Test Interpretation 2  Index


ALT (Alanine aminotransferase)

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

Primary Hepatopathies
Acute liver disease
Chronic active hepatitis (dog) - Fibrosis/cirrhosis
Poisoning/Toxicity hepatitis
Cholangiohepatitis (cat)
Lymphocytic cholangitis (cat)
Acute pancreatitis
Obstructive jaundice (slightly raised)
Pregnancy (slightly raised)
Glucocorticoid use
Hypoxia
Acute pancreatitis
Hepatic neoplasia

Secondary hepatopathiesCopper storage disease
Hyperthyroidism (cat)
Hyperadrenocorticism
Diabetes mellitus
Glucocorticoid therapy
Hypothyroidism (dog)
Post hepatic obstructive jaundice

o Equine

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.
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AMYLASE.

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

Acute Pancreatitis in the (dog)
Renal failure (dog)
Glutacorticoid administration
Pancreatic neoplasia and abscessation.
Corticosteroid administration
Urinary tract obstruction
Intestinal obstruction
and other intestinal pathology (cat)
Equine

COMPLEMENTARY TESTS

When elevated, serum lipase levels should also be determined.
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AP (Alkaline Phosphatase)

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

Cholestasis
Glutacorticoid (dog), anticonvulsants, barbiturates
Age (young growing animals)
Cholangitis-cholangiohepatitis (cat)
Other hepatopathies (see ALT)
Hyperthyroidism (cat)
Hyperadrenocorticism (dog)
Corticosteroids (dog), anticonvulsants, barbiturates.
Cholangitis-cholangiohepatitis (cat)
Hyperthyroidism (cat)
Diabetes mellitus (cat)
Hyperadrenocorticism (dog)
Tumours affecting any of the tissue sources mentioned above
(eg. carcinomas haemangiosarcomas and mastocytomas)
Pancreatitis
Chronic and acute liver disease
Pancreatitis
Healing bone fractures and bone disease
COMPLEMENTARY TESTS

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

Intestinal pathology
Biliary obstruction (chronic)
Hyperparathyroidism
Increased or abnormal bone metabolism
Vit D deficient diet
COMPLEMENTARY TESTS

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.
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AST (Aspartate aminotransferase)

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

Hepatopathies (see ALT)Hepatic disease
Muscular diseases and myopathies
Haemolysis
Recent intra-muscular injection
Myocardial infarction or ischaemia
Congestive heart failure
COMPLEMENTARY TESTS

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.

Azoturia
Acute Hhepatocellular damage
Cardiac muscle damage
Haemolysis
Training
Post exercise
COMPLEMENTARY TESTS

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.
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BILIRUBIN

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

Biliary obstruction and cholestasis (intra or post hepatic)
Reduced hepatocellular function ( loss of 70% of functional hepatocellular mass)
Haemolysis (intravascular or marked extravascular)
COMPLEMENTARY TESTS

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

Anorexia
Biliary obstruction and cholestasis (intra or post hepatic)
Reduced hepatocellular function ( particularly due to acute hepatic failure)
Haemolysis (intravascular or marked extravascular)
COMPLEMENTARY TESTS

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.
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BILE ACIDS

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

Congenital or acquired portosystemic shunt
Acquired portosystemic shunt
Reduced hepatocellular function (reduced hepatocellular mass)
Cholestasis
LOW LEVELS Intestinal obstruction
Malabsorption (severe)
COMPLEMENTARY TESTS

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

Hepatic insufficiency
Cholestasis
Portosytemic shunt
COMPLEMENTARY TESTS

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).
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CALCIUM

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.
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CHLORIDE

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

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  
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CK (Creatine kinase)

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

Trauma (surgery, i/m /injections, complicated venipuncture, recumbancy, severe exertion)
Hypothyroidism
Convulsions or seizures
Cramping in greyhounds
Myositis (infectious, immune mediated, nutritional)
Hyperadrenocorticism
COMPLEMENTARY TESTS

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

Azoturia"Tying up"
Trauma (i/m injections, surgery, severe exertion)
Myocardial infarction
Hypothyroidism
Post anaesthetic myopathy
COMPLEMENTARY TESTS

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..
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CREATININE

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

Renal, pre renal and post renal azotaemia - (see Urea)
Severe prolonged exertion or exercise
Acute myositis or muscle trauma
Cooked meat diet
COMPLEMENTARY TESTS

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

Renal, pre renal and post renal azotaemia - (see Urea)
Severe prolonged exercise or muscle catabolism
Increased pituitary activity
New born foals - may be a normal feature or may indicate birth hypoxia or placental dysfunction
COMPLEMENTARY TESTS

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

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

Uncontrolled diabetes mellitus
Poor metabolic control of diabetes mellitus
LOW LEVELS Insulinoma COMPLEMENTARY TESTS

Plasma glucose
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GGT(Gamma-glutamyltransferase)

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.

Glucocorticoid therapy (dog)
Hepatobiliary disease
Cholestasis
COMPLEMENTARY TESTS.

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

Hepatobiliary disease
Cholestasis
Hepatic insufficiency
Pancreatitis
Foals (< 3 months3months of age)
Renal pathology
COMPLEMENTARY TESTS

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

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

Hepatocellular necrosis
Secondary hepatopathies (congestive heart failure and small intestinal pathology)
COMPLEMENTARY TESTS

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

Hepatocellular necrosis
Enteropathy.
COMPLEMENTARY TESTS

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

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).
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IAP (Intestinal Aalkaline Pphosphatase)

Equine
 
Reference Range : Equine 0-150 IU/L/l

ELEVATED LEVELS

Intestinal parasitism pathology (including intestinal parasitism) COMPLEMENTARY TESTS

Protein electrophoresis (when hyperglobulinaemia present)
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LDH (Lactate Dehydrogenase)

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

Hepatocellular damage
Skeletal muscle disorders
Cardiac muscle disorders (especially ischaemia)
Exercise
Post prandial
Malignant neoplasia
COMPLEMENTARY TESTS

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

Hepatocellular damage
Skeletal muscle disorders
Cardiac muscle disorders
Pancreatitis
Renal disease
COMPLEMENTARY TESTS

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

Small Animals
 
Reference Ranges Canine 0 -< 500 IU/L/l  Feline 0 - 250 IU/L/l

ELEVATED LEVELS

Acute pancreatitis
Glucocorticoid therapy
Glutacorticoid administration
Renal failure (dog)
Other pancreatic pathology (neoplasia and , abscessation)
Hepatic disease (dog)
COMPLEMENTARY TESTS

Amylase (pancreatitis), urea and creatinine (renal failure), ALT, GLDH (hepatocellular damage).
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PHOSPHORUS (Inorganic Pphosphate)

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).
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POTASSIUM

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.
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PROTEIN (Albumin and Globulin)

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)
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SODIUM

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.
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TRIGLYCERIDE

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

Post prandial
Hypothyroidism (dogs)
Diabetes mellitus
Starvation
Hyperadrenocorticism
Biliary obstruction
Pancreatitis
Glomerulopathy
Hepatic lipidosis (cats)
Acromegally (cats)
Obesity (cats)
Antithyroid therapy (cats)
Primary lipoproteinaemias
Hyperchylomicronaemia (cats)
Idiopathic
COMPLEMENTARY TESTS

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

Hyperlipidaemia ( 5 mmol/L/l) COMPLEMENTARY TESTS

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

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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URINE CLEARANCE RATIOS

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

Sodium CRSodium:CR elevated with normal or low serum sodium suggests hypoadrenocorticism
Elevated sodium, potassium, phosphorus and chloride :CR's with renal tubular dysfunction
Elevated phosphorus :CR in primary or secondary nutritional hyperparathyroidism.
LOW LEVELS Low potassium CR due to potassium depletion in some cases of chronic laminitis Top

REFERENCES AND FURTHER READING

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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