urinalysis

review
BIEN ALFONSO B. SALVA,RMT
01
INTRODUCTION
TO URINALYSIS
HISTORY AND
SIGNIFICANCE
:Discovered albuminuria in 1694 by boiling urine
:Wrote a book about "pisse prophets", inspired the
passing of the first medical licensure laws in
England
:Developed the first method of quantitative urine
microscopic examination
:Introduced urinalysis as part of a doctor's routine
patient examination in 1827
urine composition
Urine is normally 95% water
and 5% solute INORGANIC COMPONENT

ORGANIC COMPONENT Primary inorganic component

Pimarily from salt intake

Primary organic component
Combined with chloride and other saits
Product of creatine
metabolism Combines with sodium, buffers the blooc

Product of nucleic acid Regulates blood and tissue fluid acidity

breakdown
Combines with chloride, sulfate,
Excretion form of benzoic acid phosphate
 SPECIMEN COLLECTION
CONTAINER
Clean, dry, leak-proof, wide-mouthed, flat bottom, must be made from clear material
Recommended capacity:
LABELS
Must include patient's name and identification number, date and time of collection
Additional infomation such as patient's age and location, physician's name
Must be attached not on the lid; should not be detached when specimen is
refrigerated or frozen
REQUISITION
Must accompany the specimen when delivered to the laboratory
The information on this form must match the specimen label
Additional information can include method of collection, type of specimen,
medications, clinical information. The time the specimen is received should be
recorded on the form
SPECIMEN REJECTION
1. Specimen in unlabeled containers
2. Nonmatching labels and requisition
forms
3. Specimen contaminated with feces or
toilet paper
4. Containers with contaminated exteriors
5. Specimens of insufficient quantity
6. Specimens that have been improperly
transported
 SPECIMEN HANDLING
AND PRESERVATION
Collected specimens should be delivered in the laboratory promptly
and tested within 2 hours
If testing cannot be carried out within 2 hours, an appropriate
preservative must be employed
The most routinely used method of preservation is
refrigeration at 2 to 8 degrees Celsius
 SPECIMEN HANDLING
AND PRESERVATION
Specimens must be returned to room temperature before
chemical testing by reagent strips because the enzyme reactions
on the strips perform best at room temperature
Specimens for culture should be refrigerated on transport and kept
refrigerated until culture for up to 24 hours only
When preserving samples that will be transported to another
laboratory, be sure to check with the laboratory concering the
appropriate preservative
 CHANGES OCCURING
IN UNPRESERVED URINE
CHANGE ANALYTE CAUSE

Color Oxidation or reduction of metabolites

Odor Breakdown of urea to ammonia by bacteria

Breakdown of urea to ammonia by urease-producing

pH
bacteria

Nitrite Multiplication of nitrate-reducing bacteria

Bacteria Multiplication
CHANGE ANALYTE CAUSE

Bacteria growth and precipitation of amorphous

Clarity
material

Glucose Glycolysis and bacterial use

Ketones Volatilization and bacterial metabolism

Bilirubin Exposure to light/photooxidation to biliverdin

Urobilinogen Oxidation to urobilin

RBC, WBC, and

Disintegration in dilute alkaline urine
Casts

Trichomonas Loss of motility, death

 URINE
PRESERVATIVES
Most routinely used method of preservation; Does not interfere with chemical tests
Precipitates amorphous phosphates and urates ; Prevents bacterial growth for 24 hours

Prevents bacterial growth and metabolism; Interferes with drug and hormone analysis
Keeps pH at about 6.0; Can be used for urine culture fransport

Excellent sediment preservative

Acts as a reducing agent interfering with chemical tests for glucose, blood, leukocyte
esterase and copper reduction
Rinse specimen container with formalin to preserve cells and casts
 URINE
PRESERVATIVES
A good preservative for drug analysis.
Inhibits reagent strip test for glucose, blood, and leukocytes

Does not interfere with routine test; cause an odor-change

Use 1 drop per ounce of specimen

Preserves glucose and sediments well

Interferes with acid precipation test for proteins
 URINE
PRESERVATIVES
Does not interfere with routine test
Floats on the surface of the specimen and clings to pipettes and testing materials

Preseves cellular elements; used for cytological studies

 TYPES OF URINE
SPECIMEN
Most commonly received specimen
Useful for routine screening tests to detect obvious abnormalities

Ideal screening specimen; most concentrated

Prevention of false negative pregnancy test and evaluation of orthostatic
proteinuria

Quantitative chemical tests

Measurement of analytes exhibiting diurnal variation
 TYPES OF URINE
SPECIMEN
Collected under sterile conditions by passing a hollow tube through the
urethra into the bladder.

Provides a safer and less traumatic method of obtaining urine for culture
Aternative to catheterized specimen

Collected by external introduction of a needle through the abdomen into the

bladder
Preferred sample for bacterial culture and cytolagical examination
 TYPES OF URINE
SPECIMEN
Collected by external introduction of a needle through the abdomen into the bladder
Preferred sample for bacterial culture and cytolagical examination

Collection is done using soft, clear, plastic bags with hypoallergenic skin adhesive to
attach to the genital area. Bag is checked approximately every 15 minutes until the
needed amount of sample has been collected.

Collection and handling of the specimen must follow the chain of custody
Urine volume:
Container volume:
Urine temperature:
 TYPES OF URINE
SPECIMEN
Three glass collection Pre and Post Massage Test Stamey-mears test

Prostatitis
02
RENAL FUNCTION
COMPONENTS OF
THE URINARY
SYSTEM
01
bean-shaped paired organs
located on the retroperitoneum;
site of urine formation

02
structure attached to each
kidney and caries urine to the
bladder
 03
a three-sided pyramid-like
structure which stores
urine until excretion

04
a structure longer in males
which delivers urine for
excretion
 PARTS OF THE KIDNEYS
macroscopically granular outer layer of about 1.4cm thick
contains all the glomeruli, thus it is the exclusive site of
plasma filtration process

inner layer of pyramid-shaped renal tissue. Site of urine

concentration.

funnel-shaped structure that emerges from the indented

region of each kidney and narows to join with the ureter
 NEPHRON
CORTICAL JUXTAMEDULLARY
NEPHRONS NEPHRONS
Moke up approximately 85% of Have longer loops of Henle that
nephrons extends deep into the medulla
Situated primarily in the cortex of the kidneys
Responsible primarily for the Primarily responsitble for urine
removal of waste products and concentration
reabsorption of nutrients
 PARTS OF THE NEPHRON
Glomerulus and
Renal Corpuscle

Proximal Convoluted Tubule

Descending loop of Henle

Ascending loop of Henle

Distal Convoluted Tubule

Colleting Ducts
Renal blood flow
The kidneys receive approximately 25% of the
blood pumped through the heart at all times
Renal blood flow is approximately 1200
mL/min. 600 - 700 mL/min of plasma
 GLOMERULAR
FILTRATION
1. Molecular weight: <70,000 daltons
2. Cellular structure of the capillary walls:
Capillary wall membrane:
Basement membrane:
Visceral epithelium of the Bowman’s capsule
3. Glomerular pressure:
Hydrostatic pressure
Oncotic pressure
4. Renin-Angiotensin-Aldosterone system
RAAS
 TUBULAR REABSORPTION
ACTIVE TRANSPORT PASSIVE TRANSPORT

Glucose, Salt,
Water
Amino acids

Sodium Sodium

Chloride Urea
tubular secretion
Elimination of waste products not
filtered by the glomerulus

Regulation of acid-base balance

of the body
 GLOMERULAR
FILTRATION TEST
Clearance tests
Earliest glomerular filtration test

A polymer of fructose infused at a constant rate; formerly the

reference method

Product of muscle metabolism; dependent on muscle mass

Most commonly used method
 Clearance tests
Small protein produced at a constant rate by all nucleated cells
Recommended for pediatric patients, diabetic patients, elderly and
critically ill patients

Dissociates from the human leukocyte antigens at a constant rate

Not recommended for patients who have history of immunologic
disorders

Provides a method for determining GFR through plasma

disappearance of the material
Allows visualization of the filtration in one or both kidneys
Useful in determining the viability of a transplanted kidney
CALCULATED GLOMERULAR
FILTRATION ESTIMATES
Formerly the most frequently used formula
Age, Sex and Body weight (kg) are the variables included in the original formula
Modifications: IBW and ABW(correction for weight not due to muscle mass)

Most frequently used formula

Utilizes additional variables such as ethnicity, BUN and serum albumin
Does not include bodyweight

Recommended by the NKDEP

Corrects for the discrepancy brought by methods used in measuring serum creatinine
 TUBULAR
REABSORPTION TESTS
SPECIFIC GRAVITY OSMOLARITY
WATER DEPRIVATION TEST
FISHBERG

MOSENTHAL
 OSMOMETRY
FREEZING POINT

VAPOR PRESSURE
FREE WATER CLEARANCE
Used to determine the ability of the kidneys to
respond to the state of body hydration
Determined by calculating the osmolar clearance and
subtracting it from the urine volume (ml/min)
OSMOLAR CLEARANCE - indicates how much water
must be cleared each minute to produce a urine with
the same osmolarity as the plasma
Interpretation:
(-) = less water is being concentration excreted;
possible state of dehydration
(0) = no renal concenration or dilution
(+) = excess water is being excreted
 TUBULAR SECRETION AND
RENAL BLOOD FLOW TEST
P-AMINOHIPPURIC ACID (PAH TEST)
Exogenous procedure but it meets the criteria needed to measure renal blood fow
Nontoxic substance which is loosely bound to plasma proteins and is secreted by the PCT
Clearance of this substance can be used to calculate the effective renal plasma flow

PHENOLSULFONPHTHALEIN (PSP TEST)

A dye entirely cleared by the tubules
Normal kidneys will excrete 60 to 75% of PSP in 2 hours following injection
Colorless in acid solution and red-in alkaline solution

URINARY AMMONIA AND TITRATABLE ACIDITY

Evaluates the ability of the kidney to produce an acidic urine
Tests can be run simultaneously on either fresh or toluene-preserved urine specimens
collected at 2-hour intervals from patients primed with an acid load of oral ammonium
chloride
Titratable acidity is the amount of free Hydrogen ions
Ammonium concentration = Total Acidity - Titratable Acidity
03
PHYSICAL
EXAMINATION
OF URINE
 URINE VOLUME
OLIGURIA ANURIA NOCTURIA POLYURIA

Decreased urine Cessation of urine Increased nocturnal Increased daily urine

output flow urine excretion output
Usually due to Due to serious Often associasted
dehydration damage to the with DM and DI
kidneys or decreased May be induced by
blood flow to the diuretics, caffeine, or
kidneys alcohol
URINE COLOR
Examine the specimen under good light source, looking down
through the container against a white background.
Normal urine color:

1.
causes the yellow color of urine, produced and excreted at a constant
rate
production is dependent on the body's metabolic state
increased in thyroid conditions, fasting states, specimen that stands at
room temperature
2.
a pink pigment most evident in refrigerated specimen
imparts the characteristic color of amorphous urates precipitate

3.
imparts an orange-brown color to urine specimens that are not fresh
oxidation product of urobilinogen
VARIATION OF URINE COLOR
DARK YELLOW/AMBER/ ORANGE

PATHOLOGIC NON PATHOLOGIC

VARIATION OF URINE COLOR
RED/PINK/BROWN

PATHOLOGIC NON PATHOLOGIC

VARIATION OF URINE COLOR
BROWN/BLACK

PATHOLOGIC NON PATHOLOGIC

VARIATION OF URINE COLOR
BLUE/GREEN

PATHOLOGIC NON PATHOLOGIC

URINE CLARITY REPORTING
Visually examine the
specimen in a clear TERM DESCRIPTION
container while holding it in
front of a light source
No visible particulates, transparent
Normal urine clarity:
Provides a key to
microscopic examination Few particulates, print easily seen through
results because the amount urine
of turbidity should
correspond with the amount Many particulates, print blured through urine
of material observed under
the microscope
Print cannol be seen through urine

May precipitate or be clotted

CAUSES OF TURBIDITY
NONPATHOLOGIC PATHOLOGIC

Squamous epithelial cells RBCs and WBCs

and mucus Bacteria and yeast cells
Bacterial growth Nonsquamous epithelial
Amorphous sediments cells
Semen Abnormal crystals
Fecal contamination Lymph fluid
Radiographic contrast media Lipids
Talcum powder
Vaginal creams
 URINE ODOR
Seldom of clinical significance and not part of routine
urinalysis
Normal odor:
VARIATIONS IN URINE ODOR

Foul, Ammonia-like

Fruity, Sweet

Maple Syrup

Mousy
 URINE ODOR
VARIATIONS IN URINE ODOR

Rancid

Sweaty Feet

Cabbage, Hops

Rotting Fish
 URINE ODOR
VARIATIONS IN URINE ODOR

Bleach

Unusual or Pungent

Odorless
 URINE SPECIFIC
GRAVITY
Density of solution compared to the density of similar volume of
water at the same temperature
Used to measure the concentrating and diluting ability of the
kidney
Indicator of concentration of dissolved solutes in the urine
Normal urine specific gravity:

Urine with fixed specific gravity of 1.010, seen in

end-stage renal disease

Urine with consistent specific gravity of <1.010

Urine with specific graviy of >1.010

 URINE SPECIFIC
GRAVITY METHODS
1. URINOMETER
Less accurate, not CLSI recommended
Requires large volume of specimen 10 -15 ml
Calibrated at 20 degrees Celsius
Scale reading is taken at the lower urine meniscus
Corrections:
Temperature:

Glucose:
Protein:
 URINE SPECIFIC
GRAVITY METHODS
2. HARMONIC OSCILLATION DENSITOMETRY
The frequency of soundwave entering
solution changes in proportion to its
density
Results are valid up to 1.080
 URINE SPECIFIC
GRAVITY METHODS
3. REFRACTOMETRY
Measures the refractive index (comparison of
the velocity of light in air and in the solution)
Deviation in the path of light is seen when it
enters the solution. This degree of deviation is
proportional to the solution's density
Small specimen volume requirement
Temperature compensated
 URINE SPECIFIC
GRAVITY METHODS
3. REFRACTOMETRY
Corrections:
Glucose:
Protein:
Calibration:
Distilled water:
5% NaCl:
9% Sucrose:
 URINE SPECIFIC
GRAVITY METHODS
4. REAGENT STRIP
Change in pKa of a polyelectrolyte
The higher the urine concentration, the more
H+ ions dissociate from the polyelectrolyte
Indicator:
Correction:
pH:
04
CHEMICAL
EXAMINATION
OF URINE
reagent strip
Consist of chemical-impregnated
absorbent pads attached to a plastic strip
A color reaction takes place when the pad
comes in contact with urine
Reactions are interpreted by comparing
the color pads with a chart provided by
the manufacturer
Results are described as trace, 1+, 2+, 3+, 4+
 care of
reagent strip
Store with dessicant in an opaque, tightly
closed container
Store below , do not freeze
Do not use if chemical pads become
discolored
Remove strips from the container just
before use
QUALITY CONTROL of
reagent strip
Test open bottles of reagent strips with known
positive and negative controls
Resolve control results that are out of range by
further testing
Test reagents used in backup tests with positive
and negative controls
Perform positive and negative controls on new
reagents and newly opened bottles of reagent
strips
Record all control results and reagent lot numbers
 GLUCOSE
Parameter/Principle Reagents & Results Correlation
Multistix
Glucose oxidase, peroxidase
and potassium iodide
GLUCOSE (BLUE to BROWN)
Chemstrip
(Double sequential Glucose oxidase, peroxidase
and tetramethybenzidine
enzymatic reaction)
[YELLOW TO GREEN)
Interferences
False (+)
Contamination by oxidizing
agents and detergents
False (-)
Ketones High levels of ascorbic acid,
ketones and high specific gravity
Low temperature
Improperly preserved specimens
 KETONES
Parameter/Principle Reagents & Results Correlation Interferences

Multistix False (+)

Sodium nitroprusside Phthalein dyes, highly pigmented
(PURPLE) red urine, Levodopa

KETONES Chemstrip
Medications containing free
sulfhydryl groups
(Sodium nitroprusside Sodium niroprusside and GLUCOSE
glycine False (-)
reaction)
(PURPLE) Improperly preserved specimens
 ph
Parameter/Principle Reagents & Results Correlation Interferences

Nitrite,
pH Multistix and Chemstrip
Methyl red and bromthymol
Leukocyte False (-)
(Double indicator blue
esterase, Runover from adjacent
protein pad
system) (ORANGE to BLUE) and
microscopy
 SPECIFIC GRAVITY
Parameter/Principle Reagents & Results Correlation Interferences

Multistix False (+)

Poly (methyl viny High concentrations of protein

SPECIFIC ether/maleic anhydride and

bromthymol blue False (-)

GRAVITY (BLUE to YELLOW)

Chemstrip
Highly alkaline utine (>6.5)
Add 0.005 to specific grovily
(pKa change of a Elhyleneglycol-Bis reading
(arinoethylether)
polyelectrolyte)
bromthymol blue
(BLUE to YELLOW)
 PROTEIN
Parameter/Principle Reagents & Results Correlation Interferences

Multistix Blood, False (+)

Tetrabromphenol blue Highly buffered alkalline urine
(YELLOW to BLUE-GREEN)
Nitrite, High specific gravity
Leukocyte Pigmented specimens,
PROTEIN Chemstrip esterase quaternary ammoniur compounds
(Error of indicators) Tetrachlorophenol Anfisepfics (chlorhexidine)
tetrabromosulfonohthalein
and Loss of buffer from prolonged
(YELLOW to BLUE-GREEN) microscopy exposure of reagent strip to the
specimen
 PROTEIN
Parameter/Principle Reagents & Results Correlation Interferences

False (-)
Proteins other than albumin
 BLOOD
Parameter/Principle Reagents & Results Correlation Interferences

Multistix False (+)

Diisopropylbenzenedehydro Strong oxidizding agents
peroxidetetramethylbenzid- Bacterial peroxidases
BLOOD ine Menstrual contamination

(Pseudoperoxidase (BLUE) Protein and False (-)

High specific gravity
activity of microscopy
Chemstrip High nitrite concentration
hemoglobin) Dimethyldihydroperoxidete- Formalin, captopril
tramethylbenzidine ascorbic acid (>25 mg/dL)
(BLUE) Unmixed specimen
 BILIRUBIN
Parameter/Principle Reagents & Results Correlation Interferences

Multistix False (+)

Dichloroaniline diazonium Highly pigmented urine
salt Phenazopyridine, indican. Lodine
(PINK-PURPLE) metabolites
BILIRUBIN Urobilinogen
Chemstrip False (-)
(Diazo reaction) Dichlorobenzene- Exposure to light
diazonium Ascorbic acid (>25 mg/dL)
tetrafluoroborate High nitrite concentration
(PINK-PURPLE)
 UROBILINOGEN
Parameter/Principle Reagents & Results Correlation Interferences

Multistix False (+)

UROBILINOGEN p-
direthylamninobenzaldehyde
Multistix
Porphoblinogen, p-aminosalicylic
(RED) acid, sulfonamides, methyldopa,
procaine, chlorpromazine.
Multistix Bilirubin
Chemstrip highly pigmented urine
Ehrlich's reaction Mothoxybenzenediazonium-
Chemstrip tetrafluoroborate Chemstrip
(RED) Highly pigmented urine
Diazo reaction
 UROBILINOGEN
Parameter/Principle Reagents & Results Correlation Interferences

False (-)
Multistix
Old specimen, Formalin
Chemstip
Old specimen, fomralin, high
nitrite concentration
 NITRITE
Parameter/Principle Reagents & Results Correlation Interferences

Multistix False (+)

P-arsanilic acid Improperly preserved specimen
tetrahydrobenzo (h)- Highly pigmented urine
quinoline-3-ol Protein, False (-)
(PINK] Nonreductase containing bacleria
NITRITE Chemstrip Leukocyte Insufficient contact time
Greiss reaction Sulfanilamide, esterase, and Lack of nitrate
hydroxytetrahydro microscopy Large quantities of bacteria
benzoquinolne Antibiotics
(PINK) Ascorbic acid
High specific gravity
 LEUKOCYTES
Parameter/Principle Reagents & Results Correlation Interferences

Multistix False (+)

Derivatized pyerole Strong oxidizing agents, formalin,
amino acid ester, highly pigmented urine,
diazonium salt Protein, nitrofurantoin
LEUKOCYTE (PURPLE) Nitrite, and False (-)
(Leukocyte esterase) Chemstrip High concentrations of protein,
Indoxylcarbonic acid microscopy glucose, oxalic acid, ascorbic
ester, diazonium salt acid, gentamicin, cephalosporins,
(PURPLE) tetracylines
 URINE PH
Determined based on the concentration of free hydrogen
Normal urine pH:
Most useful parameter for crystal identification

ACID URINE ALKALINE URINE

 URINE PROTEIN
Most indicative of renal disease
Normal urine protein:
Proteins normally found in urine:
: Major serum protein
found in urine
: A mucoprotein
produced bu the renal tubules; matrix
of cast formation
Serum and tubular microglobulins
Proteins from prostatic, seminal, and
vaginal secretions
 URINE PROTEIN
Clincal proteinuria
PRERENAL RENAL POST RENAL

Not indicative of Associated Caused by

actual renal disease with true proteins
Not detected by renal produced by the
reagent strip disease urinary tract
Overflow of plasma Contamination by
proteins with low proteins during
molecular weight excretion
 URINE PROTEIN

Prerenal causes
Severe infection or inflammation
Hemoglobinuria
Myoglobinuria
Multiple myeloma
 URINE PROTEIN
Renal causes
1. Glomerular proteinuria
Most common and most
clinically significant

2. Tubular proteinuria
Occurs when normal tubular
reabsorptive function is impaired
 URINE PROTEIN
Renal causes
1. Microalbuminuria
Proteinuria not detected by the
routine reagent strip
 TESTS FOR ALBUMIN
01 HEAT AND ACETIC ACID TEST
Urine is coagulated by heat and precipitated by 5-10% acetic acid. The
degree of turbidity is proportional to the amount of protein present
GRADING

1+ Diffuse cloud

2+ Granular cloud

3+ Distinct floccule

4+ Large floccule, dense, something solid

 02 SULFOSALICYLIC
ACID TEST
Most proteins are precipitated
by dilute (3%) SSA

REAGENT
SSA INTERPRETATION
STRIP

(+) (+)

(+) (-)
SSA TEST GRADING
PROTEIN RANGE
GRADE DESCRIPTION
(mg/dL)

Neg No increase in turbidity

Trace Noticeable turbidity

1+ Distinct turbidity with no granulation

2+ Turbidity with granulation, no flocculation

3+ Turbidity with granulation and flocculation

4+ Clumps of protein
URINE GLUCOSE
Most frequent chemical test
performed on urine
Clincally significant for
detection of DM
Normal urine glucose:
 URINE GLUCOSE
HYPERGLYCEMIA-ASSOCIATED RENAL-ASSOCIATED
DM ADVANCED RENAL DISEASE
ACROMEGALY FANCONI’S SYNDROME
CUSHING’S SYNDROME NEPHROTIC SYNDROME
HYPERTHYROIDISM OSTEOMALACIA
PHEOCHROMOCYTOMA PREGNANCY
 URINE GLUCOSE
TESTS FOR GLUCOSE
1. Benedicts test
General test for glucose and other reducing sugars.
Principle is based on the ability of glucose and other
reducing substances to reduce copper sulfate to cuprous
oxide in the prescence of alkali and heat.
 URINE GLUCOSE
BENEDICTS TEST GRADING
NEGATIVE Clear blue color, blue precipitate may form

TRACE Bluish green color

1+ Green color, green or yellow precipitate

2+ Yellow to green color, yellow precipitate

3+ Yellow-orange color, yellow orange precipitate

4+ Reddish-yellow color, brick red or red precipitate

URINE GLUCOSE
TESTS FOR GLUCOSE
2. Clinitest Tablet
Copper reduction method
Reagents:
Main reacting agent
Effervescent
Provides alkaline medium
Procedure:
URINE GLUCOSE
CORRELATION WITH REAGENT STRIP
Clinitest Reagent strip Interpretation

(+) (+)

(+) (-)

(-) 1+

(-) 4+
URINE KETONE
Results from increased fat metabolism
due to abnormal cabohydrate utilization
Not normally found in the urine
because metabolized fat is completely
broken down into CO2 and H20
Composition
B-Hydroxybutyric acid
Acetoacetic acid
Acetone
 URINE KETONE
TESTS FOR KETONES
1. : Reaction of ferric chloride
with acetoacetic acid forming a port wine or
bordeaux red color. Cannot detect acetone and
BHBA
2. : A nitroprusside ring test
which can detect about 1 - 5 mg/dL of
acetoacetic acid and 10 - 25 mg/dL of acetone.
Cannot detect BHBA.
 URINE KETONE
TESTS FOR KETONES
3. : Indirect method for BHBA
detection. Addition of hydrogen peroxide
converts BHBA to acetone. Acetone is then
tested by nitroprusside reaction
4. : Can be used to test urine,
serum, plasma, and whole blood. 10x more
sensitive to acetoacetic acid and acetone, but
cannot detect BHBA.
URINE BLOOD
Urine appearance is dependent
on the urine pH, amount and
duration of blood in the sample
Blood should not be detected in
the urine under normal
conditions
: Microscopic
hematuria; clincally significant
URINE BLOOD
Clinical significance
HEMATURIA

Bleeding in the kidneys or genitourinary tract

Causes:
Renal calculi Exposure to toxic
Glomerulonephritis chemicals
Pyelonephritis Anticoagulants
Tumors Strenous exercise
Trauma S. haematobium
infection
URINE BLOOD
Clinical significance
HEMOGLOBINURIA

May result from intravascular hemolysis or

from lysis of RBCs originating from the
urinary tract due to dilute, alkaline urine.
Causes:
Transfusion Malaria infection
reactions Strenous excercise
Hemolytic anemia Brown recluse
Severe burns spider bites
URINE BLOOD
Clinical significance
MYOGLOBINURIA

May result from skeletal and cardiac muscle

damage
Described as “tea”, “cola”, “black coffee”
urine
Causes:
Crush syndrome Drug abuse
Prolonged coma Extensive exertion
Convulsions Myocardial infaction
Alcoholism Statin drugs
 URINE BLOOD
Blondheim’s test
Use to differentiate:
Reagent:
Interpretation
Myoglobinuria Hemoglobinuria
urine bilirubin
Yellow pigmented product of
hemoglobin degredation
Major clinical significance is of the
screening of abnormal hepatobiliary
function
Bilirubin in the urine is excreted in very
small amounts and normally should not
be detectable in the urine
: Bilirubin fraction
that can be appear in the urine
 urine bilirubin
TESTS FOR BILIRUBIN
1. Harrison Spot Test
Bilirubin is oxidized by ferric
chloride in the prescence of TCA
into biliverdin
2. Ictotest tablet
More sensitive method than the
urine strip; less subject to
interference
 URINE
UROBILINOGEN
Colorless product of bilirubin breakdown
in the intestine
Appears in the urine as it is filtered by the
glomerulus as it passes through the
kidneys going to the liver
Excretion peaks at:
Never reported as negative in urinalysis
report
 URINE
UROBILINOGEN
TESTS FOR UROBILINOGEN
1. Ehrlichs reaction
Uses p-dimethylbenzaldehyde and sodium
acetate
Not specific for urobilinogen
2. Hoesch test
Uses Ehrlich reagent dissolve in 6M HCL
Rapid screening test for urine
porphobilinogen
 URINE
UROBILINOGEN
TESTS FOR UROBILINOGEN
3. Watson-schwartz
Classical test for the differentiation of
urobilinogen from porphobilinogen
Utilizes organic solvents:
 CORRELATION OF URINE
BILIRUBIN AND
UROBILINOGEN IN JAUNDICE
TYPE OF JAUNDICE URINE BILIRUBIN URINE URIBILINOGEN

Prehepatic

Hepatic

Post-hepatic
 URINE NITRITE
Rapid, non-culture method for the detection of UTI
Most common UTI-causing organisms:

Clincal significance:
Cystitis and Pyelonephritis
Evaluate antibiotic therapy
Monitor patients at high risk of UTI
Screen urine culture specimens
Factors influencing Nitrite results:
Organism Antibiotic use
Nitrate Heavy bacteriuria
Duration Interferences
LEUKOCYTE ESTERASE
Indicates presence of pyuria and
inflammatory process occuring in the
kidney or urinary tract
Esterase may be present in:
Clincal Significance:
UTI
Inflammation of the urinary tract
Screening of urine cukture
specimens
ASCORBIC ACID
A common cause of interference due to its
strong reducing property leading to false-
negative results for tests utilizing oxidation
reaction.
In the prescence of oxidizers, ascorbic acid is
converted to dehydroascorbic acid which is a
colorless compound
Compounds such as hydrogen peroxide and
diazonium salt are subject to Vitamin C
interference
Affects reagents strip reaction for:
05
MICROSCOPIC
EXAMINATION
 Preparation and
examination of urine
sediment
Specimen volume:
Centrifugation:
Sediment volume after decantation:
Sediment volume for examination:
Reporting:
RBC,WBC,RTE and oval fat bodies : Average #/HPF
Casts : Average #/LPF
Epithelial cells, Crystals, and other : Qualitative
sediments
Stains for microscopic
sediments
Composed of CRYSTAL VIOLET
AND SAFRANIN
Delineates structure and
contrasting colors of the nucleus
and cytoplasm
Identifies WBCs, epithelial cells,
and casts

Enhances nuclear detail

Differentiates WBCs and renal
tubular epithelial (RTE) cells
Stains for microscopic
sediments
Lyses RBCs and enhances nuclei
of WBCs
Distinguishes RBCs from WBCs,
yeast, oil droplets, and crystals

Stain triglycerides and neutral

fats orange-red
Identify free fat droplets and
lipid-containing cells and casts
Stains for microscopic
sediments
Differentiates gram-positive and
gram-negative bacteria
Identifies bacterial casts

Methylene blue and eosin Y

stains eosinophilic granules
Identifies urinary eosinophils
Stains for microscopic
sediments

Stains structures containing iron

Identifies yellow-brown granules
of hemosiderin in cells and casts
 URINE SEDIMENTS
EPITHELIAL CELLS
SQUAMOUS
Seen in the vaginal lining and lower
portions of the male urethra
Largest and most frequently seen
and least significant cell in the
urine sediment
Central nucleus about the size of
an RBC and abundant irregular
cytoplasm
: Squamous EC
infected with G. vaginalis covering
most of the cell surface extending
beyond the cell's edges.
TRANSITIONAL
Found lining the renal pelvis,
bladder and upper urethra
Spherical, caudate or
polyhedral in shape with a
centrally located nucleus
Has the ability to reabsorb
large quantities of water
: Increased
numbers of transitional cells
seen single, in pairs or in
clumps; seen after an invasive
urologic procedures
(catheterization)
RENAL TUBULAR
Lines the renal tubules
Round and slightly larger than
WBCs with a single, round and
eccentrically located nucleus
Most significant and indicates
tubular injury (>2/HPF), tubular
necrosis and renal graft rejection
: lipid-containing
RTE, found in lipiduria. Exhibit
maltese cross formation.
: RTE containing
large nonlipid filled vacuoles
 URINE SEDIMENTS
RED BLOOD CELLS

SWOLLEN CRENATED DYSMORPHIC

Describes as ghost/shadow cells Shrinking is due to Seen in glomerular

Appearance in hypotonic urine hypertonic urine membrane damage
Glomerular bleeding

Clincal significance:
Glomerulonephritis
Injury along the genitourinary tract
Renal lithiasis
 URINE SEDIMENTS
WHITE BLOOD CELLS

NEUTROPHILS EOSINOPHILS MONONUCLEAR CELLS

Most frequently seen >1% is considered Lymphocytes are the

Lyse rapidly in dilute alkaline significant
urine, loss of nuclear detail Highly associated
: are with drug induced
neutrophils absorbing water in interstitial nephritis
hypotonic urine. Characteristic May also be
sparkling appearance due to increased in UTI and
the Brownian movement of renal transplant
their cytoplasmic granules
smallest and may
resemble RBCs
Monocytes, macrophages
and histiocytes are large
and may be vacuolated or
could contain inclusions
 URINE SEDIMENTS
CASTS

Only element found in the urine that are unique to the kidneys
Formed primarily within the lumen of:
Formation is favored by urine stasis, acid urine and sodium and calcium
presence
: matrix of cast formation, produced by the RTE
: casts with tapered ends produced at the junction of ALH
and DCT
: presence of casts in the urine
Order of cast degeneration:
 URINE SEDIMENTS
CASTS

Urine examination for cast detection:

scanning is performed using the LPO along the edges of the
cover slip
observed under subdued light because cast matrix has a low
refractive index
casts are dissolved quickly in dilute alkaline urine
casts must be identified as to composition using the HPO
reported as average #/LPO
URINE SEDIMENTS
CLINCAL SIGNIFICANT CASTS

Only normal and most frequently seen cast

Colorless, homogenous and has same RI with urine, because it consist almost
entirely Tamm Horsfall protein
Nonpathologic: strenuous exercise, dehydration, heat exposure, emotional stress
Pathologic: acute glomerulonephritis, pyelonephritis, chronic renal disease,
congestive heart failure

Orange-red color, cast matrix containing RBC

Glomerulonephritis, strenuous exercise
URINE SEDIMENTS
CLINCAL SIGNIFICANT CASTS

Cast matrix containing WBCs

Pyelonephritis, Acute intersitial nephritis
Presence indicates the need to perform bacterial cultures

RTE cells attached to protein matrix

Renal tubular damage

Coarse and fine granules in a cast matrix

Glomerulonephtiis. Pyelonephritis, sfress and exercise
URINE SEDIMENTS
CLINCAL SIGNIFICANT CASTS

Highly refractile casts with jagged edges and notches

Stasis of urine flow, chronic renal fallure

Fat droplets and oval fat bodies attached to a protein matrix

Nephrotic syndrome, toxic tubular necrosis, diabetes mellitus, crush injuries

Wider than normal cast matrix

Indicates distention of tubular lumen
Granular and waxy casts. are the most common broad casts
Bile-stained broad, waxy casts are seen in tubular necrosis in viral hepatitis
Extreme urine stasis and renal failure
 URINE SEDIMENTS
CRYSTALS

Formed from the precipitation of urine solutes

Formation is affected by pH, temperature and solute
concentration
: most valuable parameter in crystal identification
Reporting
Normal crystals:
Abnormal crystals:
URINE SEDIMENTS
NORMAL CYRSTALS (ACID)

Yellow-brown granules
Pink precipitate on refrigerated specimens
Occurs at pH >5.5
Revert back to uric acid on acidification

Yellow-brown with varying shapes

Confused with cysteine crystals
Highly birefringent on polarized microscopy
occurs at pH <5.5
URINE SEDIMENTS
NORMAL CYRSTALS (ACID)

May also be seen in neutral and alkaline urine

Two forms:
Monohydrate
Ethylene glycol poisoning
Oval, dumbbell-shaped
Dihydrate
Common form
Enveloped-shaped
URINE SEDIMENTS
NORMAL CYRSTALS (ACID)

Yellow-brown spheres, may also have

spicules
Larger than ammonium biurate

Needle-shaped seen in synovial fluid during

episodes of gout
URINE SEDIMENTS
NORMAL CYRSTALS (ALKALINE)

White precipitate on refrigeration

Does not dissolve on warming

Yellow-brown, spicule-covered speheres

Dissolve at 60 degree celsius
Converts to uric acid on acidification
Old specimen
URINE SEDIMENTS
NORMAL CYRSTALS (ALKALINE)

Small, colorless, dumbell or spherical

Gas formation after addition of acetic acid
Birefringent

Colorless, flat rectangular plates or thin

prisms often rosette forms that can be
mistaken as sulfonamide crystals
Common constituent of renal calculi
URINE SEDIMENTS
NORMAL CYRSTALS (ALKALINE)

Colorless, prism-shaped, resembling coffin-

lid
Feathery appearance on disintegration
Birefriengent
Highly alkaline urine due to urea-splitting
bacteria
Struvite
URINE SEDIMENTS
ABNORMAL CRYSTALS

Colorless, refractile, hexagonal plates often

mistaken as uric acid crystals
Cystinuria and cystinosis
Cyanide nitroprusside reaction:

Colorless, flat rectangular plates with

notched corners and staircase pattern
Nephrotic conditions and lipid necrosis
Soluble in organic solvents
URINE SEDIMENTS
ABNORMAL CRYSTALS

Colorless to yellow fine delicate needles in

sheaves or rosettes
Appears black on focusing
Liver disease and aminoaciduria

Dark yellow to brown spheres with radiations

and concentric striations
Liver disease and aminoaciduria
URINE SEDIMENTS
ABNORMAL CRYSTALS

Yellow or ruby red clumps of needles or

granules
Associated with liver disease or obstruction

Long, fine and colorless structures, that form

bundles upon refrigeration
Appears following massive doses of penicillin
without adequate hydration
URINE SEDIMENTS
ABNORMAL CRYSTALS

Crystals that may take on various morphologies,

depending on form of drug involved
: wheat sheaves eccentric
binding
: brown, dense spheres or
irregular divided spheres
: brown, dense globules that
is soluble on acetone
Caused by inadequate hydration during therapy
and may result to renal tubular damage
URINE SEDIMENTS
ABNORMAL CRYSTALS

Colorless to gray or brown when aggregated, slender

featrher-like crystals that aggregate into wing-like
bundles; Antiretroviral therapy

Flat, clear, colorless, notched rhombic plates or longer

slender rectangles resembling cholesterol crystals
Easily polarized showing interference colors
Its prescence in urine should correlate with high
specific gravity
 URINE SEDIMENTS
MISCELLANOUS SEDIMENTS

BACTERIA
Significant bacteruria:
Should be accompanied by WBC to be considered
significant for UTI
Commonly enteric organisms
Acid-fast bacilli must be confirmed by culture or PCR
methods
 URINE SEDIMENTS
MISCELLANOUS SEDIMENTS

YEAST
Smooth, colorless, usually ovoid cells with double
refractile walls, often showing budding
: most common isolate
Mistaken for red blood cells but can be differentiated
by adding acid or alkali
seen in UTI especially in patients with DM
 URINE SEDIMENTS
MISCELLANOUS SEDIMENTS
PARASITES
May be seen in urine sediment due to vaginal or fecal
contamination. When noted, repeat examination must
be done on a fresh, clean-collected urine specimen
:most frequently seen; causes urethral
and bladder infection
:excreted together with RBCs
:most common contaminant
:reaches the bladder through the
lymphatics or fecal contamination
 URINE SEDIMENTS
MISCELLANOUS SEDIMENTS

SPERMATOZOA
Found in urine after sexual intercourse, masturbation
or nocturnal emission
Could result to a positive protein strip if semen is
increased in amount
MUCUS THREAD
Long, thin, wavy threads composed of Tamm-Horsfall
protein
More frequently present in female urine specimens
 URINE SEDIMENTS
MISCELLANOUS SEDIMENTS

TUMOR CELLS
Exfoliated from the renal pelvis, ureter, bladder wall
and urethra
Best identified using cytologic techniques
PLATELETS
Demonstrated on a patient with HUS using phase
contrast microscopy
 URINE SEDIMENTS
MISCELLANOUS SEDIMENTS
VIRAL INLlUSION CELLS
Virally infected epithelial cells may show characteristic
cytopathic effect
Herpes infection: syncytial giant cells containing
eosinophilic, intranuclear inclusions
CMV infection: enlarged with basophilic intranuclear
inclusions and/or cytoplasmic bodies
Polyomavirus infection: cells containing dense,
basophilic homogenous intranuclear inclusions that of
often completely fill the nucleus
 URINE SEDIMENTS
FREQUENTLY ENCOUNTERED ARTIFICATS

Highly refractile spheres with dimpled center

Starch granules Powdered gloves
Can be mistaken as fat droplets or RBCs

Highly refractile
Oil droplets Immersion oils, lotion creams
MIstaken as RBCs
 URINE SEDIMENTS
FREQUENTLY ENCOUNTERED ARTIFICATS

Highly refractile
Air Bubbles Formed when coverslip is used
Can be mistaken as RBCs

Seasonal contaminants appearing as spheres with a

Pollen grains
cell wall and concentric circles
 URINE SEDIMENTS
FREQUENTLY ENCOUNTERED ARTIFICATS

Longer and more refractile

Hair and Fibers Clothing and diapers
Mistaken as casts

Improper collection or prescence if fistule

Fecal contamination Appear as plant or meat fibers as brown amorphous
material
06
ANALYSIS
OF RENAL
LITHIASIS
GENERAL PROCEDURE
Involves visual examination of the stones,
noting its external appearance
: Yellow to brownish red and
are moderately hard
: Pale and friable
: Very hard, often of a dark
color, typically have a rough surface
: Yellow brown and greasy
GENERAL PROCEDURE
Determine its weight and approximate size
Pulverize the calculus and check its
homogenecity and nucleation
Take a small portion of the stone and ash it
over a hot burner
If entirely consumed in the flame, then is
TOTALLY ORGANIC
If it does not change on ashing then it is
MOSTLY INORGANIC
07
RENAL
DISEASES
 GLOMERULAR
DISEASE
NEPHRITIC NEPHROTIC
Immune mediated Disruption of the filtration
Acute onset of usually barier because of the damage
grossly hematuria to the membrane and changes
Presence of RBC casts in the electrical charges in the
Mild to moderate basal lamina and podocytes,
proteinuria producing a less tightly
Hypertension connected barrier
Oligouria Heavy profeinura
Hypoalbuminemia
Severe edema
Hyperlipidemia and Lipiduria
 NEPHRITIC
ACUTE POSTSTERPTOCOCCAL GLOMERULONEPHRITIS
Deposition of immune complexes, formed in conjunction with
Group A Streptococcus infection on the glomerular membranes

MEMBRANOUS GLOMERULONEPHRITIS
Thickening of the glomerular membrane following IgG immune
complex deposition associated with systemic disorders

MEMBRANOPROLIFERATIVE GLOMERULONEPHRITIS
Cellular proliferation affecting the capillary walls or the glomerular
basement membrane, possibly immune mediated
 NEPHRITIC
IMMUNOGLOBULIN A NEPHROPATHY
Deposition of IgA on the glomerular basement membrane
resulting from increased levels of serum IgA

CHRONIC GLOMERULONEPHRITIS
Marked decreased in renal function resulting from glomerular
damage precipitated by other renal disorders

RAPIDLY PROGRESSIVE GLOMERULONEPHRITIS

Deposition of immune complexes from systemic immune disorders
on the glomerular membrane
Goodpasure syndrome :
Wegener’s granulomatosis :
 NEPHROTIC
ALPORT SYNDROME
Genetic disorder showing lamellated and thinning glomerular
basement membrane

DIABETIC NEPHROPATHY
Most common cause of ESRD
Damage to the glomerular membrane occurs as a result of
membrane thickening, increased proliferation of mesangial cells
and increased deposition of cellular and noncellular material
within the glomerular matrix resulting in accumulation of solid
substances around the capillary tufts.
May be associated with deposition of glycosylated proteins
resulting from poorly controlled DM.
 NEPHROTIC
MINIMAL CHANGE DISEASE
Disruption of the podocytes occuring primarily in children
following allergic reaction and immunizations

FOCAL SEGMENTAL GLOMERULOSCLEROSIS

Disruption of podocytes in certain areas of glomeruli associated with
heroin and analgesic abuse and AIDS

HENOCH-SCHONLEIN PURPURA
Occurs primarily in children following viral respiratory infections; a
decrease in platelets disrupts vascular integrity
TUBULAR DISEASES
Acute tubular necrosis
Damage to renal tubular cells caused by
ischemia or toxic agents
Fanconi syndrome
Inherited in association with cystinosis and
Hartnup disease or acquired through exposure
to toxic agents
Uromodulin-associated kidney disease
Inherited defect in the production of normal
uromodulin by renal tubules and increased uric
acid causing gout
TUBULAR DISEASES
Nephrogenic diabetes insipidus
Inherited defect of tubular response to ADH or
acquired from medications
Renal glycosuria
Inherited autosomal recessive trait resulting to
failure to reabsorb glucose either due to
decreased number of transporters or
decreased affinity of transporters to glucose
INTERSTITIAL DISEASES
Acute pyelonephritis
Infection of the renal tubules and interstitium
related to interference of urine flow to the
bladder, reflux of urine from the bladder and
untreated cystitits
Chronic phyelonephritis
Recurrent infection of the renal tubules and
intestitium caused by strcutural
abnormalitties affecting the flow of urine
INTERSTITIAL DISEASES
Acute interstitial nephritis
Allergic inflammation of the renal interstitium
in response to certain medications
Cystitis
Ascending bacterial infection of the bladder
 RENAL
FAILURE
ACUTE RENAL FAILURE
Exhibits sudden loss of renal function and its frequently reversible
General characteristics
Decreased GFR
Oliguria
Edema
Azotemia
Causes:
Prerenal: sudden decrease in renal blood flow
Renal: acute glomerular and tubular diseases
Postrenal: renal calculi and tumor obstructions
 RENAL
FAILURE
CHRONIC RENAL FAILURE
End stage renal disease
General characteristics
Marked decreased in GFR:
Steadily rising serum BUN and cfeatinine values
Electrolyte imbalance
Isothenuric urine
Proteinuria
Renal glycosuria
Telescoped sediment
RENAL LITHIASIS
Renal stones may form in the calyces
and pelvis of the kídney, ureters and
bladder.
Formation of renal stones are favored
by these factors:
PH
Chemical concentration
Urinary stasis
 RENAL LITHIASIS
Primary calculi consituents:
: most common
constituent, approximately 75%.
Associated with metabolic calcium and
phosphate disorders and occasionally
diet
: frequently
accompanied by urinary infections
involving urea-splitting bacteria
 RENAL LITHIASIS
Primary calculi consituents:
: associated with
increased intake of foods with high
purine content
: seen in conjunction
with hereditary disorders of cysteine
metabolism
 RENAL LITHIASIS
Patient management techniques
Maintaining the urine at a pH
incompatible with crystallization of the
particular chemicals
Maintaining adequate hydration to lower
chemical concentration
Suggesting possible dietary restrictions
08
METABOLIC
DISORDERS
 CLASSIFICATION BASED ON
MECHANISM OF INCREASE
OVERFLOW METABOLIC RENAL

1. phenylketonuria 1. infantile tyrosinuria 1. hartnup disease

2. tyrosinemia 2. melanuria 2. Cystinuria
3. alkaptonuria 3. indicanuria
4. msud 4. 5-hiaa
5. organic acidemia 5. porphyria
6. cystinosis
7. porphyria
8. mucopolysaccharides
9. galactosemia
10. lesch-nyhan disease
 CLASSIFICATION BASED ON
THE PATHWAY AFFECTED
PHENYLALANINE-TYROSINE DISORDERS

1. Phenylketonuria: caused by failure to inherit the gene for production of

The urine has a charteristic mousy odor due to prescence of

Guthrie test
 CLASSIFICATION BASED ON
THE PATHWAY AFFECTED
PHENYLALANINE-TYROSINE DISORDERS
2. Tyrosyluria: characterized by prescence of excessive urine tyrosine and its
metabolites
Type 1:
Generalized renal tubular disorder and progressive liver failure
Type 2:
Persons develop corneal erosion and lesions on the palms, fingers
and soles of the feet
Type 3:
Can cause mental retardation if diet restriction for phenylalanine
and tyrosine are not done
 CLASSIFICATION BASED ON
THE PATHWAY AFFECTED
PHENYLALANINE-TYROSINE DISORDERS

3. Alkaptonuria: caused by failure to inherit the gene for the production of

Urine specimen darkens upon prolonged standing

Brown or black-stained cloth diapers and reddish-stained disposable
diapers
Deposition of brown pigment in the body tissues
 CLASSIFICATION BASED ON
THE PATHWAY AFFECTED
PHENYLALANINE-TYROSINE DISORDERS

4. Melanuria: over proliferation of melanocytes producing 5,6

dihydroxyindole (colorless precursor of melanin)
Urine specimen darkens upon exposure to air
 CLASSIFICATION BASED ON
THE PATHWAY AFFECTED
BRANCHED -CHAIN AMINO ACID DISORDERS

1. Maple Syrup Urine Disease: accumulation of ketoacids in the urine due to

defect in metabolism of amino acids
Amino acids involved are:
 CLASSIFICATION BASED ON
THE PATHWAY AFFECTED
BRANCHED -CHAIN AMINO ACID DISORDERS

2. Organic Acidemias
Isovaleric academia
Proprionic academia
Methylmalonic academia
 CLASSIFICATION BASED ON
THE PATHWAY AFFECTED
TRYPTOPHAN DISORDERS

1. Indicanuria: characteristics by excessive production of indole from

tryptophan caused by intestinal disorders
: rare inherited disorder exhibiting indicanuria; aka
blue diaper syndrome
 CLASSIFICATION BASED ON
THE PATHWAY AFFECTED
TRYPTOPHAN DISORDERS

2. Argentaffinoma: carcinoid tumor producing excessive amount of

serotonin
Increased urinary 5-HIAA which is the metabolite of serotonin
Testing in the urine requires diet restrictions
 CLASSIFICATION BASED ON
THE PATHWAY AFFECTED
CYSTINE DISORDERS

1. Cytinuria: defect in renal tubular transport of amino acids

Two forms:
Cystine and lysine are affected
Cystine, ornithine, lysine, and arginine are affected
 CLASSIFICATION BASED ON
THE PATHWAY AFFECTED
CYSTINE DISORDERS

2. Cystinosis: inborn error of metabolism where cystine crystals deposit in

many areas of the body
3. Homocystinuria: defect in methionine metabolism resulting to increased
amount of homocystine
 CLASSIFICATION BASED ON
THE PATHWAY AFFECTED
MUCOPOLYSACCHARIDE DISORDERS

Inherited disorders which results in accumulation of the incompletely

metabolized polysaccharide portions in the lysosomes of connective tissue
cells and their increased excretion in urine
1. Hurler: mucopolysaccharides accumulate in the cornea; skelatal muscle
abnormality and mental retardation
2. Hunter: skeletal structure abnormalit and mental retardation
3. Sanfilipo: mental retardation
 CLASSIFICATION BASED ON
THE PATHWAY AFFECTED
PURINE DISORDERS

Lesch-Nyhan: caused by failure to inherit the gene to produce

Associated with finding of “orange sand” in diaper
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