ⇡ angiotensin
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14
Q

What is the result of ADH?

A
  • Conserve body water to ⇣plasma osmolality & ⇡blood volume
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15
Q

What are the major events of the nephron segments that influence osmolality?

A
  • Proximal CT - removes volume
    • no change in concentration
  • Descending LoH - removes H2O
    • ⇡ concentration
  • Ascending LoH - removes solute
    • dilutes (⇣⇣ concentration)
  • Distal nephron - removes H2O
    • ⇡ concentration
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16
Q

What is needed to produce concentrated urine?

A
  • Adequate number of functional nephrons
  • Adequate production o ADH from pituitary
  • Distal nephron epithelial cells must be responsive to ADH
  • Hypertonic interstitium in the renal medulla
    • Must be a concentration gradient between tubular fluid and interstitium (osmolality of the interstitium > osmolality of the tubular fluid
    • Urea, Na+, Cl- = major contributors
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17
Q

What are the expected USG for dehydrated animals?

A
  • Dog: > 1.030
  • Cat: >1.080
  • Horses/Cattle: >1.50
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18
Q

What are the possible clinical interpretation of USG?

A
  • Urine osmolality > plasma osmolality
    • USG > 1.013
    • interpret with hydration status
  • Urine osmolality = plasma osmolality
    • Isosthenuria
    • USG = 1.007 - 1.013
    • in a dehydrated animal, indicates kidneys have not concentrated nor diluted the tubular fluid
  • Urine osmolality < plasma osmolality
    • Hyposthenuria
    • USG ≤ 1.006
    • Implies that the kidneys have actively diluted the tubular fluid
    • NOT renal failure
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19
Q

What is anuria?

A

lack of urine production

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20
Q

What is Dysuria

A

painful or difficult urination

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21
Q

what is oliguria

A

production of an abnormally small amount of urine

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22
Q

What is pollakiuria

A

indicating increased frequency of urination

Doesn’t indicate urine volume

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23
Q

what is polydipsia

A

increased water consumption

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24
Q

what is polyuria

A

production of excessive amounts of urine

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25
Q

What are the routine laboratory tests to assess renal function?

A
  • Glomerular filtration adequate (GFR)
    • Urea Nitrogen
    • Serum creatinine
    • SDMA
  • Integrity of glomerular structure
    • Urine protein
    • Urine protein : urine creatine ratio
  • Ability to concentrate and dilute urine
    • USG
      • comparison of urine & plasma osmolality
    • Provocative tests of urine concentrating ability
      • water deprivation test
  • Urinalysis
    • USG, Chemistry, and sediment examination
      • assesses more than the urinary tract
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26
Q

What is Azotemia?

A

Increased concentration of Urea Nitrogen (UN or BUN) and/or Creatinine

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27
Q

How is urea synthesized and excreted?

A
  • Ammonium (NH4+) goes through the urea cycle in the liver to become urea
  • Goes through the renal system
    • ~50% is resorbed in the proximal tubule
      • depends on flow rate and H2O resorption
      • ⇣ GFR = ⇡UN
    • ~10% resorbed in collecting tubule
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28
Q

What causes increased urea formation?

A
  • High protein diet (mild, transient effect)
  • GI hemorrhage
  • Disorders that increase endogenous protein catabolism
29
Q

What causes decreased urea formation?

A
  • Hepatic failure/shunt
  • Malnutrition
  • Diuresis
30
Q

What are alternate routes of excretion for Urea Nitrogen?

A
  • Saliva, sweat, GI tract
    • Minimal to no effect on UN concentration in dogs & cats
  • GI tract excretion of urea is significant in horses and ruminants
    • UN is not a sensitive indicator of GFR in those species
    • Bacteria in the rumen (cattle/sheep/goats) or cecum (horses) degrade urea to NH4+ to make amino acids
31
Q

How does Urea Nitrogen drive recovery of water/concentration of urine in the collecting ducts

A
  • Urea diffuses readily across most cell membranes along a concentration gradient
    • Rapid equilibration among intracellular and extracellular fluid compartments (~90min)
    • Equilibrium between erythrocytes, plasma/serum
  • Whole blood UN = Serum UN
  • Urea contributes to the renal medullary concentration gradient along with electrolytes
32
Q

What tubes need to be used when testing for UN?

A
  • Serum (red top tube)
  • Plasma (green top tube)
  • Stable for 1 day at room temp, several days at 4-6C, and 2-3 months frozen
33
Q

How is creatinine Metabolized

A
  • Creatinine is a waste product from the normal breakdown of muscle tissue
    • the amount formed daily is constant for any animal
    • Production proportional to muscle mass
  • Removed almost exclusively via renal excretion
    • Freely filtered through glomerular barrier into ultrafiltrate
    • Not resorbed by tubules
    • Excreted in urine
34
Q

How is creatinine Metabolized

A
  • Creatinine is a waste product from the normal breakdown of muscle tissue
    • the amount formed daily is constant for any animal
    • Production proportional to muscle mass
  • Removed almost exclusively via renal excretion
    • Freely filtered through glomerular barrier into ultrafiltrate
    • Not resorbed by tubules
    • Excreted in urine
35
Q

Where is creatinine measured?

A

in serum or plasma (Green or red tube) NOT whole blood

36
Q

What causes increased Creatinine (Ct) levels?

A
  • Decreased GFR
  • it does NOT increase with increased muscle catabolism
37
Q

What causes decreased Creatinine?

A
  • May not be clinically significant
  • Consider:
    • decreased muscle mass
    • hypoproteinemia
38
Q

What is the relationship between UN and Ct in dogs/cats?

A
  • UN & Ct increase in parallel when GFR is decreased as a result of renal failure
  • Prerenal azotemia can cause a disproportionately greater increase in UN than creatinine
    • increased tubular resorption of urea (urea absorbed with water)
  • GI hemorrhage ⇢ increased UN
  • many animals with renal disease are anorectic or eat a low protein diet ⇢ decreased UN relative to creatinine
  • Extremely cachectic (physical wasting) animals have decreased muscle mass and may have decreased creatinine compared with UN
39
Q

What do the levels of UN/Ct indicate in horses/ruminants

A

Creatinine more specific for renal compromise than UN because urea is metabolized by bacteria in the rumen or cecum

40
Q

What are the different types of Azotemia?

A
  • ⇡ UN and/or ⇡Crt concentration in serum or plasma (or blood)
    • Prerenal: primary cause is pre-glomerulus
    • Renal: primary cause is nephron
    • Postrenal: primary cause is after the nephron
41
Q

What are possible causes of Pre-renal azotemia?

A
  • Azotemia results from processes outside of the kidneys
    • UN & Creatinine are increased
    • Urine is concentrated
  • Possible causes:
    • Decreased renal blood flow = decreased GFR
      • Dehydration
      • hypovolemia / fluid maldistribution
      • Severely decreased cardiac output
    • increased production of urea and/or creatinine
      • Urea
        • high protein diet
        • GI hemorrhage
      • Creatinine
        • Heavily muscled animal
42
Q

What is Renal azotemia?

A
  • Primary cause is within the nephron
  • Azotemia results from any form of renal disease that causes enough damage to the kidney to decrease the GFR
  • Loss of functional nephrons ⇢ GFR is decreased even if renal blood flow is normal
    • UN and creatinine are increased
    • urine is NOT concentrated in the face of dehydration
      • decreased concentrating ability
      • Isosthenuric urine (1.007 - 1.013) indicates an inability to concentrate and dilute
43
Q

What is Post-renal azotemia?

A
  • Primary problem is after the nephron
  • Results from a problem that interferes with excretion of urine somewhere distal to the nephron
    • UN and Crt are increased
    • Urine concentration varies
  • Ex:
    • Ureteral / urethral obstruction - hydrostatic pressure within the Bowman’s capsule is increased and GFR is decreased
    • Rupture / leakage along the urinary outflow tract (kidney, ureter, bladder, urethra) causing leakage of urine into abdominal cavity
44
Q

How is Azotemia different from Uremia?

A
  • Azotemia - increased concentration of non-protein nitrogen compounds in blood (UN and Crt)
  • Uremia:
    • Clinical syndrome associated with renal failure
    • Azotemia + severe physical consequences of renal failure
      • Polyuria / polydipsia
      • Vomiting / diarrhea
      • Ammonia odor of breath
      • GI ulcers
      • Nonregenerative anemia
      • Weigh loss
      • Convulsions
      • Death
45
Q

What abnormal laboratory results are expected in azotemic animals?

A
  • Sodium and Chloride
    • ⇡ with Prerenal azotemia
    • Low / WRI with renal failure due to decreased resorption
  • Potassium (excreted by kidney)
    • ⇡ in oliguric / anuric renal failure (ARF)
    • ⇣ in cats/cows with polyuric renal failure (CRF)
      • Most common electrolyte abnormality in cats with CRF - may cause marked muscle weakness
  • Phosphate
    • Excretion is ⇣ when GFR ⇣ for any reason
    • Usually ⇡ in animals with moderate to marked azotemia
  • Magnesium
    • ⇡ with ⇣GFR
  • Calcium
    • Dogs/cats/cattle:
      • WRI / slightly decreased with renal failure
      • hypercalcemia with azotemia is more likely to be the cause for renal disease than the result (but can develop secondary to renal failure)
    • Horses rely on renal excretion of calcium
      • High in most horses with renal failure
  • Hematocrit
    • WRI / ⇡ in pre-renal azotemia and ARF
    • Non-regenerative anemia in CRF (decreased RBC life-span & Epo production)
  • Total Protein, Albumin
    • WRI / ⇡ in pre-renal azotemia +/- ARF
      • only reason for increased albumin concentration is dehydration
    • WRI / ⇣ in CRF (especially with glomerular proteinuria)
  • Acid/base
46
Q

What is SDMA?

A
  • Symmetric Dimethylarginine (SDMA)
  • Kidney excretory function biomarker
47
Q

Why would SDMA be elevated?

A
  • In dogs/cats with renal disease
    • ⇡ [SDMA] before ⇡ [Creatinine]
    • ⇡ [SDMA] before ⇡ [Urea]
  • Prerenal azotemia:
    • ⇡ proteolysis ⇢ ⇡⇡ production ⇢ ⇣ renal blood flow ⇢ ⇣ GFR
  • Renal azotemia:
    • ⇣ number of nephrons ⇢ ⇣ GFR
  • Postrenal azotemia:
    • Obstruction ⇣ ⇣ GFR
    • Urine leakage
48
Q

What is an indicator of Stage 1 CKD?

A

Persistent elevation in SDMA in a hydrated and urinating dog/cat without azotemia indicates reduced renal function

49
Q

What are the mechanisms of Polyuria?

A
  • Lack of ADH production
    • Central diabetes insipidus (pathologic)
    • Psychogenic polydipsia (behavioral)
  • Distal tubule / collecting duct cells cannot respond to ADH
    • Nephrogenic diabetes insipidus
  • Must be a concentration gradient between tubular fluid and interstitium (Must have osmolality of the interstitium > osmolality of the tubular fluid)
    • Solute diuresis
    • Reduced medullary interstitium osmolality
50
Q

What is Solute diuresis?

A
  • When water is not resorbed
  • Can occur when the kidneys are functioning normally but are presented with increased solute (eg Diabetes Miletus)
  • Can occur when there are decreased # of functional nephrons
    • ⇡ solute load on the available nephrons
51
Q

What is Chronic Renal disease?

A
  • No universally accepted definition or criteria for staging
    • Major Criteria -
      • Evidence of GFR
      • Evidence of ⇣ concentrating ability
52
Q

What are the Stages of Chronic Renal Disease? (for this course)

A
  • Decreased Renal Reserve:
    • GFR ~50% normal
    • Clinically healthy - NOT azotemic or polyuric
  • Chronic renal insufficiency:
    • 25-50% function
    • Azotemia, anemia, ⇣concentrating ability, polyuria
  • Chronic renal failure:
    • <20-25% function
    • Azotemia, anemia, ⇣ concentrating ability, polyuria
    • Electrolyte imbalance, clinical signs of uremia
  • End-stage renal disease:
    • <5% function
    • Terminal uremia signs and oliguria or anuria

Percentages Not true for cats*

53
Q

What is the cause of Polyuria in Chronic Renal Disease?

A
  • Loss of functional Nephrons
    • More solute presented to remaining functional nephrons
      • ⇡ load through nephrons
      • Solute diuresis
  • Medullary hypertonicity is not maintained
    • Medullary tissue damage or abnormal blood flow
    • ⇣Na+, Cl- and urea reabsorption
  • Damaged cells less responsive to ADH
54
Q

What is the evidence for Renal insufficiency/Failure?

A
  • Azotemia
  • Inappropriaely low USG (1.007 - 1.013)
  • Inability to concentrate or dilute
55
Q

What is the evidence that renal insufficiency/failure is chronic?

A
  • Anemia
  • Hypocalcemia or WRI (dogs, cats, ruminants)
  • Hypercalcemia (equids)
  • clinical findings including duration of signs
56
Q

What is Acute Renal failure?

A
  • Abrupt insult or disease
  • Marked decrease in GFR ⇢ Azotemia ⇢ uremia
    • degree of azotemia does not differentiate chronic vs acute
    • rate of increase of UN & Crt more rapid in acute disease
  • Reversible or Irreversible
57
Q

What happens to urine volume and USG during acute renal failure?

A
  • Volume:
    • Kidneys may filter little blood ⇢ oliguria or anuria
    • No time for compensatory hypertrophy of healthy nephrons
  • USG:
    • Variable
      • Concentrated - if formed prior to insult
      • Isosthenuric - no ability to concentrate or dilute
      • Not expected to be hyposthenuric
58
Q

What is Hemorrhagic/Inflammatory proteinuria?

A
  • Most common mechanism for additional protein in urine
  • Hemorrhage anywhere in the Urinary tract
  • Inflammation causing exudation of plasma proteins into the urinary tract
  • Magnitude varies but it does NOT lead to hypoalbuminemia
59
Q

What is Functional proteinuria?

A
  • Transient mild increase in urine protein content
    • exercise, fever, seizures, stress
    • mechanism unclear
60
Q

What is Overload proteinuria?

A
  • increased plasma concentration of small proteins that pass through glomerular filtration barrier and exceed capacity for tubular resorption
    • Hemoglobin, myoglobin, immunoglobulin light chains (Bence Jones proteins)
    • Does NOT lead to hypoproteinemia
61
Q

What is Tubular proteinuria?

A
  • Proximal tubular injury causing failure to resorb small proteins
    • Usually associated with acute renal tubule damage
      • nephrotoxic agent or ischemia
  • Does NOT result in hypoproteinemia
62
Q

What is Glomerular proteinuria?

A
  • Damage/disruption of the glomerular filtration barrier
    • immune complex deposition
    • Amyloid deposition
    • Inflammatory cells contribute - release cytokines and other mediators that can damage the glomerulus
  • Increased permeability to large and/or negatively charged proteins
    • Albumin first, globulins later with progressive damage
    • Damage often leads to selective hypoproteinemia
  • Progressive disease can lead to:
    • tubular damage and tubular proteinuria, loss of nephrons ⇢ azotemia, renal failure
  • Leads to Selective Hypoproteinemia
63
Q

What happens with severe glomerular damage?

A
  • With sever glomerular damage - entire nephron may become non-functional
    • if many nephrons are lost - signs of renal failure
      • azotemia, uremia, isosthenuria, acidemia, etc
64
Q

What is Nephrotic syndrome?

A
  • Severe, persistent proteinuria
  • Hypoproteinemia (loss of many proteins)
  • Hypercholesterolemia
  • Ascites or edema (decreased plasma oncotic pressure)
65
Q

What are the Pre and Post renal sources of Proteinuria?

A
  • Hemorrhage - red/red-brown, turbid urine with RBCs in sediment
  • Hemoglobinuria - red/red-brown urine, no RBCs in sediment, red/red-brown plasma, anemia
  • Myoglobinuria - red/red-brown urine, no RBCs, plasma normal color, not anemic, signs of severe muscle damage, increased CK
  • Inflammation -WBCs in sediment
66
Q

When should Glomerular disease be suspected when interpreting Urine Protein Assays (Dipstick)?

A
  • When there is no evidence of non-glomerular sources of proteinuria AND:
    • 1+ protein in dilute urine (USG < 1.012)
    • ≥2+ protein in concentrated urine
    • And/or hypoalbuminemia with no other cause present
67
Q

What is the Urine Protein : Urine Creatinine Ratio (UPC)?

A
  • An index of the amount of protein regardless of urine concentration
  • Measured in a single urine sample
  • most useful when pre- and postrenal sources of protein have been ruled out
  • Will be Increased with any increase in protein
68
Q

What are the different UPC ratios and their interpretations?

A
  • UPC < 0.2: healthy dogs/cats
  • UPC 0.1 - 0.4 (cats) 0.1 - 0.5 (dogs): borderline
    • not conclusive evidence of proteinuric renal disease
  • UPC 0.4 - 3.0 (C) 0.5 - 3.0 (D): proteinuria present
    • could result from glomerular or tubular disease
  • UPC > 3.0 - glomerular disease
    • tubular disease may also be present, but it is not the only one
  • UPC ~15+ : most indicative of amyloidosis

Clinical Pathology (12 decks)

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