2. Urine formation
In the normal adults approx. 1200 ml of blood
perfuses the kidney each minute .
That is 25% of the cardiac output .
The glomeruli receive blood through afferent
arterioles and an ultrafiltrate of the plasma passes into
the bowman’s space.
From there the filtrate is passed through the tubules
and the collecting ducts.
Reabsorption and secretion of various substances .
Concentration of urine occurs .
180lt of glomerular filtrate in 24 hrs is reduced to 1-
2lt .
3. Through the glomerular filtration and tubular
secretion ,numerous waste products are eliminated
from the body.
4. 1. General evaluation of health
2. Diagnosis of disease or disorders of the kidneys or
urinary tract
3. Diagnosis of other systemic disease that affect kidney
functions. ex plasma cell dyscrasias.
4. Monitoring of patients with diabetes
5. Screening for drug abuse both as a part of rehabilitation
prog and in the world of professional sports.
6. To determine ovulation and pregnancy in women.
7. SPECIMEN EVALUATION:
Before proceeding with any examination ,urine
sample must be evaluated in terms of acceptability.
It includes-proper labeling
-proper specimen for the reqs examination.
-proper preservative
-visible signs of contamination
-transportation delay.
9. .
For routine examination a clean glass or plastic
container which should be dry, chemically clean,
leak proof with a tight fitting stopper is used. 1st
specimen voided in the morning is preferred.
A MID – STREAM SAMPLE is required.
2. POST–PRANDIAL SPECIMEN is sometimes
required for glucose estimation ,to monitor
insulin therapy in diabetes mellitus.
3. 24- HOUR SPECIMEN: for quantitative
estimation of proteins ,hormones.
10. COLLECTION METHODS
1.Midstream specimen: used for all types of
examinations.
First half of stream serves to flush out contaminating
cells and microbes from urethra and perineum.
subsequent stream is collected which is from the
urinary bladder.
2.Clean-catch specimen : for bacteriologic culture.
3.Catheter specimen: in bed-ridden ,ill-patients with
urinary tract obstruction.
4.Plastic bag tied around genitals : used in infants and
incontinent adults.
14. PHYSICAL EXAMINATION
1. VOLUME :
Normal average volume = 1.5 litre/day (600-2500ml/day)
I . POLYURIA : Urinary volume > 2500mL
CAUSES :
-Excessive intake of water ( polydipsia ).
- Diabetes mellitus and diabetes insipidus.
- Drugs with diuretic effect such as caffeine , alcohol and
diuretics.
-.chronic renal failure
15. 2. OLIGURIA :
Causes –
A. PRERENAL : loss of intravascular volume
- haemorrhage
- dehydration
- severe vomiting
-severe burns
16. B. POSTRENAL :
bilateral hydronephrosis
-long standing obstruction of urinary tract .
Obstruction any where in the urinary tract :
Clots , stones , strictures , tumour, sloughed
tissuse
C .RENAL PARENCHYMAL DISEASES:
17. III . COMPLETE SUPRESSION : Of urine
< 150mL /day
is called anuria.
CAUSES :
-Retention of urine as in BPH and stricture
in urethra.
-Stone and tumuors in kidney.
18. 2. COLOUR :
Normal urine is clear , pale or straw colour due to
urochrome pigment.
Increases during - Fever
-Thyrotoxicosis
- Starvation
Small amounts of urobilins and uroerythrin.
ABNORMAL COLOURS :
a. COLOURLESS – after ingestion of large amount
of water, polyuria.
b. DEEP AMBER – after exercise, high grade fever.
c. DEEP YELLOW- Jaundice
19. d. ORANGE BROWN- excreted urobilinogen is
colourless, but it is converted in presence of light and
low pH to urobilin .
e. RED/PINK – in heamoglobinuria , haematuria ,
myoglobinuria and porphyria.
f. DARK BROWN/ BLACK- in rhabdomyolysis and
alkaptonuria .
g. GREEN- phenol poisoning
h. MILKY- presence of chyle , fat.
20. 3. APPEARANCE :
Normal urine is clear
CAUSES OF TURBIDITY :
-Crystals precipitation
-Amorphous phosphate , ammonium
-Urate , carbonate
-Cellular elements leukocytes
-Bacterial growth
21. 4. ODOUR (SMELL)
Normally urine -mild aromatic due to presence of
urinoids.It may change to :
a. FRUITY- Ketoacidosis , starvation
b. MUSTY - Phenylketonuria
c. FISHY – UTI with Proteus
d. AMMONICAL - UTI with Escherichia coli
e. FOUL- UTI
f. SULFUROUS - Cystinuria
22. 5.SPECIFIC GRAVITY
- It depends on amount of solutes in solution.
-It reflects the relative degree of conc or dilution of a
urine specimen.
- It helps in evaluating the concentrating and diluting
abilities of the kidneys
- Urea( 20 %) ,Na Cl (25%), Sulphate , Phosphate –
major contributors
- SG ranges from 1.003-1.035.
- Normal adults with adequate fluid intake 1.016 –
1.022
23. INCREASE IN SG :
Diabetes mellitus
Nephrotic syndrome
Fever
Congestive heart failure
DECREASE :<1.007 - hyposthenuric
Diabetes insipidus
Compulsive water drinking
Isothenuric –SG is fixed
24. 1. URINOMETRE METHOD:
Based on the principle of buoyancy
2.REFRACTOMETER METHOD :
measures the refractive index of the dissolved solids.
3.REAGENT STRIP METHOD : indirect method .
3 main ingredients : polyelectrolyte , indicator and a
buffer.
25.
26. pH:
Normal reaction of urine is acidic with pH 4.6 to 7.6.
CAUSES OF HIGHLY ACIDIC URINE :
a. Protein-rich diet.
b. UTI by E.coli
c. Respiratory and metabolic acidosis
d. Ingestion of acidic food.
CAUSES OF ALKALINE URINE:
a. If specimen is allowed to stand at room temperature ,
it becomes alkaline.
27. b. For the treatment of uric acid calculi
c. UTI by urea splitting bacteria – proteus,
pseudomonas
1.LITMUS PAPER TEST :
2. Ph INDICATOR PAPER :
3. PH METER :
4. REAGENTS STRIP TEST:
30. PROTEINS :
150 mg of proteins is excreted in urine daily. Average
urine protein concentration is 2-10 mg/dl.
- Albumin
- Globulin
- Retinal BP
- Immunoglobulin
- Tamn-Horsfall Proteins
31. TYPES OF PROTEINURIA :
a . GLOMERULAR - Proteinuria is due to increased
permeability of glomerular capillary.
Two types – selective and non selective
Selective- in early stages of glomerular disease , there is
increased excretion of lower molecular weight
proteins.
When larger moleculer weight proteins are excreted -
non selective proteinuria.
It indicates greater glomerular damage.
Can cause heavy proteinuria > 3-4 gms /day.
32. b. TUBULAR :
Loss of small amount of urinary protein that would
otherwise be largely reabsorbed.
These proteins are usually low molecular weight.
Seen in acute and chronic pyelonephritis , heavy
metal poisoning, interstitial nephritis.
C. OVERFLOW :
Overflow of excess levels of a protein in the
circulation , occurs in urine.
33. d. POSTURAL :
Orthostatic or postural proteinuria occurs in 3-5% of
apparantly healthy young adults.
seen at day time.
Not at night when recumbant position is assumed.
Persistent proteinuria may develop at a later date.
May result due to an exaggerated lordotic position or
inferior vena caval compression between liver and
vertebral column
Daily excretion of protein rarely exceeds 1gm.
34. e. MICROALBUMINURIA :
Presence of albumin above the normal level but
below the detectable range.
20-250mg/ day
Earliest sign of renal damage in diabetes mellitus.
Detection of microalbuminuria : It cannot be
detected by routine tests.
- Measurement of albumin –creatinine ratio in a
random urine sample.
- Measurement of albumin in an early morning or
random urine sample or in a 24 hr sample.
Exact quantitation – RIA and ELISA.
35. METHODS FOR PROTEIN DETECTION :
HEAT COAGULATION METHOD
Principle – Proteins get precipitated when boiled in
acidic solution.
For testing urine should be just acidic , if not- acidify
by adding few drops of 10% acetic acid.
37. SULPHOSALICYLIC ACID TEST
Addition of sulphosalicylic acid to the urine causes
formation of a white ppt.
Proteins are denatured by organic acids and
precipitate out.
More sensitive and reliable than boiling test.
HELLER’S NITRIC ACID
REAGENT STRIP METHOD
Bromophenol (indicator) coated readymade strips
are used.
38. This test is semi quantitative.
It is mainly reactive to albumin and false negative in
the presence of Bence- Jones proteins , myoglobin,
haemoglobin.
as protein carry a charge at physiologic ph , their
presence will elicit a ph change .
39. Negative
Trace
+ (30 mg/dL)
++ (100 mg/dL)
+++ (300 mg/dL)
++++ (2000 mg/dL)
Chemical Principle
H
H
H
H
H
H
Pr
Pr
Pr
Pr
Pr
Pr
“Protein Error of Indicators Method”
Pr Pr
Pr
Pr
Pr
Pr
Tetrabromphenol Blue
(buffered to pH 3.0)
H+
H+
H+
H+
H+
H+
Read at 60 seconds
RR: Negative
40. QUANTITATIVE ESTIMATION OF PROTEIN
IN 24 HR URINE SAMPLE
Instrument used is Esbach’s albuminometer .
Esbach’s reagent –picric acid (10g), citric acid (20) in
distilled water to make 1000 ml of solution.
Sample collection : begins at 8am in the morning and
continued till 8 am nxt day.
A small volume {100-150 ml} called aliquot is
collected.
42. BENCE –JONES PROTEINURIA
These are monoclonal immunoglobulin light chains.
Synthesized by neoplastic plasma cells.
Excess production occurs in plasma cell dyscrasias
like multiple myeloma and primary amyloidosis.
When heated , they precipitate at temperatures
between 40-60 celsius and precipitate disappears at
85-100 celsius.
Osgood & Haskins method is used besides the heating
test.
These tests are now replaced by protein
electrophoresis of concentrated urine sample.
43. GLUCOSE AND OTHER SUGARS IN URINE :
Small amount present in fasting urine which is not
detectable by chemical methods.
Presence of chemically detectable glucose in urine –
Glycosuria.
It depends on -blood sugar level
- rate of glomerular filtration
- tubular reabsorption
Normal renal threshold for glucose 180-200 mg/ dl.
Diabetes mellitus – most common cause.
Also seen in – hyperthyroidism
- hyperpitutarism
44. Other causes – myocardial infarction
- cerebral haemorrhage
-brain tumours
-uremia
- severe liver ds
Sometimes the sugar level is normal but glycosuria
occurs due to decrease in renal threshold.
Non pathological causes :
-Pregnancy
-Stress and anxiety
-Alimentary glycosuria
45. METHODS :
COPPER REDUCTION METHODS :
BENEDICT’S QUALITATIVE TEST :
Benedict’s reagent ( copper sulphate 17.3 gm
sodium carbonate 100 gm
sodium citrate 173 gm )
5 ml benedict’s reagent + 8 drops of urine
PRINCIPLE :
Cu 2+ Cu+ in hot alkaline medium
Cu + OH Cu OH
2 CuOH Cu2O (RED)
46. This is a Non specific test for glucose .
Other carbohydrates - fructose
- galactose
- lactose
- pentoses
and non carbohydrates -ascorbic acid
- salicylates
- cephalosporins
also reduce copper sulphate solution.
47. Depending on the colour of the precipitate the
sugar content is estimated
Green- 0.5%
Yellow – 1%
Orange -1.5%
Red- 2%
Brick red ->2%
48. REAGENT STRIP TEST
It is specific for glucose.
Based on glucose oxidase –peroxidase activity.
Reagent strip is impregnated with the 2 enzymes and a
chromogen.
PRINCIPLE
Glucose + O2 (room air) gluconic acid+ H2O2
H2O2 + chromogen peroxidase Oxidised chromogen
(blue) + H20
49. FALSE POSITIVE TEST :
Occurs - in the presence of strong oxidizing cleansing
agent in the urine container.
- in the low specific gravity.
FALSE NEGETIVE TEST :
Occurs - sodium Fluoride -used as a preservative.
- ascorbic acid
- glycolytic enzymes from cells and bacteria.
52. KETONES :
Inadequate carbohydrate in the diet or a defect in
carbohydrate metabolism - body tends to metabolize
increasing amount of fatty acids.
This leads to increase in intermediate products like –
Ketones appear in blood which are ultimately excreted
in urine.
Aceto acetic acid (20 %) , acetones ( 2%), 3-hydroxy
butyrate (78 %)
53. CAUSES OF KETONURIA :
Diabetic Ketonuria
Ketonuria implies the presence of ketoacidosis.
Upto 50 mg of aceto acetic acid per dl may be present
without clinical evidence of ketosis.
Type 1 diabetic patients are more prone to episodes of
ketosis , associated with -infection
-stress.
54. Non Diabetic Ketonuria
In infants and children ketonuria occurs in conditions
- acute febrile diseases
- persistent vomiting or diarrhea
Inherited metabolic disorders
In hyperemesis of pregnancy
In cachexia
also seen following severe exercise
Or with a low – carb diet for weight reduction
55. METHODS
1.ROTHERA’S TEST (CLASSIC NITROPRUSSIDE
REACTION )
5 ml urine + excess of (NH4)2SO4 (Saturate it )
Few crystals of sodium nitroprusside
Slowly add 1-2 ml of liqour ammonia
Purple ring at junction.
56. The purple colour is given by acetone and acetoacetic
acid.
B-hydroxybutyrate does not gives this test.
FALSE- POSITIVE TEST
can occur in the presence of L-dopa and in
phenylketonuria.
58. 2.ACETEST TABLET TEST :
This is Rothera’s test in the form of a tablet.
The Acetest tablet consists of sodium nitroprusside ,
glycine , and an alkaline buffer.
A purple lavender discoloration of the tablet indicates
the presence of acetoacetate or acetone (>=5 mg/dl).
The test is more sensitive than reagent strip test for
ketones.
59. 3.FERRIC CHLORIDE TEST (Gerhardt s) :
Addition of 10% ferric chloride solution drop by drop
to urine causes solution to become reddish or
purplish if acetoacetic acid is present.
This test is given only by acetoacetic acid not by the
other two substances.
If considerable amount of phosphate are present a
precipitate of ferric phosphate is produced.
It is necessary to filter this off.
The test is not specific since certain drugs (salicylate
and L- dopa ) give similar reaction.
60. These can be differentiated from acetoacetic acid by
their different behaviour towards heat.
On thoroughly boiling the urine ,acetoacetic acid loses
co2 and is converted into acetone, which no longer
gives the test.
Salicylates are unaffected by boiling the urine and
colour persists.
61. Neither of these commonly used test is given by b-
hydroxybutyrate .
To test for this compound it is necessary to oxidise it
to acetoacetic acid.
62. BLOOD IN URINE
HAEMATURIA- presence of abnormal number of red
cells in urine.
Causes- IgA nephropathy
-focal GS
- neoplasia
- trauma or calculi anywhere in the urinary
tract
- bleeding disorder
63. HAEMOGLOBINUREA
Presence of free hb in urine.
Screening test for hb is a useful adjunct to the
microscopic exam. Of the sediment .
Causes –intravascular haemolysis
extensive burns
prosthetic heart valves etc .
Free hb binds with haptoglobin ,once this binding
capacity is saturated hb appears in urine.
64. REAGENT STRIP TEST FOR HAEME COMP.
Principle –O2 is liberated from peroxide in the strip
by the peroxidase – like activity of haeme in free hb.
H2O2 +chromogen oxidised
chromogen +H2O
Color change is obtained.
Strip tests can detect 0.05-0.3 mg hb /dl urine.
BENZIDINE TEST : positive for haematuria,
haemoglobinuria,myoglobinuria.
65. 10% benzidine solution in glacial acetic acid.
1ml of this solution + 1ml urine – test
1ml of benzidine sol. + 1 drop of blood – positive
control
H2O2 1ml is added to both tubes
Appearance of bluish colour -positive for occult blood
ORTHOTOLUDINE TEST: In the place of benzidine
orthotoludine is used.it is more sensitive than
benzidine test
66. False positive:
Contamination of urine by menstrual blood in females.
Contamination by oxidizing agents, bleach etc.
False negative:
Presence of reducing agents like ascorbic acid in
high concentration.
Use of formalin as a preservative for urine.
67. BILIRUBIN
Breakdown product of hb in the RE of the spleen ,
liver , bone marrow.
Bilirubin linked to albumin – unconjugated , insoluble
in water.
In liver it is conjugated with glucuronic acid to form
bilirubin glucuronide- water soluble .
Normal adult urine contains 0.02 mg/dl of bilirubin.
68. BILIRUBINURIA -CAUSES
Obstruction to bile outflow from the liver –intra or
extrahepatic
Gallstones in CBD
CA head f pancreas
Hepatocellular disease –periportal inflammation ,
fibrosis .
Hepatotoxic drugs or toxins
Dubin –johnson and Rotor .
Bilirubinuria is associated with yellow – brown to
greenish brown urine that may have a yellow foam .
- elevated serum bilirubin , pale colored stools.
69. 1. FOUCHET’S TEST :
5ml fresh urine +2.5 ml of 10% barium chloride.
Barium sulphate - bilirubin complex is ppted.
Filter to obtain the ppt on a filter paper.
To the ppt add 1 drop of fouchet’s reagent ( 25gms of
trichloroacetic acid ,10 ml of 10% FeCl3 and DW
100ml ).
Immediate development of blue green colour.
70.
71. 2. GMELIN’S TEST :
3ml conc HNO3 +equal quantity of urine .
Test tube is shaken gently ,play of colors is seen .
3. LUGOL IODINE TEST:
4. REAGENT STRIP TEST : based on the coupling
reaction of bilirubin with a diazonium salt in acid
medium .
can detect 0.5 mg/dl bilirubin in urine .
P-nitrobenzene diazonium p-toluene sulphonate is used.
72. UROBILINOGEN :
Normal output is0.5- 2.5 mg units /24 hrs .
These are colorless substances as compared to
urobilins ,the oxidation products of urobilinogen that
imparts yellow orange color to normal urine.
73. fresh urine sample should be used.
1. EHRLICH’S ALDEHYDE TEST :
Ehrlich’s reagent ( p-dimethylaminobenzaldehyde)
Reacts with urobilinogen to produce a pink color.
Intensity of the color depends on the amount of
urobilinogen present.
Bilirubin should be removed first as it interferes with
the reaction.
5 ml of fresh urine is taken in a test tube +0.5 ml of
EHRLICH’S reagent is added. Allow to stand at
room temperature for 5 minutes.
74. both urobilinogen and porphobilinogen produce
similar reaction , they can be differentiated by
WATSON –SCHWARTZ TEST .
1-2ml of chloroform is added and the test tube is
shaken for 2 min and allowed to stand.
Pink colour in the chloroform layer ,pink coloration of
aqueous portion indicates presence of
porphobilinogen .
75. FALSE NEGATIVE : can occur in the presence of
- urinary tract infection as nitrite oxidises
urobilinogen to urobilin .
-antibiotic therapy
76. BILE SALTS
HAY’S TEST – Based on the fact that bile salts when
present in the urine lower the surface tension.
Fresh clear urine sample is taken in a small beaker at
room temperature .
A little dry ,finely powdered sulphur particles are
added on the surface .
thymol used as a preservative may give false positive
test.
77. INDIRECT TEST FOR UTI :
It is not uncommon for significant UTI to be present in
patients who do not experience typical
symptomatology.
If remain untreated , it can cause severe renal damage.
So in high risk individual – elderly
- pregnant
- diabetic
Two commonly utilized tests are :
1.) Reagent strip nitrite
2.) Leukocyte estarase
78. NITRITE
Many bacteria are able to reduce nitrate to nitrite and
thus will generate a positive urine nitrite test when
present in significant no.
E.coli, klebsiella, Enterobacter , Proteus, Staph. ,
Pseudomonas.
REAGENT STRIP TEST: it is impregnated with p-
arsanilic acid , which forms a diazonium salt when
reacts with nitrite present in the urine.
79. The compoud then reacts with benzoquinolone
to form a pink azo dye.
80. LEUKOCYTE ESTERASE
Azurophilic granules of the human nuetrophils contain
up to 10 proteins showing esterolytic activity which is
commonly used as marker for these cells.
Leukocyte esterase activity can be indicative of
remnants of cells that are not visible microscopically.
Positive leukocyte esterase results correlate with
‘significant’ numbers of neutrophils of fresh urine as a
cut off point.
81. METHODS :
Neutrophilic esterases catalyze the hydrolysis of esters
to produce their respective alcohols and acids.
It utilizes 3-hydroxy-5-phenyl-pyyrole-N-tosyl-L-
alanine as a substrate , which reacts in the presence of
leukocyte esterase to form pyrrole alcohol.
The alcohol then reacts with a diazonium salt to
produce a purple color.
The intensity of the color produced is proportional to
the amount of enzyme present, which is related to the
number of neutrophils present.
84. CELLS
ERYTHROCYTES :
Under high power, unstained erythrocytes (RBCs)
appear as pale biconcave disks that may vary
somewhat in size but are usually about 7micron in
diameter.
If the specimen is not fresh when it is examined,
erythrocytes may appearas faint, colorless circles or
shadow cells because the haemoglobin may dissolve
out.
85. They may become crenated in hypertonic urine and
appear as small, rough cells with crinkled edges.
In dillute urine, the cells will swell and rapidly lyse,
releasing haemoglobin and leaving only empty cell
membranes referred to as ghost cells.
On occasion, erythrocytes may be confused with oil
droplets or yeast cells.
Erythrocytes are found in small numbers (0-2
cells/hpf) in normal urine, more then 3 cells/hpf is
considered abnormal.
86. These include :-
1.) renal disease – glomerulonephritis
2.) lower urinary tract disease – calculus
tumor
3.) extrarenal disease – accute appendicitis
4.) toxic reactions due to drugs
5.) physiologic causes , including exercise.
87.
88.
89. DYSMORPHIC ERYTHROCYTES :
Red blood cells with cellular protusions or
fragmentation are termed dysmorphic.
Their presence in urine samples is strongly suggestive
of renal glomerular bleeding.
The so-called ‘G1 cell’ , which has a doughnut shape
with one or more membrane blebs, may be more
specific than dysmorphic cells for diagnosing
glomerular hematuria.
90. LEUKOCYTES
NEUTROPHILS :
- The polymorphonuclear leukocyte (neutrophil) is the
predominant type of leukocyte (white blood cell
[WBC] ) that appear in the urine.
- When cellular degeneration has begun , nuclear detail
may be lost, and neutrophils may then become
difficult to distinguish from renal tubular epithelial
cells.
- In dilute or hypotonic urine , neutrophils swell and
their cytoplasmic granules exihibit brownian
movement. Because of the refractility of the moving
granules, neutrophils in this setting are known as
91. ‘glitter’ cells.
- The leukocytes esterase reagent strip is valuable in the
confirmation of pyuria in hypotonic urine specimen.
- Urinary neutrophil counts greater than 30 cells/hpf
suggest acute infection, and repeated sterile cultures in
this setting may indicate tuberculosis or a nephritis.
- It is a reliable indicator of urinary tract infection.
92.
93.
94. EPITHELIAL CELLS
SQAMOUS EPITHELIAL CELLS :
- These cells are the most frequent epithelial cell seen in
normal urine, and likewise the least significant.
- The distal one third of the urethra is lined by sqamous
epithelial cells, and in the urine these cells are large
and flat, with abundant cytoplasm and small round
central nuclei.
- Their margins are often folded.
95.
96. TRANSITIONAL (Urothelial) EPITHELIAL CELLS :
- Transitional epithelial cells line the urinary tract from
the renal pelvis to the lower third of the urethra.
- These cells are smaller than squamous cells , their size
ranging from 40-200 micro m.
- They are round or pear shaped , with a round centrally
located nucleus.
- The exception is the presence of large clumps or sheets
of transitional cells in the absence of instrumentation
(i.e catheterization).
97.
98. RENAL TUBULAR EPITHELIAL CELLS :
- These are the most significant types of epithelial cells
found in urine because the finding of an increased
number indicates tubular damage.
- The Papanicolaou stain has been shown to be
especially useful in distinguishing renal tubular cells
from other mononuclear cells in urine.
- Renal epithelial cells from the proximal and distal
convoluted tubules occur singly and are large ( 14-
60micro m ) and coarsely granular eosinophilic
cytoplasm.
99.
100. PIGMENT IN RENAL TUBULAR EPITHELIAL
CELLS
- With hemoglobinuria or myoglobinuria, heme
pigment is absorbed into the cells and converted to
hemosiderin.
- The cytoplasmic granules appear yellow- brown and
stain for iron with Prussian blue.
- Melanin granules are absorbed into the tubular cells
in rare cases of melanuria.
101. CASTS :
Casts are the only formed elements of urine that have
the kidney as their sole site of origin.
Tamm-Horsfall protein is the glycoprotein secreted
by the thick part of the ascending loop of henle which
constitutes about one third of the total urinary protein
in normal individuals.
Tamm-Horsfall protein forms the matrix of all casts.
The protein forms a meshwork of fibrils that can
potentially trap any elements present in the tubular
filtrate including cells, cell fragments or granular
material.
102. Casts may be short and stubby or long and
convoluted.
Casts typically have parallel sides and blunt ends, but
with age they may begin to disintegrate and show
thinning and irregularities.
Fibrils may separate , causing a frayed appearance .
Tails and tapering ends can be seen, and these
disintegrating forms are referred to as cylindroids.
In the normal person , very few casts are seen in the
urinary sediments. In kidney diseases , they may
appear in large numbers and in many forms.
103. Large numbers of casts may also be seen in healthy
persons after strenuous exercise accompanied by
proteinuria.
Casts formation increases with lower pH, increased
ionic concentration, and when there is stasis or
obstruction of the nephron by cells or cell debris.
It is also increased when larger than normal amounts
of plasma proteins enter the tubules.
104. CLASSIFICATION OF CASTS :
CAST MATRIX
1.) HYALINE CASTS : Increased numbers are seen with
renal diseases and transiently with exercise, heat
exposure, dehydration, fever, congestive heart failure,
and diuretic therapy.
2.) WAXY CASTS : They are easily visualized. Waxy
casts are homogeneously smooth in appearance with
sharp margins, blunted ends, and cracks or
convolutions frequently seen along the lateral margins.
107. CELLULAR CASTS
3.) ERYTHROCYTE (RED BLOOD CELL) CASTS :
- They are an indication of bleeding within the
nephron. Glomerular damage allows erythrocytes to
escape into the tubule.
- Acute glomerulonephritides, lgA nephropathy, lupus
nephritis, subacute bacterial endocarditis, and renal
infarction.
109. 4.) LEUKOCYTE (WHITE BLOOD CELL) CASTS :
- White blood cell casts are refractile, exhibit granules,
and frequently multilobated nuclei will be visible
unless disintegration has begun.
- They are also seen with interstitial nephritis, lupus
nephritis.
5.) RENAL TUBULAR EPITHELIAL CELL CASTS :
- Renal tubular epithelial cell casts are seen in urine with
acute tubular necrosis, viral disease (e.g,
cytomegalovirus disease).
6.) MIXED CELLULAR CASTS :
111. INCLUSION CASTS
7.) GRANULAR CASTS : Granular casts are fairly
common and may appear in both pathologic and non
pathologic conditions.
- Granules may be small or large, and may originate
from plasma protein aggregates that pass into the
tubules from damaged glomeruli, as well as from
cells.
- These are seen in glomerular and tubular diseases,
renal allograft rejection, viral infection and chronic
lead poisoning.
113. 8.) FATTY CASTS :
- Fatty material is incorporated into the cast matrix from
lipid – laden renal tubular cells – nephrotic syndrome.
9.) CRYSTAL CASTS :
- These casts indicate deposition of crystals in the tubule
or collecting duct.
PIGMENTED CASTS
10.) HEMOGLOBIN (BLOOD) CASTS :
- Most often hemoglobin casts , also known as blood
casts are seen with erythrocyte casts and glomerular
disease.
114. 11.) HEMOSIDERIN CASTS :
- Hemosiderin granules in casts derive from pigment –
laden renal tubular cells.
12.) MYOGLOBIN CASTS :
- These casts are red- brown in color and occur with
myoglobinuria following acute muscle damage.
- These may be associated with acute renal failure.
13.) BILIRUBIN AND OTHER DRUG CASTS :
- Bilirubin is seen in urine when there is obstructive
jaundice and will color casts a deep yellow brown.
115. BROAD CASTS
Broad casts are defined as those with a diameter two
to six times that of normal casts.
They indicate tubular dilation and / or stasis in the
distal collecting duct.
All types of casts may occur in broad forms and they
are typically seen in individuals with chronic renal
failure.
They portend a poor prognosis.
116. CRYSTALS
Crystals form by the precipitation of urinary salts when
alteration in multiple factors affect their solubilities.
These include changes in pH, temperature and
concentration.
The precipitation can appear in the urine in the form of
either true crystals or amorphous material.
The majority of crystal formation takes place in
refrigerated specimens and those allowed to sit at
room temperature for several hours.
Knowledge of urine pH is a valuable aid in crystal
identification because it is the pH that determines
which chemical will precipitate.
117. CRYSTALS FOUND IN NORMALACID URINE
AMORPHOUS URATES (Calcium, Magnesium,
Sodium, and Potassium Urates)
Amorphous urates will precipitate upon standing in
concentrated urine of a slightly acid pH.
When large amounts are present , the urine sediment may
appear pink- orange to reddish brown on macroscopic
examination; this appearance has been referred to as
‘brick dust’.
Microscopically this amorphous material appears as
yellow –brown small granules that can form clumps
and adhere to fibers and mucous threads.
118. CRYSTALLINE URATES (Sodium, Potassium, and
Ammonium)
Both amorphous urates and crystalline forms will slowly
revert to uric acid plates on acidification with acetic
acid.
CRYSTALLINE URIC ACID
Uric acid crystals occur at low pH(5-5.5) and seen in a
variety of shapes including rhombic or four-sided flat
plates, prisms, oval forms with pointed ends, wedges.
The majority are colored typically yellow or reddish
brown.
120. Large numbers of uric acid crystals and urates may
reflect increased nucleoprotein turnover,
chemotherapy of leukemias or lymphoma, Lesch-
Nyhan syndrome.
They may also herald the urate nephropathy of gout.
CALCIUM OXALATES
Dihydrates may appear at pH 6 or in neutral urine.
Their classic form is that of a small, colorless,
octahedron that resembles an envelope.
Dumbbell shapes and ovoid forms may occur.
Oxalate crystals in large numbers may reflect severe
chronic renal disease.
123. CRYSTALS FOUND IN NORMALALKALINE
URINE
AMORPHOUS PHOSPHATES (Calcium and
Magnesium)
Like amorphous urates, amorphous phosphates have a
granular appearance colorless and will produce a fine
or lacy white precipitate macroscopically.
124. CRYSTALLINE PHOSPHATES
Triple phosphate (ammonium magnesium phosphate)
crystals are one of the most easily identified urine
crystal, although they commonly show a variation in
size.
They are colorless, three-to six –sided prisms with
oblique ends referred to as coffin lids.
They may form colorless sheets or flakes.
CALCIUM CARBONATE
These uncommon crystals are small and colorless , with
dumbell or spherical shapes.
They are distinguished from other production of carbon
dioxide in the presence of acetic acid.
126. CRYSTALS FOUND IN ABNORMAL URINE
CYSTINE
Cystine crystals are colorless, refractile, hexagonal plates
which appear in acid urine.
They are soluble in water at pH less than 2 or greater
than 8.
TYROSINE
In acidic urine, tyrosine forms fine silky needles that
may be arranged in clumps .
These are occasionally seen in the urine of patients with
severe liver disease.
