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Red blood cell
Haemoglobin (Hb)
Haem Globin (protein)
Iron (reused Biliverdin
Amino acids
or stored (green)
as ferritin)
Bilirubin
(yellow)
Albumin
(blood protein)
Albumin-bound
bilirubin
X and Y carrier proteins
for entry to liver
Liver
Enzyme Glucuronic acid in liver
glucuronyl transferase derived from glucose
Bilirubin
diglucuronide
Bile duct
Duodenum
BloodKidneys
Urine
Stools
Bowel bacteria
release bilirubin
(as urobilinogen) (as stercobilinogen)
172 Elimination (I)
down. Haematuria from surgery or trauma often appears as bright red urine (frank blood)
at rst, diminishing in intensity over several days until the urine appears normal and
blood can only be detected by testing. An uncomplicated recovery aided by a good uid
input during the post-operative period results in a blood-free urinalysis.
Bilirubin in the urine
Bilirubin and urobilinogen are products of haemoglobin breakdown when it is released
from old destroyed red blood cells (Figure 8.13).
Figure 8.13 T he natural history of bilirubin. Red cell breakdown causes the release of haemoglobin,
which breaks down into a haem group and the protein globin. Globin can be further
reduced to amino acids; the haem group, which contains iron, releases the iron which
can be stored or reused. The remainder is biliverdin, which is green, and this is con-
verted to yellow bilirubin. Albumin, a blood protein, binds bilirubin, and other proteins
called X and Y help to transport the bilirubin to the liver. Here, the enzyme glucuronyl
transferase causes the bilirubin to combine with the glucuronic acid to form bilirubin
diglucuronide, which becomes one component of bile. Bile arrives in the duodenum,
where further conversion of bilirubin creates stercobilinogen, a component of stools.
Some bilirubin is reabsorbed into the blood and ltered in the urine as urobilinogen.
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Elimination (I) 173
Erythrocytes (red blood cells) degrade and release haemoglobin after about 120 days
in circulation. The metabolism of the haemoglobin is shown in Figure 8.13. Normal uro-
bilinogen levels in urine are small (0.09–4.23 µmol per 24 hours), but levels will increase
in jaundice. This condition occurs if the liver is no longer able to accept or handle biliru-
bin adequately (i.e. hepatic jaundice as in liver failure, cirrhosis or hepatitis) or if the bile
drainage is obstructed (i.e. post-hepatic jaundice, caused by an impacted biliary stone
or pancreatic cancer). Pre-hepatic jaundice can also occur when the breakdown of red
cells, or haemolysis, is happening too quickly, as in haemolytic anaemia, and bilirubin
is produced faster than the liver can accept. In any of these conditions, the surplus is
removed by the kidney and lost in the urine but not before the excess bilirubin colours
yellow the skin and sclera (the white of the eyes). Bilirubin, being not normally found in
urine, will appear to make urine very dark (Plate 1) along with the raised urobilinogen.
Acid-base measurement of urine (pH)
pH
5
is a scale of acidity or alkalinity (or base)
6
of a substance. The pH scale (Figure 8.14)
is a measure of the hydrogen ion (H
+
) concentration (sometimes written [pH] as square
brackets mean ‘concentration’).
Strong concentrations give an acid solution (low pH 1–6, pH 1 being the strongest
acid) and a weak concentration gives an alkaline solution (high pH 8–14, pH 14 being
the strongest alkaline). pH 7 is neutral and is the value found in most water samples
tested, especially distilled water. In urine, the hydrogen ion concentration normally
varies from pH 5 to pH 8 according to the diet and tissue metabolism, but usually
stabilises around pH 6 (Plate 3). Hydrogen ions are the end waste product of energy
(ATP) production by the cells, from glucose or fatty acids (see Chapter 1) and also from
ketone production (see page 168) and from acids taken in the diet. Because hydrogen
ions cause acidity they are potentially hazardous. They have to be transported in the
blood to the kidneys and need to be excreted. Blood pH is critical at pH 7.35–7.45
(see Chapter 4), and it must be stabilised within this range. Hydrogen ions entering
the blood must be buffered then removed by the kidneys for excretion. Buffers are a
means of ‘tying up’ hydrogen ions into compounds so that they are unable to contribute
to the hydrogen ion concentration. This allows them to be carried safely in the blood
without affecting the blood pH. Examples are bicarbonate, proteins, haemoglobin and
pH Scale
0 1 2 3 4 5 6 7 8 9 10 11 12 13 14
STRONGEST
Increasing NEUTRAL Increasing
STRONGEST
ACID
acidity pH 7 alkalinity
ALKALI
(BASE)
Figure 8.14 The pH scale. The lower part of the scale (shown here on the left) is acidic, with the
lowest numbers being the strongest acid (pH 1). The higher part of the scale (shown
on the right) is alkaline, with the highest numbers being the strongest alkaline (pH 14).
Neutral is pH 7 on the scale (centre).
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174 Elimination (I)
phosphate buffers. Of these, haemoglobin (Hb) is very important for buffering hydrogen
ions in the blood (Hb + H
+
→ HHb), followed by blood proteins, which have a nitrog-
enous component (NH
2
) which is able to take up surplus H
+
(NH
2
+ H
+
→ NH
3
+
). Bicar-
bonates (HCO
3
−
) are ltered from the blood in the glomerulus and serve to buffer urine
in the proximal tubule (HCO
−
+ H
+
→ H CO → H O + CO ), where CO is absorbed
3 2 3 2 2 2
back into the tubular cells and then into the blood. It is nally excreted from the blood
via the lungs. The water (H
2
O) remains in the ltrate and is excreted in the urine. Phos-
phates (HPO
4
2−
) are major buffers in the renal ltrate of the distal tubular cells (HPO
4
2−
+
H
+
+ Na
+
→ NaH
2
PO
4
). Phosphates prevent urine from becoming too acidic or alka-
line, which would otherwise damage the tract lining and cause great discomfort, espe-
cially when passing urine (micturition). Increased urinary pH (above pH 8, i.e. alkaline
urine) occurs in alkalosis (high blood pH, as may occur in a vegetarian diet). It occurs
naturally soon after a meal. Low urinary pH (below pH 5, i.e. acidic urine) appears in
acidosis, i.e. low blood pH as in diabetic ketoacidosis or aspirin overdose or after the
consumption of prunes or cranberries or as a result of starvation. Disturbance of blood
pH (and thus urinary pH) can happen in various therapies that inuence the uid bal-
ance of the body (see Chapter 6). Since H
+
and K
+
share the same excretory mechanism
in the distal tubule and collecting duct cells, the excretion of large quantities of K
+
(as
may be the case with excessive intravenous potassium chloride [KC1] treatment or diu-
retic therapy) may cause retention of H
+
.
Nitrites in urine
Nitrites can be tested for as an indicator of the presence of a urinary tract infec-
tion (UTI). Nitrites are the result of the breakdown of nitrates in the urinary system.
Nitrates
7
are a component of our diet and are excreted normally in the urine. The
presence of nitrites, however, indicates that there is a bacterial infection by a type of
organism that is capable of producing an enzyme, nitrate reductase, necessary for
converting nitrate to nitrite. Ninety per cent of UTIs are caused by organisms of this
type (e.g. gram-negative bacteria such as Escherichia coli), and therefore the nitrite
test stick is of increasing clinical importance as a quick, accurate means of detecting
UTIs. The remaining 10% of urinary infections include staphylococci, Pseudomonas
species and enterococci. These are organisms that do not produce the enzyme, and
therefore the test is not sensitive to them. Chemical stick reagent tests can often
replace the more expensive laboratory tests and give quicker results. The problems
have centred around the accuracy of the chemical test strip. If they are used routinely
for the identication of UTIs before laboratory cultures are taken, the risk is that they
may miss some clinically signicant infections. Stick analysis of urine for infection
is now accurate enough to be used to identify only those urines that need laboratory
culture and analysis (Doley and Nelligan 2003).
Leucocytes in urine
Leucocytes (white blood cells; see Chapter 4) of the granulocyte type (especially neutro-
phils) produce another enzyme, leucocyte esterase, that can be detected in urine. This
test will identify the presence of intact and lysed (broken down) granulocytes in the urine
either with or without infection. The presence of leucocytes indicates an inammation,
either with organisms (infection) or without (sterile).
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Elimination (I) 175
Other urine tests
Midstream urine (MSU) is the procedure for collecting a clinically clean sample of urine
for laboratory culture. Ideally, the sample collected is as clean as possible. However, even
though urine is produced sterile, it does pick up contaminants (mostly bacterial organ-
isms) from the urethra. Therefore, at the start of urination, the rst ush of urine will gather
most of these contaminants and wash these out of the urethra. This rst part of the urine
stream is then discarded. A sterile container is then used to collect the next stream of
urine (the midstream sample), which will now ow down a cleaner urethra and therefore
will have far fewer contaminants. Any remaining urine in the bladder after that can then
be discarded as usual. This midstream specimen is then sent to the laboratory, and any
organisms grown from it are most likely to be from a urinary infection requiring treatment
and not just a urethral contaminant (Gilbert 2006).
Creatinine clearance is a test to assess the amount of creatinine that is lost through the
kidneys. The test requires urine collected over a 24-hour period. The result is compared
with the creatinine present in the blood (see Test: Creatinine, Chapter 4). In Chapter 4, cre-
atinine was described as a breakdown product of creatine, a molecule in muscle essential
for energy recycling. The amount of creatine present is dependent on the person’s size, age,
sex and muscle bulk. Measuring creatinine clearance not only estimates creatinine levels
(an indication of the rate of muscle cell breakdown and renewal; see muscle wasting, page
148), but it also is a measure of renal function. This is because creatinine removal from the
blood depends on the glomerular ltration rate (GFR; the average adult GFR is about 120 ml
per minute; see page 159). A poor GFR gives a low creatinine clearance value.
Renal (or urinary) stones (called calculi) that form in the urinary tract, anywhere from
the renal pelvis down to the bladder. They have several different compositions and there-
fore different causes (Table 8.4).
Renal calculi can cause extreme pain when passing down the urinary tract, especially
down the narrow ureters and urethra. Stones passing down the ureters often cause very
severe pain in the loins known as renal colic. They may also cause trauma to the lining of
the tract, which then bleeds creating a haematuria. They may obstruct urine ow, and this
can dam back to the kidney, causing a hydronephrosis, i.e. excessive urine accumulation
within the kidney, with resulting loss of renal function.
Pregnancy tests can detect the presence of human chorionic gonadotropin (hCG) in
urine. Human chorionic gonadotropin is produced by the developing placenta, which
Table 8.4 Types of renal stones
Type of renal stone Notes (percentages are approximate)
Calcium oxalate (CAOX) The most common of the stones (67%). Dietary oxalate is found in
many fruits and vegetables.
Calcium phosphate 8% of stones. They form in alkaline (pH higher than 7) urine.
Uric acid 8% of stones. Made from uric acid, they form in acidic urine (pH
below 6). They occur with diets rich in proteins and purines.
Cystine 2% of stones. Caused by a rare genetic disorder (cystinuria) that
allows the amino acid cystine to leak into urine and form crystals.
Struvite 15% of stones. Made from magnesium ammonium phosphate.
Caused by renal tract infections. Often large stones, sometimes
called ‘staghorn calculi’. More common in women.
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176 Elimination (I)
can only happen after implantation of the fertilised ovum into the uterine lining (i.e. after
10 days following fertilisation). Before this, the fertilised ovum is still in the fallopian tube
and the test is liable to create a false negative result.
When to test urine
Urinalysis has become a standard routine test carried out on admission to hospital and
in the doctor’s surgery. The tests are quick, cheap and non-invasive, with instant results,
and they can provide a wealth of information by virtue of there being multiple tests on
one stick. For reagent strip analysis, all that is required is a very small quantity of fresh
urine, one stick and a few minutes of time. If the results are recorded as nothing abnor-
mal detected (NAD), then it is known that the renal system appears to be functioning
normally, the chance of trauma is less and there is probably no diabetes, ketoacidosis,
bleeding or jaundice. For these reasons, methods for putting other urine tests on a rea-
gent strip are being considered. The nitrite and leucocyte tests are two of the results of
these initiatives. Laboratory analysis will still be necessary to identify the organism and
the antibiotic required for treatment. By making it possible to do a test in the clinical
area, the test itself becomes far less labour-intensive, more cost-effective and reduces
the time factor to minutes, an important point for patient comfort and recovery.
Ascorbic acid (vitamin C) has become a common food supplement that is excreted in
the urine and can interfere with urine tests results. Ascorbic acid test pads are now added
to some urine test sticks to test for vitamin C levels in urine. High levels of ascorbic acid in
the urine can cause false negative results for several of the other tests, notably the glucose,
blood, nitrite and bilirubin test pads. By testing for ascorbic acid in the urine at the same
time as the other tests, it becomes possible to say if the other tests results are reliable,
provided the ascorbic acid level remains below 20mg/dL.
As a standard screening device, reagent strip urinalysis can be carried out as routine
almost anywhere, e.g. test strip urinalysis done in the accident department can quickly
rule out injury to the kidneys (Worrall 2009). In the community, it can be used in the doc-
tor’s surgery or in the patient’s own home.
New and potential urine tests which would require laboratory tests include identifying
disorders not directly affecting the urinary system:
• Testing for a distinctive metabolite pattern in urine produced by the bacteria staphy-
lococcus pneumonia. This is an important organism for causing community-acquired
pneumonia (CAP), a serious lung disease. Early detection of this organism can result in
rapid treatment and the saving of many lives (Watt et al. 2010).
• The possibility of testing for the protein biomarker called leucine-rich alpha-2-glyco-
protein (LRG), which, if present, indicates the presence of appendicitis in young chil-
dren’s urine (Kentsis et al. 2010).
• The levels of 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanol (NNAL) can be measured
in urine. NNAL is a metabolite of 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone
(NNK), a component of tobacco smoke. Both NNK and NNAL are potent pulmonary
carcinogens and the presence of raised NNAL in urine can suggest a higher risk of lung
cancer (Hecht et al. 2001).
• A ‘PCA3 assay’ test identies genetic evidence of prostate cancer in urine. The test
identies a small piece of ribonucleic acid (RNA) from an overactive gene that is 95%
specic to prostate cancer. Therefore, it can signicantly reduce the need for pain-
ful prostatic biopsies. However, more recently, questions have arisen concerning the
accuracy of this test, but combining it with tests looking for two other genes that are
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Elimination (I) 177
linked to high-risk cancer increases the reliability. These two genes (TMPRSS2 with
ERG) are abnormally fused in prostate cancer (called ‘TMPRSS2:ERG fusion’). If this
fusion is found in the urine, it is highly specic for prostate cancer. In another devel-
opment, a urine test called ‘urine exosome gene expression assay’ also improves the
reliability of the PCA3 test by combining it with tests for ERG and another gene called
SPDEF. This test requires a ‘rst-catch’ urine sample, i.e. the rst ush of urine to leave
the urethra.
• Motor neuron disease (MND) is a neurodegenerative disorder affecting several motor
systems (see Chapter 14), causing progressive limb weakness and leading to paralysis,
muscle wasting, gradual loss of speech and swallowing. Sufferers may live for two to
ve years depending on the different types of the disease (see Chapter 14, page 302),
and there is no known cure. There is a conrmed genetic basis to some forms of the
disease (see page 301) and relatives of the sufferer may carry the gene involved. A new
urine test has been developed to identify the presence of a protein in the urine of suf-
ferers with one type of MND called amyotrophic lateral sclerosis (ALS; see page 302).
The protein is called ‘p75NTRECD’, often abbreviated to ‘75ECD’ or even ‘p7’. Protein
is not normally found in urine, so any protein found there suggests an abnormality is
present. 75ECD is not only present in the urine of MND sufferers, but it increases as
the disease get worse, making it a useful measure of the disorder’s progress. It can also
be used to screen other members of the sufferer’s family to see if they are at risk before
symptoms begin. If the protein was found, early administration of an anti-glutamate
medication may help to protect neurons and slow the onset of symptoms (Shepheard
et al. 2017).
Drugs active on the urinary system
Diuretic drugs are those that induce a diuresis (a large urine output) for medical purposes,
i.e. to treat oedema, hypertension or cardiac failure that is causing oedema (see Chapter
6). Several groups of drugs achieve a large urine output, and the patient should be warned
that he/she will be passing a lot of urine. Where relevant, diuretics could make inconti-
nence of urine worse.
• The thiazides (e.g. Bendroumethiazide, Chapter 3, Table 3.8) prevent the reab-
sorption of sodium from the distal parts of the tubule. The sodium remains in the
ltrate and is lost in the urine. Water follows sodium, so a sodium loss creates a
diuresis.
• Loop diuretics (e.g. furosemide [frusemide]) and bumetanide, Table 8.5) work
by preventing reabsorption of sodium at the loop of Henle. They are the most
potent diuretics, producing the largest urine output but with the greatest potential
for causing unwanted reactions. They may promote the loss of potassium as well,
and this can be a complication. The potassium-sparing diuretics (e.g. amiloride
and spironolactone) conserve potassium while causing mild diuresis as a result of
sodium loss.
• Some drugs (e.g. spironolactone; Table 8.6) are aldosterone antagonists, i.e. they
reduce the activity of aldosterone and this promotes further sodium and water loss.
They are referred to as potassium-sparing diuretics because they signicantly reduce
the loss of potassium in the urine, a problem that may occur with other diuretics.
They can be used to reduce the circulatory volume and therefore reduce the work
load on the heart and to relieve oedema in specic sites (e.g. ascites = oedema of the
abdomen).
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178 Elimination (I)
Table 8.5 Loop diuretic drugs
Drug Possible side effects Use and other notes
Bumetanide
Co-amilofruse
Furosemide (Frusemide)
Torasemide
Dehydration, skin rash,
hypotension.
Acute urinary retention, nausea,
headache, bowel disturbance.
Fever, skin and mucosal
reactions, malaise.
Gastric disturbance, asthenia
(loss of energy), urinary
retention.
Oedema.
Oedema.
Oedema and hypertension.
With or without triamterene
(
Table8.5).
Oedema and hypertension.
Table 8.6 Aldosterone antagonists
Drug Possible side effects Use and other notes
Co-umactone Gut disturbance, tiredness,
confusion, headache.
Eplerenone Arrhythmias, cough, nausea,
diarrhoea, dizziness, insomnia.
Spironolactone Hair loss, confusion, cramp, skin
reaction, dizziness, malaise.
Congestive heart failure. A
combination of hydroumethiazide
and spironolactone.
Specic situations related to heart
failure.
Oedema, heart failure, ascites,
hypertension. With or without
furosemide.
Key points
• The functional unit of the kidney is the nephron. About 1 million nephrons exist in
each of the two kidneys.
• Urine forms in three steps: ltration from the glomerulus, reabsorption from the convo-
luted tubules and secretion from the straight collecting ducts.
• Urine is formed at an average rate of 1 ml per minute.
• For accurate results, urine must be tested when fresh using the correct technique.
• Normal urine is a pale straw colour, clear with no deposits.
• On testing, normal urine should show negative results for glucose, blood, protein,
ketones and bilirubin.
• Urinary pH ranges from 5 to 8, with an average about 6.
• The specic gravity measures the density of dissolved solutes in urine compared with
water, normally about 1,010 (water = 1,000).
• Nitrite and leucocyte tests for infection or inammatory cells in urine.
• Diabetes is an important cause of polyuria (causing thirst) and glycosuria (due to
hyperglycaemia).
• Some diseases cause polyuria (diuresis), including diabetes insipidus, diabetes mellitus
(types 1 and 2), maturity onset diabetes of the young (MODY) and latent autoimmune
disease in adults (LADA).
• Diuretic drugs induce a large urine output as a treatment for hypertension, oedema or
cardiac failure.
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Elimination (I) 179
Notes
1 Proposed additional types of diabetes mellitus (e.g. type 3, type 4 etc.) are not ofcially recog-
nised as they lack an internationally accepted solid research base conrming their existence.
Some are linked to autoimmune conditions and others to insulin receptor resistance.
2 Sweet refers to the old days when the only way to test for sugar in the urine was to taste it. Fortu-
nately, this practice has stopped thanks to the introduction of chemical reagent tests.
3 Beta (β) cells, along with alpha (α) and delta (δ) cells, form the islets of Langerhans in the pan-
creas. Beta cells produce insulin.
4 Penetrance is the degree (or amount) the gene product affects the body. With low penetrance the
gene has little effect, but in high penetrance the gene has a big effect on the body.
5 This must always be small p and capital H, not any other combination, as explained in Chapter
4, note 5.
6 Base is any substance that reacts with acids and neutralises them, and an alkali is a base dis-
solved in solution.
7 Don’t get nitrates muddled with nitrites.
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Plate 1 Different colours of urine and sedimentation. Far left: chalky sedimentation, which may
indicate the excretion of too much calcium. Left of centre: concentrated urine, as may be
passed on a hot day or because of reduced uid intake. Centre: dilute urine, as may be
passed when uid intake is high. Right of centre: blood in the urine (frank haematuria). Far
right: dark urine seen in jaundice, when the urine is rich in bilirubin.
Plate 2 Different densities of urine and specic gravity. Left: dense (darker) urine, which indicates less
water is lost through the kidneys, as occurs when dehydrated. Right: dilute urine, as may be
passed when uid intake is high. Note the hydrometer (urinometer) oats lower on the right
than on the left, and deeper urine on the right is needed to stop the hydrometer from touching
the bottom. The hydrometer is a measure of the density observed. Left: the dense urine meas-
ures between 30 and 40 on the hydrometer scale (where the urine level crosses the scale).
Right: the dilute urine measures close to 0 on the scale. Zero on this scale (or 1,000 on other
scales) is the specic gravity of pure water, so the urine on the right is not much denser than
pure water. Note that the hydrometer appears ‘broken’ in the left sample due to the different
refraction (bending) of light seen through dense urine.
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on the strips after immersion in urine. The tests are, from top to bottom, pH (measuring the
acidity or alkalinity of urine), protein, glucose, ketones, urobilinogen, bilirubin, blood and
haemoglobin. (A) A stick essentially normal with pH approximately 7 (neutral). (B) A stick
with pH 5 (acidic). (C) Protein is present. (D) Large amounts of glucose. (E) Positive for
ketones. (F) Positive for blood.
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