July 2022 Clinical Chemistry 1

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Clinical chemistry 1:
what comes from where
Clinical chemistry, or biochemistry, is the cornerstone
of any laboratory. It is the most common automated
laboratory modality utilised by veterinary nurses,
usually on a daily basis. But what do the numbers
mean? And where in the body do the measurands
come from? The aim of this two­part series is to give
you a whistle­stop tour of the common measurands
found on the feline biochemical profile. Matthew Garland
BSc RSciTech SAC DIP Cert Nat Sci Vn MRSB
Matthew Garland is a veterinary nurse and
A s with any laboratory-based
methodology, the results you achieve
are only as good as the sample you use. In
registered science technician with a degree
in chemistry and molecular biology, and over
essence, if the sample is compromised for any 20 years’ experience in the veterinary field.
reason (most commonly haemolysed samples He is currently a deputy director and
with feline patients but also consider lipaemic veterinary laboratory manager, and teaches
and icteric samples), then the results will also student veterinary nurses key laboratory
be compromised. Always make a note of the skills. Matthew has contributed to several
sample quality when processing samples as it published research projects, has had several
is directly reflected in the interpretation. The articles on veterinary haematology and
full range of the artefactual changes are clinical biochemistry published and delivers
beyond the scope of this article, but regular CPD. Being passionate about team
references to the most important changes as development and the development of others,
we move through the body systems and Matthew sits on the registers assessors
analytical groups will be made. board of the Royal Society of Biology (RSB)
and is also a judge for the RSB Apprentice
of the Year award.

This article is the first in a two-


part series. The second part will
discuss the common measurands
connected with hepatic and
metabolic laboratory testing and
their use for our feline patients.

Routine biochemistry can be


processed on serum gel, plain serum
(clot activator tubes) or lithium
heparin tubes, with most ‘in-house’
instruments using the latter sample1,2
(Figure 1). Ideally, patients should be
Figure 1: Example of an in-house instrument

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starved before sampling, but water
should always be offered. Serum
samples should be spun down after
30 mins of standing or once the clot
has formed. If you are using lithium
heparin tubes these can be spun
once adequate mixing is achieved.
Once separated, the serum/plasma
should be kept in the fridge if not
being processed in the next hour or
frozen if prolonged storage is
required.1

Interpretation is very much the


remit of the clinical pathologist
Figure 2: Example feline biochemistry profile report
or veterinary surgeon in charge of
the case, but having a sound of the artefactual changes due to
knowledge of how to interpret will poor sample handing (see above)
allow nurses to aid the veterinary or poor analytical technique.
surgeons as well as spot any
erroneous results (Figure 2). Listed Common biochemical measurands
below are some basic considerations can be grouped in to four categories
when interpreting biochemical (Table 1), which aids us in
results: interpretation; however, measurands
• Interpret results in conjunction can cross categories depending on
with the clinical signs. If the certain conditions so it is patterns
results do not fit the case then that we use to determine a
reassess the blood work. diagnosis. It is important to look at
• Interpret the measurands in the whole clinical picture and utilise
conjunction with those from multiple diagnostic techniques while
the same organ or group. formulating a diagnosis.3
• Develop an understanding of the
magnitude of change expected in Renal
the results for the condition you Without doubt, the most assessed
are testing for. parameters for older feline patients
• Develop a keen understanding are those for renal function. The

Table 1: Common groupings of clinical biochemistry measurands


Renal Hepatic Metabolic Other common
measurands

Urea Alanine aminotransferase Proteins (total Lipase


Creatinine (ALT) protein and albumin) Creatine kinase (CK)

Inorganic Alkaline phosphatase Calcium Amylase


phosphate (ALP, ALKP) Glucose
Gamma Cholesterol
glutamyltransferase (GGT)
Sodium
Bilirubin
Potassium
Bile acids
Chloride

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Table 2: Common conditions that lead to azotaemia

Prerenal Renal Postrenal


Hypovolaemia Lymphoma and other Urinary tract obstruction
Dehydration cancerous lesions (after the nephron)

Shock Trauma
Toxicity

Table 3: Other causes of urea and creatinine abnormalities

Urea Creatinine Both


Gastrointestinal bleeding Muscle wastage Dehydration
Liver failure Shock
Heart disease

‘gold standard’ method to assess and creatinine can become elevated


renal function is to directly measure for other non-renal-related
glomerular filtration rate (GFR) but conditions (Table 3).
this is rarely utilised in veterinary
medicine.2,3 Instead, we utilise a Inorganic phosphate
simpler, less accurate indirect Phosphorus has multiple functions
method by monitoring urea and within the body, being responsible
creatinine. Abnormalities in urea and for structure in the phospholipids
creatinine are only observed after an and phosphoproteins.2,3 It is also
estimated 75% of the renal nephrons utilised in cell signalling, metabolism
are damaged.1 Damage can be and nucleic acid formation.
caused for a variety of reasons, Phosphate is usually absorbed
including inflammation, old age,
trauma, etc. Elevations in both
measurands are termed azotaemia
and can be classified as pre-renal,
renal and post renal (Table 2).1–3

Urea and creatinine


The most important function of the
urinary system is to excrete urea and
creatinine.1,2 These are both waste
products generated by the
metabolism of nitrogenous products.
Urea is the main metabolite from the
metabolism of dietary protein
formed in the liver from ammonium
and bicarbonate.2,3 Creatinine is
derived from the catabolism of
muscle creatine and creatine
phosphate.1,2 Both waste products
are filtered by the kidneys and, as
such, can be used as an indication of Figure 3: An older feline patient with chronic
kidney function. However, both urea kidney disease

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Table 4: Common reasons for hyperphosphataemia when, in fact,
hypophosphataemia and hyperphosphataemia the level is normal for their age.
Hypophosphataemia Hyperphosphataemia This is largely due to bone growth.2,3

Hyperglycaemia Kidney dysfunction Assessing renal function should


always be completed with a full
Insulin therapy High phosphate diet urine analysis with a bare minimum
of a urine specific gravity. Renal
Hypercalcaemia Tissue damage insufficiency can cause other blood
panel abnormalities such as
Osteolytic lesion
electrolyte disturbances and
elevations in lipase.
into the bloodstream from the
gastrointestinal (GI) tract and is Other common measurands
usually stored in bones and teeth, The brand of your point of care
with excess being excreted through analysers will dictate which tests
the kidneys. Hyperphosphataemia are commonly available to you in
usually occurs when GI absorption practice. Listed below are two
or cellular release exceeds excretion commonly asked about measurands
and/or tissue requirements.1,2 and their relevance to feline patients.
Chronic kidney disease is a common
reason for the presence of a Serum amylase and lipase
hyperphosphataemia on a feline A commonly asked question
profile, though there are other is regarding the diagnosis of
possible causes (Figure 3). pancreatitis in feline patients and
Hypophosphatemia is also observed the use of serum amylase and lipase.
in feline patients though is unlikely Serum amylase and lipase activity
to be related to renal problems are measured by a variety of
(Table 4). methods, and all detect amylase
from a variety of tissue sources
Hyperphosphatemia can also other than the pancreas. Indeed,
be caused by incorrect sample elevated amylase and lipase are
handling. As mentioned previously, not specific for pancreatic injury
a haemolysed sample will cause and in some cases and species they
elevations in phosphate as well as a can be related to renal disease.1,2
sample that has not been separated
from the red blood cells in the Amylase and lipase are not
correct time. If adult reference considered specific for pancreatitis
ranges are used in young animals, in cats as cats with spontaneous
then there will be a perceived pancreatitis have normal to slightly

Table 5: Common causes of creatine kinase elevations


Skeletal muscle Cardiac muscle Smooth muscle
Road traffic accident Endocarditis Endometritis
Seizures Thrombus
Inflammation
Parasitic disease
Intramuscular injections
Anorexia

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elevated amylase levels. It has also
been observed that cats with
pancreatitis have low levels of
serum amylase.

Both serum amylase and lipase are


much more sensitive and specific in
canine patients and can be utilised
with a great deal of success. If
pancreatitis is a concern in a feline
patient, then the feline pancreatic
lipase immunoreactivity (fPLI) test
should be considered along with
diagnostic imaging.1,2,3

Creatine kinase (CK)


Creatine kinase (CK) is an enzyme
found in high concentrations in
theskeletal, cardiac and smooth
muscles. CK is a component
(isoenzyme) of the cytoplasm of
muscle cells and is released when
these cells are damaged. CK is
considered specific for muscle
damage, and activity can peak
6-12 h post-trauma but will also
decrease rapidly due to a short half-
life (studies suggest 2 h).2,3

Please see Table 5 for a list of the


common causes of CK elevations.

Erroneous CK can also be caused by


poor sample handling. Haemolysed
samples can cause artificially
elevated results, so great care must
be taken when interpreting these
results.1

References
1 Stockham SL, Scott MA. Fundamentals of
veterinary clinical pathology. 2nd ed. Hoboken,
NJ: Wiley-Blackwell.
2 Villers E and Ristic J. BSAVA manual of canine
and feline clinical pathology. 3rd ed. Gloucester:
BSAVA, 2016.
3 Latimer KS. Duncan and Prasse’s veterinary
laboratory medicine. 5th ed. Hoboken, NJ:
Wiley-Blackwell, 2011.

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