Small Animals
 

Reference Ranges

Canine

0-<30 IU/L/l

Feline

10-25 IU/L/l

ALT is almost liver specific in dogs and cats. It is found in the cytoplasm of hepatocytes and is released into the blood during changes in cell membrane permeability or necrosis. Its superficial location means that a relatively mild insult ,e.g. hypoxia, may lead to increased serum levels. Half life is about 60 hours in the dog and shorter in the cat.. In chronic hepatic disease with loss of functional mass levels may be deceptively low. In acute disease a rapid decline in levels may be a favourable sign. Recent work has demonstrated that ALT levels may also increase due to increased synthesis and release by healthy hepatocytes.

ELEVATED LEVELS

ALT is of no value in the horse due to its low liver activity.

COMPLIEMENTARY TESTS

Plasma ALT activity is usually determined in conjunction with other tests of hepatocellular damage or hepatic function specifically AP, AST, GGT, GLDH and Bile Acids.
Top

Small Animals
 

Reference Ranges

Canine

300-2000 IU/L/l

Feline

0-1500 IU/L/l

Only alpha amylase is found in animals. Pancreas, liver and small intestine are the main sources of serum amylase. In the healthy dogs and cats most amylase is derived from the small intestine.

ELEVATED LEVELS

COMPLEMENTARY TESTS

When elevated, serum lipase levels should also be determined.
Top

AP isoenzymes are found in a variety of tissues including intestine, liver, bone, placenta, kidney and leukocytes. Unlike ALT, AST and GLDH, increased serum levels of AP are due to increased synthesis of the enzyme.

Small Animals
 
 

Reference rRanges

Canine

0-<100 IU/L/l (adult)

Feline

0-40 IU/L/l

Hepatic AP isoenzyme has a half life of 3 days in the dog and only 5.8 hours in the cat. Increases are usually of greater magnitude in dogs but of greater significance in cats. Other isoenzymes have a half life of only minutes so can effectively be ignored. Steroid induced AP can be determined in dogs but is of questionable value as a diagnostic aid. AP levels will remain elevated during hepatic repair and this is not a poor prognostic indicator as AP is released by healthy hepatocytes.

ELEVATED LEVELS

Plasma AP activity is usually determined in conjunction with other tests of hepatocellular damage or hepatic function, specifically ALT, AST, GGT, GLDH and Bile Acids.

Equine
 

Reference Range

Equine

0-145 IU/L/l

In the horse a significant amount of AP intestinal isoenzyme is released from the intestinal mucosa and this can be distinguished from total AP by performing an intestinal AP assay. Elevated AP is a useful indicator of cholestasis.

ELEVATED LEVELS

Plasma AP activity is usually determined in conjunction with other tests of hepaticocellular function and damage or hepatic function, specifically AST, GGT, GLDH and Bile Acids.
Top

AST occurs in the liver, erythrocytes and all types of muscle. It is found in the both the cytoplasm and mitochondria of cells hepatocytes and is released into the blood due to hepatucellular damage and during changes in cell membrane permeability or necrosis. Half life is about 12 hours in the dog, less in cats and 7 to 8 days in horses

Small Animals
 

Reference Ranges

Canine

0-< 30 IU/L

Feline

10 - 30 IU/L/l

ELEVATED LEVELS

Plasma AST activity is usually determined in conjunction with other tests of hepatocellular damage and skeletal muscle damage eg. specifically AP, ALTALT GGT, and GLDH for hepatocellular damage and CK for skeletal muscle damage.

Equine
 

Reference Range :

Equine

0 - 250 IU/L/l

ELEVATED LEVELS.

Plasma AST activity should be assessed along with GLDH and GGT (hepatic disease) and CK (azoturia). Following an episode of azoturia, AST levels peak at 24 - 48 hours and decline slowly over 7 to 10 days returning to baseline levels by 10-21 days. This contrasts with CK which peaks after 6-122 hours and declines rapidly over 2 days returning to baseline levels. by 3-4 days.
Top

Bilirubin is formed from the metabolism of haem groups in the liver, spleen and bone marrow and is taken up and conjugated by hepatocytes before excretion in the bile.

Small Animals
 

Total bilirubin	Canine	0-< 5 m mol umol/L/ll	Feline	0 - 4.0 m umol/L/l
Direct bilirubin	Canine	0-<1.7 um mol/L/l	Feline	0 - 1.5 um mol/L/l

ELEVATED LEVELS

The differentiation of total serum bilirubin into direct acting (conjugated) and indirect acting (unconjugated) bilirubin is routinely performed but is of strictly limited diagnostic value. As a rule of thumb, 90% of bilirubin must be either direct acting or indirect acting before it is of diagnostic value (direct acting indicating biliary tract obstruction and indirect acting indicating haemolysis). A haemogram should be used to rule out haemolysis. Bile acids will be elevated due to loss of hepatocellular mass or biliary obstruction but not due to haemolysis. Marked increases in AP and GGT will be seen with post hepatic cholestasis.

Equine
 

Reference Range
Total bilirubin	Equine	10.0 - 40.0 um mol/L/l
Direct bilirubin	Equine	4.2 - 14.8 um mol/L/l

ELEVATED LEVELS

In contrast to small animals, only modest increases in direct acting bilirubin are seen in either liver failure or in cholestasis. Where direct acting bilirubin forms 25 - 50% of the total bilirubin , this indicates significant cholestasis.
Top

Bile acids are synthesised in the liver from cholesterol and are conjugated with taurine or glycine before excretion as bile salts into the bile. Bacterial action in the intestine deconjugates some to bile acids and converts the rest to secondary bile salts. These products ienter the portal circulation and are extracted and recycled by the hepatocytes. It is those bile acids not extracted which are measured in the peripheral blood.

Small Animals
 

Reference rRanges
Fasted	Canine	<0- 1030 mm mol/L/l	Feline	<0-2 5 mm mol/L
2 hours post feeding	Canine	< 0-350 mm mol/L/l	Feline	< 0-2530 mm mol/L/l

The measurement of fasting bile acid levels is at least as sensitive as either the bromsulphthalein clearance test or the ammonium tolerance test as a measure ofr hepatic function. Pre and post feeding bile acids are measured on a 12 hour fasted sample and a sample taken 2 hours post feeding (canned food). This is more sensitive than a single fasted sample and is recommended where the fasted result is less than 10 x normal (dog) or < 5x normal (cat)..

ELEVATED LEVELS

Tests for cholestasis (AP, GGT and bilirubin) and hepatic function (albumin and urea) are indicated along with tests for hepatocellular damage (ALT, AST and GLDH).

Equine
 

Reference Range :

Equine

< 0-20 mm mol/L/l.

As in the dog and cat, bile acids are conjugated largely with taurine. The rate of enterohepatic circulation is fairly constant so fasting is not required before sampling.

ELEVATED LEVELS

Tests for cholestasis (AP, GGT and bilirubin) and hepatocellular damage (AST and GLDH). Albumin is less useful as an indicator of hepatic insufficiency in the horse than in small animals due to its long half life (hypoalbuminaemia only seen in advanced liver failure).
Top

Calcium is an essential mineral which is involved in many body systems. These include the skeleton, enzyme activation, muscle metabolism, blood coagulation and osmoregulation. In the blood calcium exists as 50% ionisedionized, 40% protein bound and 10% complexed with anions such as citrate and phosphate. Only ionisedionized calcium is biologically active in bone formation, neuromuscular activity, cellular biochemical processes and blood coagulation. Factors governing the total plasma concentration are complex and include interaction with other chemical moieties, proteins and hormones. Calcium, phosphorous and albumin metabolism are interdependent. Serum calcium values must be adjusted to take account of low albumin levels. This calculated value is shown on the report.

Small Animals
 
 

Reference rRanges

Canine

2.3 - 3.0 mmol/L/l

Feline

2.0 - 2.8 mmol/L/l

Homeostatic mechanisms in small animals maintain plasma calcium levels within tight reference ranges. Elevated and low levels are generally significant.
 
 

ELEVATED LEVELS	LOW LEVELS
Hypercalcaemia	Hypocalcaemia
Lymphoproliferative disease(dogs)	Hypoalbuminaemia
Hypoadrenocorticism (dogs)	Malabsorption
Malignant neoplasia	Acute pancreatitis
Primary renal failure (CRF or familial)	Renal secondary hhyperparathyroidism
Primary hyperparathyroidism	Eclampsia
Hypervitaminosis D	Primary hypoparathyroidism
	Post thyroidectomy (cats)
	Nutritional secondary hyperparathyroidismHyperthyroidism (cats)
	Ethylene glycol poisoning Nutritional secondary hyperparathyroidism
	Acute renal failure (especially post renal obstruction)Ethylene glycol poisoning
	Glucocorticoid therapy Acute renal failure (especially post renal obstruction)

COMPLEMENTARY TESTS

PTH assay (primary hyperparathyroidism), serum electrolytes and ACTH stimulation test (hypoadrenocorticism), urea and creatinine (primary renal failure, hypoadrenocorticism, acute tubular necrosis secondary to hypercalcaemia), amylase and lipase (pancreatitis), albumin (hypoalbuminaemia), T4 (hyperthyroidism), phosphorus (primary hyperparathyroidism and malignant neoplasia).

Equine
 

Reference Range :

Equine

2.6 - 3.9 mmol/L/l

Homeostatic mechanisms are efficient in maintaining plasma calcium levels within the reference range. Elevated and low levels are therefore significant.
 
 

ELEVATED LEVELS			LOW LEVELS
Hypercalcaemia		Hypocalcaemia
Chronic renal failure			Lactation tetany
Malignant neoplasia			Transit tetany
Vit D toxicosis			Acute renal failure
Primary hyperparathyroidism			Abdominal crisis
Nutritional secondary			Primary hypoparathyroidism
Hyperparathyroidism			Acute pancreatitis
			Hypoalbuminaemia

COMPLEMENTARY TESTS

Albumin and phosphorous determinations should always be included. Differentiation of diseases causing abnormal calcium levels can be facilitated by the determination of fractional clearance of calcium in blood and urine.
Top

Equine
 

Reference Range :

Equine

89 - 106 mmol/L/l

Chloride is present in highest concentrations in the ECF and tends to accompany sodium movement by passive diffusion.
 

ELEVATED LEVELS	LOW LEVELS
Hyperchloraemia	Hypochloraemia
Dehydration	Gastro-intestinal loss (higher bowel obstruction)
Acidosis	Low salt diet
Respiratory alkalosis	Respiratory acidosis.
Renal dysfunction	Oesophageal obstruction

COMPLEMENTARY TESTS

In equines the calculation of urine clearance ratios will assist interpretation of serum electrolyte and mineral levels.

Cholesterol is produced in the liver and acquired by diet. Plasma cholesterol occurs at high concentration in the esterified form and at much lower concentration in the free form, and tthese are measured together as total cholesterol. Cholesterol is esterified in the liver and is the precursor of steroid hormones. Cholesterol is also utilisedbroken down in the liver to synthesise bile acids. and eliminated via Surplus cholesterol is excreted via the bile. duct.

Small Animals
 

Reference Rranges

Canine

3.8 - 7.9 mmol/L/l

Feline

2.0 - 3.9 mmol/L/l

ELEVATED LEVELS	LOW LEVELS
High fat diet/post prandial	Hepatic failure
Hypothyroidism	Primidone therapy (dogs)
Nephrotic Syndrome	Low fat diet/ malabsorption/ EPI
Cholestatic disorders
Diabetes mellitus
Acute pancreatitis
Hyperadrenocorticism
Glucocorticoid therapy
Idiopathic hyperlipidaemias

COMPLEMENTARY TESTS

Triglyceride levels as both triglycerides and cholesterol combine in lipoproteins. Triglyceride levels determine visible lipaemia.

Equine
 

Reference Range

Equine

2.3 - 3.6 mmol/L/l

ELEVATED LEVELS	LOW LEVELS
Cholestasis	Liver disease
Hypothyroidism	Sepsis
Starvation

Top

Also known as creatine phosphokinase (CPK). CK occurs in high levels in skeletal muscle, cardiac muscle and brain tissue though only skeletal and cardiac muscle are of major significance. The enzyme is essential for the rapid conversion of ADP to ATP to release energy for muscle contraction. Thus if muscle tissue is disrupted the enzyme is released into the blood stream and is readily detected.

Small Animals
 
 

Reference rRanges

Canine

<0 - 300 IU/L/l

Feline

0 - 300 IU/L/l

Experience has shown that levels can rise slightly with muscular exertion alone but where pathological conditions exist the levels are usually very high. Increase associated with cardiomyopathies is are much less than with rhabdomyopathies in small animals. Generally, re-sampling in 2 to 3 days is recommended to exclude trauma as a cause of elevated levels.

ELEVATED LEVELS

Usually determined along with AST to assess possible muscle damage. A TRH stimulation test is indicated if hypothyroidism is suspected.

Equine.
 
 

Reference Range :

Equine

0 -100 IU/L/l

ELEVATED LEVELS

Usually determined along with AST. Following an episode of azoturia, CK peaks after 6 - 12 hours and declines rapidly over 2 days returning to baseline levels by 3 - 4 days. AST peaks after at 24-48 hours and declines slowly over 7 to 10 days returning to baseline levels by 10 -21 days..
Top

Creatinine is produced at a steady rate due to muscle catabolism and is not reabsorbed by the kidney tubules after filtration. Its measurement provides an indirect assessment of the glomerular filtration rate (GFR). The relationship between the GFR and creatinine excretion are is not linear; with creatinine levels of less than 180 nmol/L/l (in the dog) there may be up to three quarters of the nephrons lost, thereafter even small losses may result in substantial increases in creatinine levels. Unlike urea it is not markedly affected by diet or any aspect of liver function and therefore the test is more specific for renal dysfunction.

Small Animals
 
 

Reference rRanges

Canine

0 - <106 um mol/L/l

Feline

40 - 180 um mol/L/l

ELEVATED LEVELS

Urea (azotaemia), phosphorus and urine specific gravity (see Urea).

Equine.
 

Reference Range

Equine

87 - 163 umol/L/l

Urea levels are influenced to a large extent by diet in horses making creatinine a more suitable guide to the GFR.

ELEVATED LEVELS

Urea (azotaemia), phosphorus, urine clearance ratios (renal dysfunction).
Top

Serum fructosamine measures the glycation of serum proteins (principally albumin) and is an accurate measure of the average serum glucose concentration over 1 to 2 weeks (dogs) or 1 to 3 weeks (cats).

Small Animals
 

Reference Ranges

Canine

240 - 350 umol/L

Feline

130 - 280 mmol/L

ELEVATED LEVELS

Plasma glucose
Top

The highest concentration of GGT is found in the renal tubule cells but, as it is excreted in the urine, levels do not rise in response to renal damage. Circulating enzyme is considered to originate from the liver (biliary endothelial cells and hepatocytes).

Small Animals
 

Reference rRanges

Canine

0 - 10 IU/L/l

Feline

<0 - 5 IU/L/l

GGT is considered a specific indicator of hepatobiliary disease in the cat.

ELEVATED LEVELS.

AP (increases in AP largely parallel those in GGT). ALT and GLDH (hepatocellular damage), bile acids (hepatic function) and bilirubin (cholestasis).

Equine
 

Reference Range :

Equine

0 - 41 IU/L/l

As in cats, GGT is considered a specific indicator of both acute and chronic hepatobiliary disease. GGT has a long half life and levels may remain elevated after the pathology resolves.

ELEVATED LEVELS

AST and GLDH (hepatocellular damage), bile acids (hepatic function) and bilirubin (cholestasis) (bilirubin).
Top

Practically liver specific, this enzyme is localised almost exclusively in the mitochondria of hepatocytes. It is generally considered that a severe insult is required to bring about its release and it is therefore not a sensitive general marker for hepatic disease (but see below).

Small Animals.
 

Reference Ranges

Canine

0 -< 9.0 IU/L/l

Feline

0 - 6.0 IU/L/l

GLDH has been demonstrated to be a sensitive marker of hepatocellular necrosis in the dog irrespective of its severity. It is considered to be at least as specific as ALT as a marker of hepatic disease in the dog.

ELEVATED LEVELS

ALT and AST (hepatocellular damage) and bile acids (hepatic function).

Equine
 

Reference Range

0 - 9.0 IU/L/l

GLDH has a relatively short half life in the horse (12 - 14 hours) compared to LDH, AST and GGT. Elevated levels therefore indicate active hepatocellular damage.

ELEVATED LEVELS

AST,LDH and GGT (hepatocellular damage) and bile acids (hepatic function).
Top

Glucose is the source of energy in the body and is regulated by insulin and glucagon. Glucose passes freely through the renal glomeruli and is totally reabsorbed in the renal tubules. As plasma glucose levels rise this mechanism is saturated and the "renal threshold" exceeded, glucose then appears in the urine.

Small Animals
 

Reference Ranges
Canine	3.0 - 5.5 mmol/L/l (fasting)	Feline	4.3 - 6.6 mmol/L/l (fasting)

Renal thresholds for the dog and cat are approximately 10 mmol/L/l and 16 mmol/L/l respectively.
 

ELEVATED LEVELS	LOW LEVELS
Hyperglycaemia	Hypoglycaemia
Diabetes mellitus	Hepatic insufficiency
Stress (cats)	Insulinoma
Steroid therapy	Insulin therapy
Post prandial	Hypoadrenocorticism
Hyperadrenocorticism	Starvation (especially neonates)
Acute pancreatitis	Septicaemia
Megoestrol acetate therapy
Acromegally (especially cats)

COMPLEMENTARY TESTS

Urine glucose. (Glycosuria in the absence of hyperglycaemia indicates a primary renal problem or poisoning),. Fructosamine (diabetes mellitus, stress hyperglycaemia), ACTH stimulation test (hyperadrenocorticism, hypoadrenocorticism), IGF1 (acromegally), amylase and lipase (pancreatitis), insulin (insulinoma), bile acids (hepatic insufficiency).

Equine
 

Reference Range

Equine

3.4 - 5.9 mmol/L/l

ELEVATED LEVELS	LOW LEVELS
Hyperglycaemia	Hypoglycaemia
Post prandial	Insulinoma
Pituitary adenoma	Malabsorption
Post exercise	Scouring
Pancreatic destruction (rare)
Obesity (non- insulin dependant d. mellitus)
Pregnancy

COMPLEMENTARY TESTS

Oral or i/v glucose tolerance test (diabetes mellitus). TRH response test (pituitary adenoma).
Top

Equine
 

Reference Range :

Equine

0-150 IU/L/l

ELEVATED LEVELS

Protein electrophoresis (when hyperglobulinaemia present)
Top

This enzyme is present in large amounts in all organs and tissues (including red blood cells). It is found in the cell cytoplasm and is released into the blood during changes in cell membrane permeability or necrosis. Five isoenzymes are recognised.

Small Animals
 
 

Reference Ranges

Canine

0 -< 150 IU/L/l

Feline

0 - 150 IU/L/l

ELEVATED LEVELS

Increases in LDH activity are not organ specific. Isoenzyme analysis is not performed in small animals.

Equine
 

Reference Range

Equine

76 - 409 IU/L/l

ELEVATED LEVELS

Isoenzyme analysis may be indicated when total LDH activity is elevated in order to localise the affected organ.
Top

Small Animals
 

Reference Ranges

Canine

0 -< 500 IU/L/l

Feline

0 - 250 IU/L/l

ELEVATED LEVELS

Amylase (pancreatitis), urea and creatinine (renal failure), ALT, GLDH (hepatocellular damage).
Top

Serum phosphorus is primarily regulated by the kidney through the action of parathyroid hormone . Abnormal levels are caused by variations in dietary intake, decreased renal excretion and the hormonal imbalances that affect serum calcium.

Small Animals
 

Reference Ranges

Canine

0.9 - 1.6 mmol/L/l

Feline

0.81 - 1.61 mmol/L/l (< 2yr)

ELEVATED LEVELS	LOW LEVELS
Prerenal, renal and post renal azotemia (see Urea)	Malignant neoplasia
Young animals (< 1yr)	Glucocorticoid therapy
Hyperthyroidism (cats)	Primary hyperparathyroidism
Nutritional secondary hyperparathyroidism	Oral phosphate-binding agents
Primary hypoparathyroidism	Osteomalacia
Hypervitaminosis D	Hyperadrenocorticism
Tissue necrosis	Hypovitaminosis D
OsseousOsseus neoplasia	Renal tubular defects

COMPLEMENTARY TESTS

Calcium, urea and creatinine. Urine specific gravity (azotaemia), T4 (hyperthyroidism), PTH (primary hyperparathyroidism).

Equine
 

Reference Range

Equine

0.8 - 1.8 mmol/L/l

Serum phosphate levels fall readily after exercise therefore samples should be taken at rest.
 

ELEVATED LEVELS	LOW LEVELS
Post prandial	Primary hyperparathyroidism
Hypoparathyroidism	Scouring
Vit D excess	Vit D deficiency
Nutritional secondary hyperparathyroidism	Chronic renal failure

COMPLEMENTARY TESTS

Urea and creatinine (renal failure). Urine clearance ratios (renal failure, primary hyperparathyroidism, nutritional secondary hyperparathyroidism).
Top

Small Animals
 

Reference Ranges

Canine

3.5 - 5.6 mmol/L/l

Feline

3.5 - 5.5 mmol/L/l

Plasma potassium levels are not always a good indicator of intracellular levels; in acidosis the exchange of H+ and K+ ions leads to the depletion of intracellular potassium and elevated plasma potassium. The converse occurs in alkalosis. Hypokalaemia may lead to neurological, muscular and cardiac signs. Hypokalaemia is of particular significance in the cat. In most cases, hyperkalaemia arises due to a diminished ability to excrete potassium. Marked hyperkaelaemia is potentially life threatening causing bradycardia and cardiac arrest.
 

ELEVATED LEVELS	LOW LEVELS
Hyperkalaemia	Hypokalaemia
Acute renal failure	Diuretic therapy
Hypoadrenocorticism	Diabetes mellitus
Iatrogenic (KCl)	Polyuric disorders
Massive tissue damage	Vomiting and diarrhoea
Metabolic acidosis (e.g. liver failure)	Chronic renal failure (particularly cats)
Low sodium intake	Insulin therapy
Urethral obstruction	Steroid administration
Drug action (e.g. digitalis)	Excessive bicarbonate therapy
Bladder rupture	Administration of potassium depleted fluids
Diabetes mellitus	Excessive mineralocorticoid therapy
	Chronic renal failure (terminal event)
	Chronic hepatic disease
	Thrombocytosis
	Hyperadrenocorticism
	Acute renal failure (polyuric phase)
	Fanconi's syndrome
	Alkalosis (respiratory or metabolic)
	Hypothermia
	Hypomagnesaemia

COMPLEMENTARY TESTS

In small animals a sodium:potassium ratio is useful information for an aid to the diagnosis of hypoadrenocorticism; a ratio of <27:1 is suspicious, <25:1 is suggestive. An ACTH stimulation test should be considered for confirmation.

Equine
 

Reference Range

Equine

2.7 - 5.9 mmol/L/l

Potassium levels in the extracellular fluid are influenced most by renal function and do not always reflect potassium levels in the intracellular compartment. Potassium distribution depends on the acid-base status as it is exchanged for hydrogen ions across the cell membrane. Hyperkalaemia is a potential emergency due to induction of cardiac dysrrythmias.
 
 

ELEVATED LEVELS	LOW LEVELS
Hyperkalaemia	Hypokalaemia
Reduced extra-cellular fluid volume	Reduced intake
AnaemiaHaemolysis	Gastrointestinal tract loss ( lower bowel obstruction)
Muscle damageAnaemia	Polyuric conditions including renalenal failure
HypoadrenocorticismMuscle damage	Alkalosis
Anuric renal failure Hypoadrenocorticism	Enterocolitis
Urinary tract disruption Anuric renal failure	Anorexia
Urinary tract disruption	Renal tubular acidosis
	Iatrogenic (diuretics, bicarbonate or insulin administration)

COMPLEMENTARY TESTS

In equines the calculation of urine clearance ratios will assist interpretation of serum electrolyte and mineral levels.
Top

Serum proteins vary widely in their size, structure and function. Abnormal levels of these proteins are termed dysproteinaemias. Total protein and albumin concentrations are determined and the globulin concentration arrived at by subtraction. Total protein levels are affected by physiological as well as pathological factors. Total protein levels are low in neonates rising to adult levels by 6 months to 1 year of age. In older animals total protein levels are high due mainly to IgG synthesis. Serum total protein levels are approximately 5% less than those of plasma due to the loss of fibrinogen in the clotting process.

Small Animals
 

Reference Ranges	Canine	Feline
Total Protein	55 - 75 g/L/l	55 - 78 g/L/l
Albumin	31 - 40 g/L/l	26 - 40 g/L/l
Globulin	18 - 38 g/L/l	19 - 48 g/L/l

ELEVATED LEVELS	LOW LEVELS
Hyperalbuminaemia	Hypoalbuminaemia
Dehydration	Hepatic insufficiency
	Protein losing enteropathy
Hyperglobulinaemia	Protein losing nephropathy
ImmuneImmmune response	Haemorrhage
Infection	Protein malnutrition/ malabsorption
Inflammation	Trauma
Neoplasia	Exudation
Immune mediated disorders	Sepsis
Compensatory for hypoalbuminaemia	Congestive heart failure
	Compensatory for a hyperglobulinaemia
	Hypoglobulinaemia
	Haemorrhage
	Protein losing enteropathy
	Congenital immunodeficiency
	Neonates

COMPLEMENTARY TESTS

Serum Pprotein electrophoresis (hyperglobulinaemia). Urine protein electrophoresis. Radial immunodiffusion for IgG, IgA and IgM (canine) (suspected immunodeficiency and classification of myelomas).

Equine
 

Reference Range
Total protein	60 - 80 g/L/l
Albumin	27 - 40 g/L/l
Globulin	17 - 34 g/L/l

ELEVATED LEVELS	LOW LEVELS
Hyperalbuminaemia	Hypoalbuminaemia
Dehydration	Advanced hepatic insufficiency
	Protein losing enteropathy
Hyperglobulinaemia	Protein losing nephropathy
Infection	Endoparasitism
Inflammation	Chronic infection
Neoplasia	Neoplasia
Immune response Hyperglobulinaemia	Trauma
Compensatory for a hypoalbuminaemia	Haemorrhage
	Compensatory for a hyperglobulinaemia
Hyperglobulinaemia	Hypoglobulinaemia
Infection	Inadequate transfer of colosterum (neonates)

COMPLEMENTARY TESTS

Protein electrophoresis (hyperglobulinaemia)
Top

The distribution of sodium in the body differs from that of potassium. Sodium is predominantly extracellular due to the sodium pump mechanism. In contrast, only 2% of potassium is extracellular, the rest being intracellular. Renal function is the single most important homeostatic mechanism in relation to plasma concentrations of sodium and potassium.

Small Animals
 

Reference Ranges

Canine

135-150 mmol/L/l

Feline

141-155 mmol/L/l

Slight hyponatraemia is common in small animals. Marked hyponatraemia or a sodium:potassium ratio < 27:1 indicates further investigation. Marked hyponatraemia may cause fluid movement into cells with an effect on neurological function. Hypernatraemia is uncommon in small animals. It almost always indicates water intake which is inadequate to balance fluid losses. Marked hypernatraemia may lead to neurological signs due to the net movement of water out of the cells.
 

ELEVATED LEVELS	LOW LEVELS
Hypernatraemia	Hyponatraemia
Diabetes mellitus	Hypoadrenocorticism
Diabetes insipidus	Severe dehydration (vomiting and diarrhoea)
Insensible losses	Diabetes mellitus
Hyperadrenocorticism	Ruptured urinary tract
Increased sodium intake	Administration of low sodium fluids
Moderate dehydration	End stage chronic renal failure
Pyometra	Diuretic therapy
High protein diets	Psychogenic polydipsia
Osmotic diuresis	Acute renal failure (polyuric phase)
Osmotic cathartics	Hypertension (congestive heart failure)
Water restriction	Hypoalbuminaemia
Extreme exercise	Drug therapy (e.g. NSAID's)
Drug therapy (e.g. corticosteroids)	Osmotic diuresis
Severe hypokalaemia

COMPLEMENTARY TESTS

In small animals a sodium:potassium ratio is useful as an aid to the information for the diagnosis of hypoadrenocorticism; a ratio of <27:1 is suspicious, <25:1 is suggestive. An ACTH stimulation test should be considered for confirmation.

Equine
 

Reference Range

Equine

133 - 143 mmol/L/l

Sodium levels reflect the relative amounts of water and electrolytes in the extra-cellular fluid . It is the principle determinant of ECF volume. Hyponatraemia occurs more commonly due to excessive losses than to reduced intake. Hypernatraemia indicates water loss in excess of electrolytes.
 

ELEVATED LEVELS	LOW LEVELS
Hypernatraemia	Hyponatraemia.
Dehydration	Gastrointestinal loss (especially high obstruction)
Excess saline therapy	Chronic renal disease (PU/PD)
Enterocolitis	Oesophageal obstruction.
Excessive sweating	Enterocolitis
Water deprivation	Urinary tract disruption
	Inappropriate ADH secretion.

COMPLEMENTARY TESTS

In equines the calculation of urine clearance ratios will assist interpretation of serum electrolyte and mineral levels.
Top

Triglycerides may be ingested or synthesised in the liver. They are complexed with cholesterol, phospholipids and plasma proteins to form lipoproteins.

Small Animals
 

Reference Ranges

Canine

0.6 - 1.2 mmol/L/l

Feline

0.6 - 1.2 mmol/L/l

Triglycerides are the main constituent both of chylomicrons and very low density lipoproteins (VLDL's) which are responsible for the gross lipaemia often seen in serum or plasma samples. Chylomicrons separate and form a fatty layer after overnight refrigeration whilst VLVDL's remain dispersed in the serum/plasma. Where a sample is lipaemic after a 16 hour fast then a pathological lipaemia is said to exist.

ELEVATED LEVELS

Cholesterol (hyperlipidaemia). TRH stimulation test (hypothyroidism). ACTH stimulation test or low dose dexamethasone screening test (hyperadrenocorticism). Glucose/fructosamine (diabetes mellitus). Amylase and lipase (pancreatitis). Urine protein:creatinine ratio and albumin (nephrotic syndrome).

Equine
 

Reference Range :

Equine

0 - 0.6<0.57 mmol/L/l

ELEVATED LEVELS

Bile acids (hepatic function). Urea and creatinine (renal function).
Top

Urea is principally a product of amino acid deamination in the liver. Urea is primarily excreted by the kidneys and is the most commonly used test of renal function.

Small Animals
 

Reference rRanges

Canine

3.5 - 7.0 mmol/L/l

Feline

3.5 - 8.0 mmol/L/l

ELEVATED LEVELS	LOW LEVELS
Renal Azotaemia	Polydipsia/ polyuria
Acute renal failure	Hepatic insufficiency
Chronic renal failure	Protein malnutrition
Prerenal Azotaemia.	Overhydration
Dehydration	Late pregnancy
Shock	Portosystemic shunt
High protein diet	Anabolic steroids
Fever
Reduced cardiac output
Hyperthyroidism (cats)
Hypoadrenocorticism
Gastrointestinal haemorrhage
Prolonged exercise
Glutacorticoid Corticosteroid therapy
Postrrenal Azotaemia
Feline urological syndrome
Bladder rupture
Calculi
Neoplasia
Perineal herniation
Prostatic enlargement

COMPLEMENTARY TESTS

Creatinine and phosphorus (azotaemia). Urine specific gravity (azotaemia); pre renal azotaemia 1.030 (dog) and 1.035 (cat), renal azotaemia 1.008 - 1.030 (dog) and 1.008 - 1.035 (cat), post renal azotaemia any value (dog and cat).

Equine
 

Reference Range

Equine

3.5 - 7.3 mmol/L/l

ELEVATED LEVELS	LOW LEVELS
Renal Azotaemia	Hepatic insufficiency
Acute renal failure	Young foals (normal by 60 days)
Chronic renal failure

Prerenal Azotaemia
Dehydration
Excessive muscle catabolism
High protein diet
Postrenal Azotaemia
Grass sickness
Obstruction
Neonatal foals

COMPLEMENTARY TESTS

Creatinine and phopsphorus (azotaemia). Urine specific gravity (<1.020 in a dehydrated or azotaemic horse suggests renal tubular dysfunction). Urine clearance ratios (renal tubular dysfunction). Urinalysis;. Urinary indices for urea and creatinine given by ; urine urea conc./serum urea conc. and urine creatinine conc./serum creatinine conc. Prerenal azotaemia; urea index 14, creatinine index 50, renal azotaemia; urea index <15, creatinine index <37.
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Equine
 

Reference Rranges
Sodium	0.02 - 1.0 %
Potassium	15 - 65 %
Phosphorus	0 - 0.5 %
Chloride	0.04 - 1.6 %

Urine clearance ratios measure the clearance of electrolytes and minerals from the plasma against that of creatinine. Creatine is selected as it is neither secreted or resorbed by the renal tubules and compares favourably with the use of endogenous substances such as inulin. Creatinine and electrolyte/mineral concentrations are measured on both urine and serum/plasma and the results are expressed as a % clearance ratio.

ELEVATED LEVELS

SMALL ANIMAL CLINICAL BIOCHEMISTRY.

Blaxter,A. (1987). Diagnosis and management of hepatic disorders in the cat. In Practice. 9 (5). p 178 - 185.

Bruijne,J.J. and Rothuizer,J. (1988). The Value of Serum Bile Acid and GLDH in the Screening for Canine Liver Function Disorders. In: Animal Clinical Biochemistry - the Future. Ed. Blackmore, D.J. Cambridge University Press. Cambridge. p 175 - 180.

Bush,B.M.(1991). Interpretation of Laboratory Results for Small Animal Clinicians. Blackwell Scientific Publications. Oxford.

Dunn,J.(1992). Assessment of liver damage and dysfunction. In Practice. 14 (4). p 193 - 200.

Evans,R.J. (1988). Hepatobiliary Damage and Dysfunction ; a Critical Overview. In: Animal Clinical Biochemistry - the Future. Ed. Blackmore, D.J. Cambridge University Press. Cambridge. p 117 - 150.

Meyer,D.J. and Carter,S.A.(1986). Approach to the diagnosis of liver disorders in dogs and cats. Comp. Contin. Educ. Pract. Vet. Small Animal. 8 (12). p 880 - 888.

Simpson,K. and Lamb, L.(1995). Acute pancreatitis in the dog. In Practice. 17 (7). p 328 - 337.

Small Animal Clinical Diagnosis by Laboratory Methods (198994). 2nd Edition, Eds. Willard,M.D.,Tvedten,H. and Turnwald,G.H. W.B.Saunders Company. Philadelphia.

Watson,T.D.G.(1993). Why is this sample lipaemic? Canine Practice. 18 (5). p 26 - 31.

Watson,T.D.G.(1994). Hyperlipidaemia in cats. The Journal of the Feline Advisory Bureau. 31 (3). p 111 - 114.

EQUINE CLINICAL BIOCHEMISTRY.

Blackmore,D.J. and Brobst,D. (1981). Biochemical Values in Equine Medicine. The Animal Health Trust. Newmarket.

Milne,E.M. (1990). Differential diagnosis of hepatic disorders in horses. In Practice. 12 (6). p 252 - 258.

Traver, D.S. et al. (1976). Urine clearance ratios as a diagnostic aid in equine metabolic disease. Proc. 22nd. A. Conv.Am.Assoc.Eq.Pract. p 177 - 183.

The Equine Manual. (1995). Eds. Higgins,A.J. and Wright, I.M. W.B.Saunders Co. Ltd. London.

Watson,T.D.G.(1994). Hyperlipaemia in ponies. In Practice. 16 (5). p 267 - 272.

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