URINALYSI

S
By

Roderick D. Balce, RMT

ANATOMY OF THE KIDNEY
RENAL FUNCTIONS
1. Renal Blood Flow
Afferent arterioles
Efferent arterioles
Peritubular capillaries
Proximal convoluted tubule
Distal convoluted tubule
Vasa recta
Ascending loop of Henle
Descending loop of Henle
2. Glomerular Filtration
 Glomerulus
 GFR = 120 ml/min
 Factors Affecting Glomerular Filtration
a. Cellular structure
 Capillary Wall Membrane
 Basement Membrane
 Visceral Epithelium
b. Hydrostatic pressure
 Blood Colloidal Oncotic Pressure
 Capsular Pressure
c. Renin-Angiotensin-Aldosterone
Mechanism
3. Tubular Reabsorption
 Mechanisms involved:
a. Active Transport
 Actively transported: Glucose,
Amino acids
Salts
Chloride
Sodium
 Renal threshold –important in distinguishing

between:
 Excess solute filtration
 Renal tubular damage
b. Passive Transport
Passively Transported: Water
Urea
Sodium

c. Counter-Current Mechanism
Osmotic Gradient of Medulla
Vasopressin
4. Tubular Secretion
 Major Functions:
a. Elimination of waste products not
filtered by the glomerulus

b. Regulation of acid-base balance

through secretion of H ions
Renal Function Tests
1. Glomerular Filtration Test
 Clearance test
a. Urea
b. Radioisotope
c. B2 microglobulin
d. Creatinine
C = UV/P
Normal values:
Creatinine Clearance: F = 75-112 ml/m
M = 85-125 ml/m
Plasma Creatinine = 0.5-1.5 mg/dl
e. Inulin
2. Tubular Reabsorption Tests
a. Fishberg Test
b. Mosenthal Test
c. Osmometry

3. Tubular Secretion and Renal Blood Flow

Tests
a. PAH
b. PSP
c. Indigo Carmine Test
Renal Diseases
A. Glomerular Disorders:
1. Glomerulonephritis – blood, protein, and casts
in urine
a. Acute Poststreptococcal – caused by deposition
of immune complexes and antibodies in the
glomerular membrane following group A
streptococcal infection.
b. Rapidly Progressive ( Crescentic) – more
serious, can lead to renal failure; arises as a result
of another form of glomerulonephritis or an immune
systemic disorder.
c. Good Pasture’s Syndrome – attachment of
cytotoxic autoantibody (anti-glomerular
basement membrane antibody) to the
glomerular and alveolar basement
membranes during viral respiratory
infections.
Lab Findings:proteinuria, hematuria, RBC
casts
2. Vasculitis
- immune-mediated disoders affecting the
systemic vascular system resulting to
glomerular damage.
a. Wegener’s granulomatosis – granuloma-
producing inflammation of the small blood
vessels in the lungs and kidney.The
antibody causing the damage is the anti-
neutrophilc cytoplasmic antibody (ANCA)
 Lab findings: hematuria, proteinuria, rbc casts,
and increased BUN and crea
b. Henoch-Schonlein Purpura – characterized
by a decrease in platelets that causes
disruption of vascular integrity
 Lab findings: heavy proteinuria and hematuria
with rbc casts
Wegener’s Granulomatosis
3. Immunoglobulin A nephropathy
- deposition of immune complexes on the
glomerular membrane resulting from
increased levels of serum IgA
 Lab
findings: macroscopic/microscopic
hematuria and increased IgA

4. Membranous Glomerulonephritis
- thickening of the glomerular membrane
due to deposition of IgG immune
complexes.
 Lab findings: microscopic hematuria and
increased IgG and protein excretion
5. Membranoproliferative Glomerulonephritis
– immune mediated disorder characterized
by cellular proliferation in capillary walls or
glomerular basement membrane.
 Lab findings: hematuria, proteinuria, and decreased
serum complement levels
6. Chronic Glomerulonephritis – glomerular
damage as a result of other renal disorders
leads to marked decrease in renal functions
and eventually to renal failure
 Lab findings: hematuria, proteinuria, glucosuria,
varieties of casts including broad cast, markedly
decreased GFR with increased BUN and crea
levels, and electrolyte imbalance
7. Nephrotic Syndrome – disruption in the
electrical charges in the basal lamina and
podocytes, producing a less tightly
connected barrier.
 Lab Findings: massive proteinuria, low albumin, high
serum levels of lipids, and pronounced edema

8. Minimal Change Disease – podocytes appear

to be less tightly fitting allowing increased
filtration of protein; seen in children
following allergic reaction and immunization.
 Lab Findings: edema, heavy proteinuria, transient
hematuria
9. Focal Segmental Glomerulosclerosis
- only a certain number and areas of
glomeruli are affected. The disease is
caused by disruption of the podocytes
associated with analgesics and heroin
abuse and AIDS. Immunoglobulins M and
C3 are seen in undamaged
glomeruli.
•Lab Findings: heavy proteinuria, microscopic
hematuria
II. Tubulointerstitial Disorders
1. Acute Tubular Necrosis – damage to the
renal tubular cells by toxic agents or
ischemia

2. Fanconi’s Syndrome – generalized failure

of tubular reabsorption in the PCT; may
be hereditary or acquired
3. Cystitis – ascending bacterial infection of
the bladder
4. Acute Pyelonephritis – infection of the upper
urinary tract involving the interstitium and
tubules due to interference of urine flow
to the bladder, reflux of urine from the
bladder, or untreated cystitis
5. Chronic Pyelonephritis – recurrent infection
of the tubules and interstitium caused by
structural abnormalities affecting urine
flow
6. Acute Interstitial Nephritis – inflammation of
the renal interstitium associated with
allergic reaction to medications
C. Vascular Disorders
1. Renal Failure – may be gradual progression
from the original disorder to chronic renal
failure or end-stage renal disease.

2. Renal Lithiasis – deposition of renal calculi or

kidney stones in the calyces and pelvis of
the kidney, ureters and urinary bladder.
 Chemical Composition of Renal Calculi:

a. Calcium oxalate or phosphate

b. Magnesium ammonium
phosphate
c. Uric acid
d. Cystine

 Lab Findings: microscopic hematuria

Composition of Urine
1. water
2. analytes
 organic
 inorganic

3. hormones, vitamins, medications,

formed elements, etc.
 Types of Urine Specimens
Timed Specimen:
24-hour Quantitative chemical tests,
hormone studies
12-hour Addis count
2-hr Postprandial Diabetic monitoring
Afternoon Specimen Urobilinogen determination
Glucose Tolerance Test Accompaniment to blood
samples in GTT
Random Routine screening
First Morning Routine screening
Pregnancy Tests
Orthostatic Proteinuria
Fasting/Second Morning Diabetic screening /
monitoring
Catheterized Bacterial culture
Midstream clean-catch Routine screening
Bacterial culture
Suprapubic aspiration Bladder urine for bacterial
culture
Cytology
Three-glass collection Prostatic infection
Drug Specimen Drug testing
 Voiding cystourethrogram
Examining bladder function by injecting dye that is
visible on X-rays through a catheter to fill the
bladder. X-rays are taken while the bladder is full
and while the patient is urinating to determine if
fluid is forced out of the bladder through the
urethra (normal) or up through the ureters into the
kidney (vesicoureteral reflux).
DRUG SPECIMEN COLLECTION
Chain of Custody (COC) Form
 the process that provides the
documentation of proper sample
identification from the time of collection to
the receipt of laboratory results
 a standardized form that documents that
the specimen collected by the patient is
the same one that is analyzed and
reported
Urine Specimen Collection
- the most vulnerable part of a drug testing program
- may be witnessed or unwitnessed; a same-gender
collector is required in witnessed collection

Required Volume - 30-45 ml taken within 4 minutes

Temperature - 32.5ºC to 37.7ºC

Procedure:
 The collector washes hands, wears
gloves, adds bluing agent or dye to the
toilet water reservoir, and tapes the toilet
lid and faucet handles.
 The donor provides identification from
employer.
 The collector completes step 1 COC
Form and has the donor sign the form.
 The donor leaves all his belongings outside,
washes hands, and receives a specimen cup.
 The collector remains in the restroom, outside
the stall (unwitnessed) listening for
unauthorized water use.
 The donor hands specimen cup to the
collector and the latter checks the urine for
abnormal color and for the required amount.
 The collector checks the temperature using a
temperature strip, records the reading on the
COC Form (step 2). If the temperature is out
of range, recollection is needed.
 With the donor watching, the collector seals the
capped bottle with identification strips (COC step
3) covering both sides of the cup. The seals
contain the date and time.
 The donor initials the seals and completes COC
step 4 after which, the collector accomplishes
COC step 5.
 Each time the specimen is handled, transferred
or stored, every individual must be identified, the
date and purpose of the change must be
recorded, and specific instructions on labeling,
packaging or transport must be followed.
Methods of Preservation
1. Physical (Refrigeration)
2. Chemical
 Phenol – causes an odor change
 Toluene –not effective for bacteria and molds
 Thymol crystals – preserves glucose and
sediments well
 Formalin – excellent sediment preservative
 Boric acid – preserves protein well
 Sodium fluoride – good for drug analysis
 Sacomanno’s fixative – preserves cellular
elements
Changes in Unpreserved Urine
 Color - modified  Decreased:
or darkened  Clarity
 Glucose

 Increased:  Ketones

 Odor  Bilirubin
 Urobilinogen
 pH
 Red blood cells
 Nitrite
 White blood cells
 Bacteria
 Casts
Clinical Utilities of Routine Urinalysis
Indicators of the State of the Kidney
or Urinary Tract
 Appearance
 SpecificGravity
 Chemical tests
 Leukocyte Esterase
 Urinary Sediment
Indicators of Metabolic and Other
Conditions or Disease
 pH
 Appearance
 Glucose and Ketones
 Bilirubin
 Urobilinogen
Indications of Other Systemic
(Nonrenal) Conditions or
Disease
 Hemoglobin
 Myoglobin
 Light-chainproteins
 Porphobilinogen
 PHYSICAL
EXAMINATION
I. Volume
 Average daily output: 1,200-1,500 ml
 Variations:
a. Polyuria
 Indications: Diabetes mellitus
Diabetes insipidus
b. Diuresis
c. Oliguria
d. Anuria
e. Nocturia
II. Specific Gravity
 Performed using:
a. Urinometer
 Corrections done
b. Refractometer
 Instrument Calibration
c. Reagent strip
d. Harmonic Oscillation Densitometry
 Variations in S.G.:
a. Hypersthenuria
b. Hyposthenuria
c. Isosthenuria

III. pH
IV. Color
• Pigments
Variations in Color:
 Colorless  Yellow green/
 Pale yellow Yellow brown
 Dark yellow  Green
 Orange Red/  Blue green

Reddish brown  Milky white

 Amber/Orange  Pink/Red
 Brown/Black
V. Odor
Normal: Aromatic
Variations in Urine Odor:
 Amoniacal/Putrid/  Mousy
Foul  Rancid
 Mercaptan  Sweaty feet
 Fecaloid  Rotting fish
 Fruity, sweet  Cabbage
 Maple syrup  Bleach
 Sulfur odor
VI. Transparency
Urine Clarity
Clear No visible particulates, transparent
Hazy Few particulates, print easily seen
through urine
Cloudy Many particulates, print blurred
through urine
Turbid Print cannot be seen through urine
Milky May precipitate or be clotted
 Nubecula
Nonpathologic Causes of Urine
Turbidity
 Epithelial cells
 Normal crystals
 Bacteria (old urine)
 Semen, prostatic fluid
 Fecal contamination
 Radiographic contrast media, mucus,
talcum powder
 Vaginal creams
Pathologic Causes of Urine
Turbidity
 Red blood cells
 White blood cells
 Bacteria
 Yeasts
 Nonsquamous epithelial cells
 Abnormal crystals
 Casts
 Lymph fluid/Chyle
 Lipids
 Fecal matter
CHEMICAL
ANALYSIS
I. pH
 Normal values: average-6; random-4.5-8.0;
fasting-5.5-6.5
 Clinical Significance
a. respiratory or metabolic acidosis/ketosis
b. respiratory or metabolic alkalosis
c. renal tubular acidosis
d. renal calculi formation
e. treatment of UTI
f. precipitation/identification of crystals
g. determination of unsatisfactory specimen
Causes of Acid and Alkaline Urine
Acid Urine Alkaline Urine
 Emphysema Hyperventilation
 Diabetes mellitus Vomiting
 Starvation Renal tubular acidosis
 Dehydration Presence of urease-
producing bacteria
 Diarrhea Vegetarian diet
 Presence of Old specimens
acid-producing
bacteria
 High protein diet
 Cranberry juice
 Medications
 II. Protein
 Most indicative of renal disease
 Normal urine contains <10 mg/dl or 100 mg/24
hours
 Types of Proteinuria (according to the amount of
protein excreted per day)
Degree of Grams Excreted
Proteinuria per 24 hours
Mild <1 g/day
Moderate 1- 4 g/day
Heavy >4 g/day
Types of Proteinuria
(according to cause)
1. Pre-renal
 Intravascular hemolysis
 Muscle injury
 Severe infection and inflammation
 Multiple myeloma
2. Renal
a. Glomerular
 Conditions that cause damage to the glomerulus
 Orthostatic or Postural Proteinuria

b. Tubular
• Fanconi’s Syndrome
• Toxic agents/Heavy metals
• Severe viral infections
3. Post-renal
a. lower UTI/inflammation
b. injury/trauma
c. menstrual contamination
d. prostatic fluid/spermatozoa
e. vaginal secretions
Tests for Albumin
 Heat and Acetic Acid Test
 Positive Results: 1+ - diffused cloud
2+ - granular cloud
3+ - distinct flocculi
4+ - large flocculi
 Reagent Strips
 SSA/Cold Protein Precipitation
 Correlation of Reagent Strip and SSA Results
(+) Rgt. Strip, (-) SSA = albumin present
(+) Rgt. Strip, (+)SSA = proteinuria
(-) Rgt. Strip, (+) SSA = BJP, globulins, etc.
III. Glucose
 Normal concentration: 15 mg/dl
 Melituria
 Glycusoria
 Clinical significance
a. DM
b. endocrine disorders
c. pancreatitis, carcinoma, cystic fibrosis,
hemochromatosis
d. CNS disorders
e. disturbance in metabolism
f. liver disease
g. renal glycusoria
h. drugs
 Glycusoria without hyperglycemia
a. renal tubular dysfunction
b. tubular necrosis
c. Fanconi’s syndrome

Tests for Glucose

1. Benedict’s Test – general test for glucose and
other reducing sugars
2. Clinitest – subject to interference from other
reducing sugars
• Pass-though phenomenon
3. Glucose Oxidase – specific for glucose
Correlation of Glucose Oxidase and Clinitest
GOD Clinitest Interpretation
1+ neg small amount of glucose
present

4+ neg possible oxidizing agent

interference on rgt
strip

neg 1+ non-glucose reducing

substance present
IV. Ketones
 Represents 3 intermediate products of fat
metabolism:
a. acetone
b. acetoacetic acid
c. β-hydroxybutyric acid

 Accumulation in blood leads to:

a. electrolyte imbalance
b. dehydration
c. acidosis
d. diabetic coma
 Clinical significance:
a. DM
b. insulin dose monitoring
c. diabetic acidosis
d. starvation/fasting
e. weight reduction/dieting/strenuous exercise
f. vomiting
g. malabsorption/pancreatic disorders
h. inborn error of amino acid metabolism
V. Blood
 Hematuria
 Clinical Significance:
a. renal calculi
b. glomerulonephritis
c. tumors
d. trauma
e. pyelonephritis
f. toxic chemicals
g. strenuous sxercise
h. menstrual contamination
 Hemoglobinuria

 Clinical significance:
a. hemolytic anemia
b. transfusion reaction
c. PNH
d. severe burns and infections
e. malaria
f. strenuous exercise
 Myoglobinuria
 Clinical significance:
a. muscular trauma/crush syndrome
b. prolonged coma
c. convulsions
d. muscle-wasting diseases
e. alcoholism/overdose
f. drug abuse
g. extensive exertion
Tests to Differentiate Hemoglobin
and Myoglobin
 Ammonium Sulfate Method
 Hb is precipitated by ammonium sulfate
 Absorption Spectrophotometry
 Immunodiffusion Technique
 Protein Electrophoresis
 Differentiation of Hematuria,
Hemoglobinuria, and Myoglobinuria
Finding Red Cells Hemoglobin Myoglobin
Rgt. Strip Positive Positive Positive
Microscopic (RBCs) Present Absent or few Absent or few

Urine Appearance Cloudy red Clear red Clear red

Plasma Appearance Normal Pink to red Normal

Total serum CK Normal Slight Marked

elevation elevation
Total serum LD Normal Elevated Elevated
LD1 and LD2 Normal Elevated Normal
LD4 and LD5 Normal Normal Elevated
VI. Bilirubin
 Clinical Significance
 Hepatitis, cirrhosis, other liver disorders
 Biliary obstruction

 Tests
 Foam-Shake Test
 Oxidation Test – acidic oxidation of bilirubin
into rainbow array of colors
 Diazotization Test
 Ictotest
 Reagent Strip
VII. Urobilinogen
 found in urine in small amounts

 Clinical Significance
 Early detection of liver disease
 Hemolytic disorders
 Hepatitis, cirrhosis, carcinoma

 Tests
 Ehrlich’s Tube Test
 Schwartz-Watson Differentiation Test
 Reagent Strip
 Watson-Schwartz Test Interpretation
Urobilinogen Ehrlich-reactive Porphobilinogen
Substances

Chloroform Extraction

Urine Colorless Red Red

(Top layer)

Chloroform Red Colorless Colorless

(Bottom layer)

Butanol Extraction

Butanol Red Red Colorless

(Top layer)

Urine Colorless Colorless Red

(Bottom layer)
 Laboratory Findings in Various Types of
Jaundice
Blood Urine Urine
Bilirubin Bilirubin Urobilinogen

Normal 0–1.3 mg/dL Negative ≤1 mg/dL

Hemolytic Increased Negative +++

Hepatic Increased + or - ++

Obstructive Normal +++ Normal

 Urobilin – brown pigment which result from
oxidation of urobilinogen upon
exposure to light; tested when
urobilinogen is negative
 Porphyrins – cyclic compounds derived from ALA
 Clinical Significance: Porphyrias
 Tests for Porphyrinuria
 Ehrlich Test – requires the addition of acetylacetone
prior to performing the test
 Fluorescence – involves extraction into a mixture of
glacial HAc and ethyl acetate and
examination of solvent layer
 faint blue fluorescence = (-)
 violet, pink, or red = (+)
VIII. Nitrite
 Clinical Significance
 Cystitis
 Pyelonephritis
 Evaluation of antibiotic therapy
 Monitoring of patients at high risk for
UTI
 Screening of urine culture specimens
IX. Leukocyte Esterase
 Clinical Significance
 Bacterial
and nonbacterial UTI
 Inflammation of the urinary tract
 Screening of urine culture
specimens
 Urine Reference Values
Property Reference Value
Color Yellow
Transparency Clear
pH 5-7
Specific Gravity 1.001-1.035
Protein (albumin) Negative or Trace
Blood (hemoglobin) Negative
Nitrite Negative
LE Negative
Glucose Negative
Ketones Negative
Bilirubin Negative
Urobilinogen ≤1 mg/dL
 Confirmatory Urinalysis Tests
Substance Test
Protein SSA Test
Blood Microscopic Examination
Hemoglobin, Myoglobin Centrifugation; then test
supernatant with rgt. strip
for blood
Hemosiderin Rous Test
Glucose Clinitest
Bilirubin Ictotest
Urobilinogen Watson-Schwartz Test
Porphobilinogen Hoesch Test
Ascorbic Acid EM Quant
 SPECIAL URINALYSIS
SCREENING TESTS
Amino Acid Disorders
1. Phenylalanine-Tyrosine Disorders
a. Phenylketonuria
Tests:
 Ferric Chloride Test
 Phenistix
 DPNH
 Robert Guthrie Bacterial Inhibition
Test
b. Tyrosyluria
Tests:
 Millon’s Test
 Nitrosonaphthol Test

 Ferric Chloride Test

 Phenistix

 DPNH
c. Melanuria
Tests:
 Sodium nitroprusside Test
- interference due to a red color from
acetone and creatinine can be avoided by
adding glacial HAc
 Ferric Chloride Test
 Acetest

 Blackberg and Wanger Test

 Ehrlich’s Test
d. Alkaptonuria
Tests:
 Ferric chloride Test
 Alkali Test
 Addition of silver nitrate or ammonium
hydroxide
 Benedict’s Test or Clinitest
2. Branched Chain Amino Acid Disorders
a. Maple Syrup Urine Disease
Tests:
 DNPH
 Amino Acid Chromatography

 Ferric Chloride Test

 Nitrosonaphthol

 Acetest
b. Organic Acidemias
 Isovaleric Acidemia
 DNPH
 Acetest

 Chromatography

 Propionic Acidemia
 DNPH

 Acetest

 Methylmalonic Acidemia
 DNPH

 Acetest

 p-nitroaniline
3. Tryptophan Disorders
a. Indicanuria
Clinical Significance:
 Obstruction
 Presence of bacteria

 Malabsorption syndrome

b. Hartnup’s Disease
 production of blue color when indican is
oxidized upon exposure to air
c. 5-HIAA
Tests:
 Ferric Chloride Test
 Sjoerdsma Test.

Clinical Significance:
 Elevated in malignancy involving Argentaffin
cells
4. Cystine Disorders
a. Cystinuria
Tests:
 + Cystine crystals
 Cyanide nitroprusside
b. Cystinosis
Tests:
 Cyanide nitroprusside
 Clinitest
c. Homocystinuria
Tests:
 Cyanide nitroprusside
 Silver nitroprusside
Mucopolysaccharide Disorders
 Hurler’s Syndrome
 Hunter’s Syndrome
 San Filippo’s Syndrome

Tests:
 AcidAlbumin
 CTAB Turbidity Test
 Metachromatic Staining Spot Test
Purine Disorders
 Lesch-Nyhan Disease
 lackof the enzyme HGPT
 Manifestations: severe motor defects,
mental retardation, tendency toward
self-destruction, gout and renal calculi,
orange sand in diapers
MICROSCOPIC
EXAMINATION
 Types of Microscope
 Bright Field – objects appear dark against a light
background
 Phase Contrast – works by retardation of light
rays diffused by the object in
focus
 Polarizing – used to confirm the identification of
fat droplets, oval fat bodies, and
fatty casts
 Interference Contrast – object appears bright
against a dark background but
without the diffraction halo
associated with Phase Contrast
Microscope
Microscopic Sediment Stains
 Sternheimer-Malbin
 0.5% Toluidine Blue
 Sudan III
 Oil Red O
 Prussian Blue
 Hansel Stain
 Reference Values for Urine Sediment
Constituent Reference Value
Red Blood Cells 0-2/hpf
White Blood Cells 0-5/hpf (female>male)
Casts 0-2 hyaline/hpf
Squamous Epithelial Cells Few/hpf
Transitional Epithelial Cells Few/hpf
Renal Tubular Epithelial Cells Few/hpf
Bacteria Negative
Yeast Negative
Abnormal crystals Negative
Standardization of Procedure
1. Urine Volume – 12 mL
2. Time of Centrifugation – 5 minutes
3. Speed of Centrifugation
 Relative Centrifugal Force of 400 g
4. Volume of Sediment Examined – 20 μL
5. Reporting Format
 Reporting System for Urine Sediment
Average Number per Low-Power Field
Casts Neg 0-2 2-5 5-10 10-25 25-50 >50

Abnormal crystals Neg 0-2 2-5 5-10 10-25 25-50 >50

Squamous ECs Few Moderate Many
Mucus Present
Average Number per High-Power Field
Red Blood Cells 0-2 2-5 5-10 10-25 25-50 50-100 >100
White Blood Cells 0-2 2-5 5-10 10-25 25-50 50-100 >100
Normal Crystals Few Moderate Many
Epithelial Cells Few Moderate Many
Miscellaneous Few Moderate Many
Sperm Present
Organized
Sediments
 Red Blood Cells

•Normal appearance
•N.V.
•Variations in shape and
appearance
•Clinical Significance
Non-glomerular hematuria: RBCs
are uniform in size and shape but
show two populations of cells
because a small number have lost
their hemoglobin pigment.
 Glomerular hematuria: RBCs are
small and vary in size, shape, and
hemoglobin content.
White Blood Cells
Bacteria

Amoeboid

•Normal appearance
•N.V.
•Clinical Significance
•Glitter cells
•Eosinophils
•Mononuclear cells
Squamous Epithelial Cells
• Clue Cells
Transitional Epithelial Cells
 smaller than squamous cells, spherical,
caudate, or polyhedral with central
nucleus

 Clinical Significance
 Transitional that appear singly, in pairs,
or in clumps
 Transitional cells with abnormal
morphology
Renal Tubular Epithelial Cells

•Clinical Significance
•Oval Fat Bodies
•Bubble Cells
 Casts

Mechanisms of Cast Formation

 Hyaline Cast

•Strenuous exercise, dehydration, heat

exposure, emotional stress
•Acute glomerulonephritis, pyelonephritis,
chronic renal disease, CHF
Red Blood Cell Cast
 WBC Cast

•Epithelial Cell Cast

Coarsely Granular Cast
Finely Granular Cast
Waxy Cast

•Fatty Cast
•Broad Cast
Bacteria
 Yeast Cells

There are no PMNs seen

suggestive of contamination and
not of UTI.
Mucus Thread
Unorganized
Sediments
Crystals
 Normal Crystals in Acidic Urine
1. Amorphous Urates
2. Uric Acid
3. Sodium Urates
4. Calcium Sulfates
5. Calcium Oxalate
6. Hippuric Acid
Amorphous Urates
Uric Acid
Dihydrate Calcium Oxalate
Normal Crystals in Alkaline Urine

1. Amorphous Phosphate
2. Calcium Carbonate
3. Ammonium biurate
4. Calcium Phosphate
5. Triple Phosphate
Amorphous Phosphate
Calcium Carbonate
Ammonium biurate
Calcium phosphate
Triple phosphate
Abnormal Crystals of Abnormal Crystals of
Metabolic Origin Iatrogenic Origin
 Cystine  Sulfonamides

 Cholesterol  Radiographic contrast

media
 Leucine
 Ampicillin
 Tyrosine  Acyclovir
 Bilirubin  Indinavir sulfate
 Hemosiderin
Cystine
Cholesterol
Leucine
Tyrosine
Sulfa Crystals
Starch