MAKERERE UNIVERSITY

COLLEGE OF HEALTH SCIENCES

DEPARTMENT OF BIOCHEMISTRY

BIOCHEMISTRY PRACTICAL REPORT

DATE OF THE PRACTICAL;

AUTHORS;

MAYANJA Caroline MBChB 19/U/20400/PS

KISEKKA Enock PHA 19/U/0867

MUKIIBI Simon Blair PHA 19/U/0874

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TITLE: ANALYSIS OF URINE.

ABSTRACT

This experiment involved physical and chemical analyses of three urine samples as a laboratory
technique used to diagnose and disclose presence of some diseases.
The experiment involved tests that investigated the physical properties i.e. smell, color, turbidity,
specific gravity, foam of the urine and also its chemical properties like presence of reducing sugars
using benedict’s test, ketone bodies using Rothera’s test, proteins, bilirubin using Foucher’s test and
urobilinogen using Ehrlich’s test. These tests were done on three urine samples D, S and N.
It was found out in the experiment that sample D had diabetes mellitus and ketonuria, Sample S had
proteinuria an indication of renal disease and sample N had normal parameters except that urobilinogen
was present. Urinalysis is key in the diagnosis and monitoring of illness, however it should be noted
that some findings from a urinalysis need the support of other diagnostic procedures like physical
examination by a physician.

INTRODUCTION

Urinalysis is done in microbiology to investigate cells, pus cells and microbes under microscopes as
well as in biochemistry to determine the concentration of different substances like glucose, ketone
bodies, bilirubin etc. This can disclose evidence of diseases even some that have not caused significant
signs and symptoms and is therefore a common procedure of routine health screening. It’s used to
diagnose a urinary tract or kidney infection, to evaluate causes of kidney failure, to screen for
progression of some chronic diseases like kidney stones, inflammation of the kidneys
(glomerulonephritis) or muscle breakdown (rhabdomylosis). Interpretation of urinalysis is based on
reviewing all the components of the test as well as the clinical signs and symptoms of the patient. A
clinical examination of urine can provide a convenient, cost effective and non-invasive means of
assessing kidney function and providing an overall assessment of our body's health.

The aim of this practical was to appreciate the importance of urinalysis as a screening and diagnostic
tool for diseases and disorders in the clinical setting.
The objectives of the practical included the following, to obtain a simplified knowledge about routine
urinalysis, to perform physical and chemical analyses on urine samples and to establish the relationship
between physical characteristics of urine and the chemical composition.

The practical is thus significant as observation of these characteristics provides preliminary information
concerning disorders such as glomerular bleeding, liver disease, inborn errors of metabolism, and
urinary tract infection, diabetes mellitus and hypertension among others. These characteristics can also
be used to determine the prognosis of a treatment schedule especially those that involve drugs that can
be excreted in urine or those that affect body chemical components that can be excreted in urine

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BACKGROUND

The ability of the kidneys to selectively reabsorb essential chemicals and water from the glomerular
filtrate is one of the body’s most important functions. The intricate process of reabsorption is often the
first renal function to become impaired; therefore, an assessment of the kidney’s ability to reabsorb is
a necessary component of the routine urinalysis.
Urine examinations are classified into physical, chemical and microscopic examinations.
1. Physical characteristics of urine
The physical characteristics of urine include observations of color, turbidity, odor and measurement of
specific gravity, pH and volume. Visual observation of a urine sample can give important clues as to
evidence of pathology.
I. Color
The color of urine varies from almost colorless to black. These variations may be due to normal
metabolic functions, physical activity, ingested materials, or pathologic conditions. A noticeable change
in urine color is often the reason a patient seeks medical advice; it then, becomes the responsibility of
the laboratory to determine whether this color change is normal or pathologic.
Common descriptions include pale yellow, yellow, dark yellow, and amber. Care should be taken to
examine the specimen under a good light source, looking down through the container against a white
background. The yellow color of urine is caused by the presence of a pigment, which Thudichum named
Urochrome in 1864. Urochrome is a product of endogenous metabolism, and under normal conditions
the body produces it at a constant rate. The actual amount of Urochrome produced is dependent on the
body’s metabolic state, with increased amounts produced in thyroid conditions and fasting states.
Urochrome also increases in urine that stands at room temperature.
Because Urochrome is excreted at a constant rate, the intensity of the yellow color in a fresh urine
specimen can give a rough estimate of urine concentration. A dilute urine will be pale yellow and a
concentrated specimen will be dark yellow. Remember that, owing to variations in the body’s state of
hydration, these differences in the yellow color of urine can be normal
Two additional pigments, uroerythrin and urobilin, are also present in the urine in much smaller
quantities and contribute little to the color of normal, fresh urine. The presence of uroerythrin, a pink
pigment, is most evident in specimens that have been refrigerated, resulting in the precipitation of
amorphous urates. Uroerythrin attaches to the urates, producing a pink color to the sediment. Urobilin,
an oxidation product of the normal urinary constituent Urobilinogen, imparts an orange-brown color to
urine that is not fresh. The photo-oxidation of large amounts of excreted Urobilinogen to urobilin also
produces a yellow-orange urine; however, yellow foam does not appear when the specimen is shaken.
Photo-oxidation of bilirubin imparts a yellow-green color to the urine. (Susan King Strasinger &
Marjorie Schaub Di Lorenzo, 2008).

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 II. Smell
Normal urine is aromatic but odor of urine depends on diet as well as medication. Sweetish fruity smell
is seen in uncontrolled diabetes mellitus due to excretion of acetone in urine, also when urine is retained
in the bladder, a putrid or strongly ammoniacal odor develops due to decomposition of urine by bacteria.
(N.Mallikarjuna Rao, Medical biochemistry, 2006)
III. Turbidity
Clarity is a general term that refers to the transparency/turbidity of a urine specimen. In routine
urinalysis, clarity is determined by visually examining the mixed sample while holding it in front of a
light source. The sample should, of course, be in a clear container. Color and clarity are routinely
determined at the same time. Common terminology used to report clarity includes clear, hazy, cloudy,
and turbid. Freshly voided normal urine is usually clear, particularly if it is a midstream clean-catch
specimen. Precipitation of amorphous phosphates and carbonates may cause a white cloudiness. The
presence of squamous epithelial cells and mucus, particularly in specimens from women, can result in
a hazy but normal urine. (Susan King Strasinger & Marjorie Schaub Di Lorenzo, 2008).
The most commonly encountered pathologic causes of turbidity in a fresh specimen are RBCs, white
blood cells (WBCs), and bacteria caused by infection or a systemic organ disorder. Other less frequently
encountered causes of pathologic turbidity include abnormal amounts of non-squamous epithelial cells,
yeast, abnormal crystals, lymph fluid, and lipids. The clarity of a urine specimen certainly provides a
key to the microscopic examination results, because the amount of turbidity should correspond with the
amount of material observed under the microscope (Susan King Strasinger & Marjorie Schaub Di
Lorenzo, 2008).
Urinary tract infections in which the urine appears cloudy because it contains pus cells and bacteria and
Bancroftian filariasis in which the urine may appear milky-white because it contains chyle (Monica
Cheesbrough, 2009)
IV. Foam
Normal urine produces only a small amount of rapidly disappearing foam when shaken, and a large
amount of white foam indicates an increased concentration of protein, yellow foam appears bilirubin is
suspected, red/brown foam indicates hemoglobin.
(Susan King Strasinger & Marjorie Schaub Di Lorenzo, 2008).

V. pH
Along with the lungs, the kidneys are the major regulators of the acid-base content in the body. They
do this through the secretion of hydrogen in the form of ammonium ions, hydrogen phosphate, and
weak organic acids, and by the reabsorption of bicarbonate from the filtrate in the convoluted tubules.
A healthy individual usually produces a first morning specimen with a slightly acidic pH of 5.0 to 6.0
this is due to acid, base, organic and inorganic ions present in the urine all which contribute to the

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titratable acidity of urine. A more alkaline pH is found following meals (alkaline tide) due to secretion
of H+ in gastric juice and also after a fruit and vegetable diet as well as during alkalosis and alkaline
therapy. (N Mallikarjuna Rao, Medical biochemistry 2006) The pH of normal random samples can
range from 4.5 to 8.0.pH decreases after a protein meal and is acidic in uncontrolled diabetes, starvation
and fevers. Consequently, no normal values are assigned to urinary pH, and it must be considered in
conjunction with other patient information, such as the acid-base content of the blood, the patient’s
renal function, the presence of a urinary tract infection, the patient’s dietary intake, and the age of the
specimen
(Susan King Strasinger & Marjorie Schaub Di Lorenzo, 2008).
VI. Specific gravity
Specific gravity is defined as the density of a solution compared with the density of a similar volume of
distilled water at a similar temperature. Because urine is actually water that contains dissolved
chemicals, the specific gravity of urine is a measure of the density of the dissolved chemicals in the
specimen. As a measure of specimen density, specific gravity is influenced not only by the number of
particles present but also by their size. Large urea molecules contribute more to the reading than do the
small sodium and chloride molecules. For purposes of routine urinalysis, however, the specific gravity
provides valuable preliminary information and can be easily performed by direct methods using a
Urinometer (hydrometer) .It is also influenced by volume i.e. specific gravity is inversely proportional
to volume
The specific gravity of the plasma filtrate entering the glomerulus is 1.010. The term isosthenuric is
used to describe urine with a specific gravity of 1.010. Specimens below 1.010 are hyposthenuric, and
those above 1.010 are hypersthenuric. One would expect urine that has been concentrated by the kidneys
to be hypersthenuric; however, this is not always true. Normal random specimens may range from 1.003
to 1.035, depending on the patient’s amount of hydration. Specimens measuring lower than 1.003
probably are not urine. Most random specimens fall between 1.015 and 1.025, and any random
specimen with a specific gravity of 1.023 or higher is generally considered normal. Specific gravity
increases in diabetes mellitus due to increased glucose in urine as well as fever and nephritis and it
decreases in diseases that cause increase in volume i.e. diabetes inspidus.

2. Chemical analysis of urine.

I. Protein
Of the routine chemical tests performed on urine, the most indicative of renal disease is the protein
determination. The presence of proteinuria is often associated with early renal disease, making the
urinary protein test an important part of any physical examination. Normal urine contains very little

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protein: usually, less than 10 mg/dl or 100 mg per 24 hours is excreted. This protein consists primarily
of low-molecular weight serum proteins that have been filtered by the glomerulus and proteins produced
in the genitourinary tract. Owing to its low molecular weight, albumin is the major serum protein found
in normal urine. Even though it is present in high concentrations in the plasma, the normal urinary
albumin content is low because the majority of albumin presented to the glomerulus is not filtered, and
much of the filtered albumin is reabsorbed by the tubules. Other proteins include small amounts of
serum and tubular micro globulins, Tamm-Horsfall protein produced by the tubules, and proteins from
prostatic, seminal, and vaginal secretions.
Demonstration of proteinuria in a routine analysis does not always signify renal disease; however, its
presence does require additional testing to determine whether the protein represents a normal or a
pathologic condition. Clinical proteinuria is indicated at ≥30 mg/dL (300 mg/L). The causes of
proteinuria are varied and can be grouped into three major categories: pre renal, renal, and post renal,
based on the origin of the protein.
Pre renal proteinuria is caused by conditions affecting the plasma prior to it reaching the kidney and,
therefore, is not indicative of actual renal disease. This condition is frequently transient, caused by
increased levels of low molecular- weight plasma proteins such as hemoglobin, myoglobin, and the
acute phase reactants associated with infection and inflammation. The increased filtration of these
proteins exceeds the normal re-absorptive capacity of the renal tubules, resulting in an overflow of the
proteins into the urine. Because reagent strips detect primarily albumin, pre-renal proteinuria is usually
not discovered in a routine urinalysis.
Renal Proteinuria associated with true renal disease may be the result of either glomerular or tubular
damage.
Sulfosalicylic Acid Precipitation Test
The SSA test is a cold precipitation test that reacts equally with all forms of protein (Table 5–2). Various
concentrations and amounts of SSA can be used to precipitate protein, and methods vary greatly among
laboratories. All precipitation tests must be performed on centrifuged specimens to remove any
extraneous contamination. Of course, any substance precipitated by acid produces false turbidity in the
SSA test.
The most frequently encountered substances are radiographic dyes, tolbutamide metabolites,
cephalosporins, penicillins, and sulfonamides. The presence of radiographic material can be suspected
when a markedly elevated specific gravity is obtained. In the presence of radiographic dye, the turbidity
also increases on standing due to the precipitation of crystals rather than protein. The patient’s history
provides the necessary information on tolbutamide and antibiotic ingestion. In contrast to the reagent
strip test, a highly alkaline urine produces false-negative readings in precipitation tests, as the higher
pH interferes with precipitation. Use of a more concentrated solution of SSA may overcome the effect
of a highly buffered, alkaline urine
(Susan King Strasinger & Marjorie Schaub Di Lorenzo, 2008).

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The reagent on most dipstick tests is sensitive to albumin but may not detect low concentrations of γ-
globulins and Bence Jones proteins. Dipstick tests for trace amounts of protein yield positive results at
concentrations of 5 to 10 mg per dL—lower than the threshold for clinically significant proteinuria. A
result of 1+ corresponds to approximately 30 mg of protein per dL and is considered positive; 2+
corresponds to 100 mg per dL, 3+ to 300 mg per dL, and 4+ to 1,000 mg per dL. Dipstick urinalysis
reliably can predict albuminuria with sensitivities and specificities of greater than 99
percent. Asymptomatic proteinuria is associated with significant renal disease in less than 1.5 percent
of patients. (Rabinovitch Albert. 2001).
II. Reducing sugars
Owing to its value in the detection and monitoring of diabetes mellitus, the reducing sugar test is the
most frequent chemical analysis performed on urine.
Under normal circumstances, almost all the glucose filtered by the glomerulus is reabsorbed in the
proximal convoluted tubule; therefore, urine contains only minute amounts of glucose. Tubular
reabsorption of glucose is by active transport in response to the body’s need to maintain an adequate
concentration of glucose. Should the blood level of glucose become elevated (hyperglycemia), as occurs
in diabetes mellitus, the tubular transport of glucose ceases, and glucose appears in the urine
(glucosuria). The blood level at which tubular reabsorption stops (renal threshold) for glucose is
approximately 160 to 180 mg/dL. Blood glucose levels fluctuate, and a normal person may have
glycosuria following a meal with a high glucose content.
(Susan King Strasinger & Marjorie Schaub Di Lorenzo, 2008).
Normally, the urine contains about 0.05 gm% of sugar. Such a small quantity cannot be detected by
Benedict’s test, but under certain circumstances, a considerable amount of glucose or other sugar may
be excreted in the urine. (Pakanja Naik, 2012).
Glycosuria can result from either an excessive concentration of glucose in the blood, such as may be
seen in people with uncontrolled diabetes mellitus, or a reduction in the renal threshold.
Glycosuria occurs when the filtered load of glucose exceeds the ability of the tubule to reabsorb it (i.e.,
180 to 200 mg per dL). Etiologies include diabetes mellitus, Cushing’s syndrome, liver and pancreatic
disease, and Falcone’s syndrome (Arthur Guyton and John Hall, 2006).It can also be due to
hyperactivity of pituitary, adrenal and thyroid glands as well as dysphyxia and ether anesthesia. Also
lactose can appear in urine (lactosuria) in pregnant and lactating mothers.
Measurement of reducing sugars by the copper reduction method Benedict’s test was one of the earliest
chemical tests performed on urine. The test relies on the ability of glucose and other substances to
reduce Copper sulfate to cuprous oxide in the presence of alkali and heat. A color change progressing
from a negative blue (CuSO4) through green, yellow, and orange/red (Cu2O) occurs when the reaction
takes place.
Heat CuSO4 (cupric sulfide) + reducing substance →
Alkali Cu2O (cuprous oxide) + oxidized substance →color (blue/green →orange/red)

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(Susan King Strasinger & Marjorie Schaub Di Lorenzo, 2008).
III. Ketones
The term ketones represents three intermediate products of fat metabolism, namely, acetone, acetoacetic
acid, and betahydroxybutyric acid. Normally, measurable amounts of ketones do not appear in the urine,
because all the metabolized fat is completely broken down into carbon dioxide and water. Clinical
reasons for increased fat metabolism include the inability to metabolize carbohydrate, as occurs in
diabetes mellitus; increased loss of carbohydrate from vomiting; and inadequate intake of carbohydrate
associated with starvation and malabsorption. Testing for urinary ketones is most valuable in the
management and monitoring of insulin-dependent (type 1) diabetes mellitus. Ketonuria shows a
deficiency in insulin, indicating the need to regulate dosage.
(Susan King Strasinger & Marjorie Schaub Di Lorenzo, 2008).
Ketones in urine can give an early detection of insufficient insulin in a person with diabetes. Severe
exercise, exposure to cold, poisoning from drinking rubbing alcohol, and Von Gierke’s disease. Low
levels of ketones are sometimes found in the urine of healthy pregnant women.
Ketones are detected by the Rothera’s test. Acetone and acetoacetic acid react immediately to give a
violet color but hydroxybutanote does not react in this test.
The principle of reactivity is as below; Acetoacetate + Nitroprusside = Colored complex
(Monica Cheesbrough, 2009)
IV. Bilirubin
Dark yellow or amber urine may not always signify a normal concentrated urine but can be caused by
the presence of the abnormal pigment bilirubin. If bilirubin is present, it will be detected during the
chemical examination; however, its presence is suspected if a yellow foam appears other than white
foam when the specimen is shaken. A urine specimen that contains bilirubin may also contain hepatitis
virus, reinforcing the need to follow standard precautions.
The appearance of bilirubin in the urine can provide an early indication of liver disease. It is often
detected long before the development of jaundice.
Conjugated bilirubin appears in the urine when the normal degradation cycle is disrupted by obstruction
of the bile duct (e.g., gallstones or cancer) or when the integrity of the liver is damaged, allowing leakage
of conjugated bilirubin into the circulation. Hepatitis and cirrhosis are common examples of conditions
that produce liver damage, resulting in bilirubinuria. Not only does the detection of urinary bilirubin
provide an early indication of liver disease, but also its presence or absence can be used in determining
the cause of clinical jaundice.
(Susan King Strasinger & Marjorie Schaub Di Lorenzo, 2008).
Urine normally does not contain detectable amounts of bilirubin. Bilirubin is a waste product that is
produced by the liver from the hemoglobin of red blood cells that are removed from the circulation. It
becomes a component of bile. Unconjugated bilirubin is water insoluble and cannot pass through the

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glomerulus; conjugated bilirubin is water soluble and indicates further evaluation for liver dysfunction
and biliary obstruction when it is detected in the urine.
In certain liver diseases, such as biliary obstruction, or hepatitis, bilirubin leaks back into the blood
stream and is excreted in urine. The presence of bilirubin in urine is an early indicator of liver disease
and can occur before clinical symptoms such as jaundice develop.
Bilirubin is detected using the Fouchet’s test where the urine sample is mixed with barium .The
precipitate which contains any bilirubin remains on paper and a drop of Fouchet’s reagent is added to
the dried the dry sample. If bilirubin is present a green precipitate is formed.
Caution: Prolonged exposure of the urine sample to sunlight leads to the oxidation of bilirubin, hence
compromising the sensitivity of the test. (Monica Cheesbrough, 2009)
V. Urobilinogen
When conjugated bilirubin is excreted through the bile duct into the intestine, the intestinal bacteria
convert the bilirubin to a combination of Urobilinogen and stercobilinogen. Some of the urobilinogen
is reabsorbed from the intestine into the blood, recirculates to the liver, and is excreted back into the
intestine through the bile duct.
Urobilinogen appears in the urine because, as it circulates in the blood and route to the liver, it passes
through the kidney and is filtered by the glomerulus. Therefore, a small amount of urobilinogen, less
than 1 mg/dL or Ehrlich unit is normally found in the urine.
Increased urine urobilinogen (greater than 1 mg/dL) is seen in liver disease and hemolytic disorders.
Measurement of urine urobilinogen can be valuable in the detection of early liver disease; however,
studies have shown that when urobilinogen tests are routinely performed, 1% of the non-hospitalized
population and 9% of a hospitalized population exhibit elevated results. Addition of Ehrlich reagent to
urine produces a cherry-red color. Addition of sodium acetate enhances the color reaction. In the tube
method, one part Ehrlich reagent was added to 10 parts of urine. The tube was mixed and examined for
a red color (Susan King Strasinger & Marjorie Schaub Di Lorenzo, 2008)
Hemolysis and hepatocellular disease (such as hepatitis and cirrhosis) can elevate urobilinogen levels,
and antibiotic use and bile duct obstruction can decrease urobilinogen levels.
When urobilinogen levels are low or absent in a patient with urine bilirubin and/ or signs of liver
dysfunction, it can indicate the presence of hepatic or biliary obstruction.
The chemistry behind detection of Urobilinogen concentration is as per the reaction below;
Urobilinogen + Diethylaminobenzaldehyde (Ehrlich’s Reagent) Colored Complex.

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Materials and Methods
Materials used include;

 12 Test tubes
 burette
 3 urine samples (D, S and N)
 Benedict’s solution
 Urinometer
 1ml and 2ml pipettes
 Filter papers
 6% Sulphosalicylic acid (SSA)
 Rothera’s powder (Nitroprusside dry reagent)
 0.5 mol/L barium chloride
 Foucher’s reagent
 Ehrlich’s reagent
 Pipette filler.
 2 test tube racks
 Water bath
The methods used are categorised into physical examination methods and chemical examination
methods.
PHYSICAL EXAMINATION
Among the physical examination methods, the following parameters were investigated:
 Colour.
 Transparency.
 Smell.
 Foam.
 Specific gravity.
The following were the procedures followed for each of the parameters investigated for all the 3 urine
samples.
Specific gravity
 The Urinometer was placed in the sample of urine in the measuring cylinder
 The Urinometer as then rotated to make sure it was not touching the sides or bottom of the
measuring cylinder
 The scale was read at the bottom of the meniscus
 The temperature of the urine was noted and the calibration temperature of the Urinometer

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  The observed specific gravity was then corrected by adding 0.001 for each 3 0C above the
calibration temperature.
 The procedure was repeated for the remaining 2 urine samples
Foam.
 The urine sample was shaken to check for foam and its properties and the observations
recorded accordingly for each urine sample.
Colour and transparency
 The urine sample was critically viewed against a light background to observe its colour and
against the relevant background for transparency. Observations were recorded accordingly for
all the urine samples
Smell.
 The urine samples were further investigated for their smell and observations recorded
accordingly for each of the samples.
CHEMICAL EXAMINATION
Among the chemical examination methods, the following parameters were investigated:
 Protein.
 Reducing sugars.
 Ketone bodies.
 Bilirubin.
 Urobilinogen.
 pH
The following were the procedures followed for each of the parameters investigated for all the 3 urine
samples D, S and N
PH
A broad range indicator paper was used followed by a narrow range indicator paper to get the
value to 0.2 units
Protein
 The urine samples which were cloudy were filtered through a fluted filter paper
 2 ml of clear urine of each of the samples were put into clean test tubes
 2ml of 6% Sulphosalicylic acid (SSA) were added from a burette to each test tube and mixed
by swirling
 Then each of the tubes was examined for turbidity against a dark background
Reducing sugars (Benedict’s test)
 0.2 ml of urine sample was mixed with 2 ml of Benedict’s qualitative reagent in a test tube.
 The tube was heated in a boiling water bath for 5 minutes.

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  The tubes was then removed, cooled on the bench; and the colour of the solutions was
observed and recorded.
 The procedure was repeated for the remaining urine samples.
Ketone bodies (Rothera’s test)
 A small sample of dry Nitroprusside reagent (Rothera’s powder) was put in a dry test tube,
enough to cover the bottom.
 1 ml of urine sample was then added to each test tube, the color observed and recorded.
Bilirubin (Foucher’s test)
 5ml of urine was added into a test tube, and 2ml of 0.5 mol/L barium chloride were added
and mixed.
 The mixture was filtered into another tube using a filter paper.
 The filter paper was unfolded and dried by placing it on another dry paper.
 A drop of Foucher’s reagent was added to the precipitate and the color change observed and
recorded.
 The procedure was repeated for the other urine samples.

Urobilinogen (Ehrlich’s test)

 5ml of fresh urine was put into a test tube
 0.5ml of Ehrlich’s reagent was added and mixed
 The color against a white paper background was observed after 5 minutes

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Results:

Sample Test Observation Deduction

D Colourless Polyuria
S Colour Pale Polyuria
N Yellow Normal
D Clear Normal
S Transparency Cloudy Mucus and Cells
N Clear Normal
D Sweet fruity Ketone bodies
S Smell Odourless
N Aromatic Normal
D Small amount of white foam Normal
S Foam Stable white foam Protein
N Small amount of white foam Normal
D 1.019 Normal

Specific gravity Nephritis, Diabetes inspidus etc.

S 1.010
N 1.018 Normal
D 5.5 Normal, mixed diet
S pH 5.6 Normal, mixed diet
N 5.8 Normal, mixed diet
D Urine remains clear No protein
S Protein Definite turbidity Proteins present; Positive+
N Urine remains clear No protein
D Brown ppt Reducing sugars present; ++
S Reducing sugars Solution remains blue No reducing sugars
N Solution remains blue No reducing sugars
D Pale purple solution Ketone bodies present
S Ketone bodies Pale yellow solution Ketone bodies absent
N Orange solution Ketone bodies absent
D No colour change No bilirubin
S Bilirubin No colour change No bilirubin
N No colour change No bilirubin
D No pink colour No urobilinogen
S Urobilinogen No pink colour No urobilinogen
N Pink to light red solution Urobilinogen present

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DISCUSSION
During the practical, it was discovered that a sweet fruity smell in urine always indicates the presence
of ketone bodies in that urine as in sample D which had a sweety fruity smell and tested strongly positive
to the presence of ketone bodies. Diabetic ketones always produce a sweet or fruity odor in urine. (Susan
King Strasinger & Marjorie Schaub Di Lorenzo, 2008)
It was also observed that formation of much white foam on shaking which is stable usually occurs in
cases of proteinuria. This was based on sample S which formed much white foam on shaking which
foam was stable and later was positive for the presence of much proteins. A large amount of white foam
indicates an increased concentration of protein (Susan King Strasinger & Marjorie Schaub Di Lorenzo,
2008).
It was further observed that normal urine always has small quantities of urobilinogen. This was based
on the fact that sample N taken to be our normal contained little trace of urobilinogen. This is also
consistent with both (Monica Cheesbrough 2009), and (Suzan King, 2008).

CONCLUSION
It was established from the practical analysis that specimen N was normal. Specimen S had proteinuria
and indication of renal disease and specimen D had glycosuria and Ketonuria.
The Urinalysis is key in the diagnosis and monitoring of illness, however it should be noted that some
findings from a urinalysis need the support of other diagnostic procedures like physical examination by
a physician, the complaints (signs and symptoms of the patients), radiological and other laboratory test
(Complete blood count, glucose tests among others).

REFERENCES
 Arthur Guyton & John Hall (2006). Text book of medical physiology, 11th edition, Philadelphia
(USA), Published by Elsevier Sauders, pages 347, 404-413
 Monica Cheesbrough (2009). District Laboratory Practice in Tropical Countries, 2ndedition,
Published by Cambridge University Press-New York, pages 369- 378
 Pakanja Naik (2012). Essentials of Biochemistry. 1st edition. Jaypee Brothers Medical
Publishers, New Delhi-India, Page 182.
 Rabinovitch Albert (2001). Urinalysis and collection, transportation, and preservation of urine
specimens: approved guideline. 2nd ed. Wayne, Pa.: National Committee for Clinical
Laboratory Standards, NCCLS document GP16-A2
 Susan King Strasinger & Marjorie Schaub Di Lorenzo (2008). Urinalysis and Body fluids, 5th
edition. F. A DAVIS COMPANY, Philadelphia. Pages 42-74

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