Quick test interpretation


Artifact Water loss from blood sample (inadequate capping)
Iatrogenic Hypertonic fluid administration
Water deficit Excess water loss: Panting, fever, hyperventilation, diabetes insipidus
Inadequate intake: Water deprivation, primary adipsia/hypodipsia
Hypotonic fluid loss and inability to conserve water or drink:
Renal: Osmotic/chemical diuresis, renal failure
Non-renal: Gastrointestinal, cutaneous, third space losses
Salt gain Excess intake: Salt poisoning (with concurrent water deprivation)
↑ Renal retention: Hyperaldosteronism


Artifact Lipemia (chylomicrons, high VLDL), hyperproteinemia, hyperosmolar states
Iatrogenic Diuretic therapy, hypotonic fluid administration
Volume overload (hypervolemic hyponatremia with inappropriate ADH release due to perceived volume depletion) Congestive heart failure, hepatic disease, nephrotic syndrome, advanced renal failure
Fluid losses with dilution (ADH or drinking) (hypovolemic hyponatremia) Renal: Proximal renal tubule dysfunction, hypoadrenocortisim, hypoaldosteronism, osmotic diuresis (diabetes mellitus)
Non-renal: Gastrointestinal (vomiting/diarrhea), cutaneous (equine sweating), third space losses (ruptured or obstructed urinary tract, peritonitis, chylothorax)
Other Intracellular translocation (muscle injury), decreased intake (anorexia)


Interpret with: Electrolytes (K+, Cl), urinalysis, HCT, protein, urea nitrogen, creatinine, osmolality  




Artifact Serum K+ > plasma K+ (release from WBC, platelets); anticoagulant (K+ EDTA), hemolysis (horses, camelids, some cattle, some breeds of dogs, pigs), leukocytosis (release from cells with clotting), age (> foals), K administration and intravenous (IV) line contamination
Iatrogenic IV fluids or IV line contamination with K+ supplementation (rare unless renal disease)
Transcellular shifts
Hyperkalemic myopathy, tissue necrosis, hypertonicity (diabetes mellitus), uroperitoneum (foals), hyperchloremic metabolic acidosis (transient)
↓ Renal excretion Anuric/oliguric renal failure, chronic kidney disease (horses), uroabdomen, hypoadrenocorticism, hypoaldosteronism


Artifact Lipemia due to chylomicrons or high VLDL (mild effect)
↓ Intake Anorexia (large animals, especially ruminants and foals; small animals – rare)
Transcellular shifts (ECF→ICF) Primary respiratory or primary metabolic alkalosis, hyperinsulinemia, catecholamine release, endotoxemia (may work via insulin)
↑ Loss GI: Gastric vomiting, abomasal stasis, outflow obstruction/torsion, and choke (horses, cattle);
Third space loss/sequestration
Cutaneous: sweating (horses)
Renal: ↑ aldosterone, ↑ distal tubular flow rate, renal tubular disease


Interpret with: Electrolytes, UN, creatinine, urinalysis, bicarbonate, AG, blood gas analysis



Artifact Lipemia (chylomicrons, high VLDL), anticonvulsant medication (KBr, zonisamide)
Iatrogenic Administration of Clcontaining fluids (hypertonic saline, ammonium chloride)
Metabolic acidosis  
(i) Bicarbonate loss (Hyperchloremic metabolic acidosis)
 – Primary GI loss/sequestration of Cl/HCl: Vomiting (biliary, pancreatic fluids), secretory diarrhea (e.g. calves), sequestration (e.g.. distal intestine in horses), diarrhea, loss of saliva (ruminants, horse)
Renal loss: Proximal renal tubular acidosis, Addison’s disease
 – Secondary Compensatory response to a primary respiratory alkalosis (hyperventilation or hypocapnea – hypoxemia, primary pulmonary disease, pain)
(ii) Bicarbonate consumption (Titration acidosis) Production of noncarbonic acid: Lactic acidosis, ketosis (e.g. diabetes mellitus)
↓ Excretion of noncarbonic acid: Sulfates, phosphates (renal failure)
Toxicity (ethylene glycol, salicylate, methanol)


Iatrogenic Administration of sodium-rich fluids, loop diuretics (e.g. spironolactone)
Loss of Cl > Na+ GI: loss of Cl rich fluid (vomiting, ptyalism; gastric reflux, gastroduodenal ulcers in horses)
Sequestration of Cl rich fluid: displaced abomasum, abomasal atony, gastric rupture, gastric dilatation volvulus, proximal intestinal ileus (horses)
Renal: Renal disease (especially cattle)
Cutaneous: Sweating (horses)


Interpret with: Electrolytes (Na+, K+), urinalysis, bicarbonate, AG, blood gas analysis,



Artifact Severe muscle injury (rare)
Iatrogenic Administration of HCO3 containing solutions
Metabolic alkalosis  
   (i) Primary GI loss/sequestration of HCl: Vomiting gastric contents (small animals), gastric reflux or proximal enteritis (horse), abomasal atony/torsion/displacement
Cutaneous loss: Sweating (horses, loss of KCl)
Renal loss: Loop (e.g. furosemide) or thiazide diuretics, severe hypokalemia, excess aldosterone (stimulation of H+ antiporter)
   (ii) Secondary Compensation for primary respiratory acidosis by increasing renal excretion of acid (increased ammoniagenesis, stimulation of H+ antiporter)


Artifact Aged samples (production of lactate in tube), heparin over-dilution, prolonged venous stasis
Iatrogenic Ammonium chloride administration (induces a primary hyperchloremic metabolic acidosis)
Metabolic acidosis  
  (i) Bicarbonate loss  Usually yields a hyperchloremic metabolic acidosis
       – Primary GI loss: Vomiting of biliary or pancreatic fluids (rich in bicarbonate)), secretory diarrhea, sequestration (e.g. ileus in horses), diarrhea (horse), loss of saliva (ruminants, horse)
Renal loss: Proximal renal tubular acidosis, Addison’s disease
       – Secondary Compensation for primary respiratory alkalosis via decreased ammoniagenesis
  (ii) Bicarbonate consumption Results in a high anion gap or titration acidosis
Production of non-carbonic acids: Lactic acidosis (L or D), ketoacidosis (e.g. diabetes mellitus in small animals, excess negative energy balance in camelids or ruminants)
↓ Excretion of non-carbonic acids by the kidney: Renal failure (decreased excretion of sulfates, hippurates, citrates, phosphates
Gain of a non-carbonic acid: Toxicity (ethylene glycol, salicylate, methanol)
  (iii) Failure of acid excretion Usually yields a hyperchloremic metabolic acidosis: Defective function of the H+ antiporter, resulting in excessive acid excretion, e.g. distal renal tubular acidosis, hyperaldosteronism.


Interpret with: Blood gas analysis – Anion gap, electrolytes (corrCl, K+), urinalysis, glucose, urea, creatinine


Anion Gap

Artifact Artifactual ↑ of sodium/potassium or ↓ chloride/bicarbonate
Iatrogenic Sodium-containing drugs (e.g. penicillin, sodium salts)
Metabolic acidosis (titration) Accumulation of non-carbonic acid (e.g. lactate, ketones, uremic acids), toxins (methanol, salicylate, ethylene glycol, metaldehyde)
Alkalemia (typically secondary to a primary respiratory alkalosis) Stimulates lactic acid production (small amount, mild increase in anion gap)
↑ Albumin Dehydration, increased albumin production (e.g. hepatocellular carcinomas)
↓ “Unmeasured” cations Ionized calcium, ionized magnesium (exceedingly rare)


Artifact Falsely high chloride/bicarbonate, anticonvulsants (potassium bromide), pyruvate and LDH accumulation (muscle injury, false increase in bicarbonate)
Iatrogenic Bicarbonate-rich fluid administration
↓ Albumin Hypoalbuminemia (e.g. protein-losing nephropathy, negative acute phase response)
↑ “Unmeasured” cations Ionized magnesium/calcium (unlikely), paraproteins or neoplastic immunoglobulins (monoclonal gammopathy, e.g. multiple myeloma)


Interpret with: Bicarbonate, electrolytes, blood gas analysis, urinalysis



Physiologic Post-prandial, increased counterregulatory hormones, pregnancy (progesterone)
Iatrogenic Drugs inducing insulin resistance (xylazine, detomidine, propanalol, megestrol acetate, ketamine)
Sustained hyperglycemia Lack of insulin or insulin resistance: Diabetes mellitus, hyperadrenocorticism, acromegaly, hyperglucagonemia, hyperpituitarism/pituitary pars intermedia dysfunction (horses), pheochromocytoma


Artifact Bacterial contamination of blood, serum not separated from clot, severe hematrophic Mycoplasma infection (camelid, ruminant)
Iatrogenic Insulin administration
↓ Production Glycogen storage diseases (e.g. Pompe’s disease, von Gierke’s disease)
Juvenile hypoglycemia
Hepatic insufficiency
↓ Intake Starvation, malabsorption, high grain diet (horse)
↑ Use Sepsis
Idiopathic hypoglycemia of hunting dogs and endurance horses
Bovine ketosis (type 1), ovine pregnancy toxemia
Exertional hypoglycemia
↑ Insulin secretion Neoplasia: insulinoma, mesenchymal tumors (leiomyoma, leiomyosarcoma, hepatic and renal tumors, secrete insulin-like growth factor)
Xylitol (dogs)


Interpret with: Urinalysis, fructosamine, ketones, liver analytes


Urea Nitrogen

↑ Protein catabolism Fever, burns, corticosteroid administration, starvation, exercise
↑ Protein digestion Hemorrhage into the the upper GI, high protein diet, ammonia toxicity cattle (increased protein production in rumen)
↓ GFR Pre-renal, renal, post-renal causes


↓ Protein intake,
protein anabolism
Diet, young animals
↓ Production Hepatic disease
↑ Excretion Causes of polyuria (e.g. hyperadrenocorticism, diabetes mellitus)
↑ GFR Portosystemic shunts


Interpret with: Creatinine, urinalysis, total protein, albumin, HCT, electrolytes, anion gap, calcium, phosphate, hepatic tests



Artifact Presence of acetoacetate, glucose, vitamin C, uric acid, pyruvate, cephalosporins and amino acids in sample with Jaffe but not enzymatic reaction
Physiologic Neonatal foals, heavily-muscled horses, Greyhounds, post-high protein meal
↓ GFR Pre-renal, renal, post-renal causes


Physiologic Pregnancy (↑ GFR)
↓ Production Starvation, cachexia, decreased muscle mass
↑ GFR Portosystemic shunts


Interpret with: Urea nitrogen, liver analytes


Uric acid

Artifact Dehydation, fecal urate contamination
Physiologic Post-prandial
Renal disease ↓ GFR, Loss of >70% functional renal capacity
↑ Deposition Articular gout


Bilirubin (indirect, unconjugated)

Physiologic Fasting (horses), anorexia (cattle), neonates (especially foals)
↑ Production Heme breakdown (hemolytic anemia – extravascular > intravascular but definitely both). Called prehepatic icterus
↓ Hepatic uptake
(primarily indirect)
Hepatic insufficiency or dysfunction (hepatocellular disease , portosystemic shunts). This may also occur as a consequence of cholestatic disorders (hepatic dysfunction from retained bile acids). Called hepatic icterus, but can also result in increased direct or conjugated bilirubin.
↓ Hepatic conjugation Hepatic insufficiency or dysfunction. This may also occur as a consequence of cholestatic disorders (hepatic dysfunction from retained bile acids). Called hepatic icterus, but can also result in increased direct or conjugated bilirubin.
Inherited Southdown sheep (defect in uptake)


Interpret with: Hepatocellular injury (ALT, AST, SDH, GLDH) and cholestatic enzymes (ALP, GGT), urinalysis, CBC, cholesterol (decreases with insufficiency)


Bilirubin (direct, conjugated)

↓ Hepatic excretion, i.e. Cholestasis Rate limiting step of bilirubin synthesis pathway is excretion of conjugated bilirubin into bile via hepatic transporters. Decreased bile excretion could be due to a physical obstruction to bile flow (structural cholestasis) or downregulation of transporters by cytokines (functional cholestasis). 
Structural (intra/extra-hepatic) e.g. hepatocellular swelling, extrahepatic biliary tract obstruction (cholelithiasis, gallbladder mucocele, neoplasia, parasites), bile sludging in cats (with anorexia or dehydration). This falls into hepatic icterus and post-hepatic icterus (latter due to biliary issues)
– Functional: Bacterial sepsis, severe inflammation
Inherited Corriedale sheep (Dubin-Johnson syndrome): Defect in biliary or canalicular transporters excreting bilirubin into bile


Interpret with: Hepatocellular injury (ALT, AST, SDH, GLDH) and cholestatic (ALP, GGT), enzymes, urinalysis, CBC, cholesterol (often goes up in cholestatic disorders)


Physiologic Young animals, breed-associated (Siberian Huskies – benign familial hyperphosphatasemia; endogenous corticosteroids (chronic stress in dogs)
Iatrogenic Liver injury: Anticonvulsants (e.g. phenobarbital, primidone), thyroxine
Induction: exogenous corticosteroid (dogs)
Hepatobiliary Cholestasis (structural/functional)
Endocrine Hyperthyroidism (cats, bone isoform)
Bone Hyperparathyroidism, fracture healing, osteosarcoma (dogs)


Interpret with: Other hepatic enzymes, bilirubin



Physiologic Neonates – colostral GGT (except horses); breed (donkeys, burros have higher GGT activity than horses)
Iatrogenic Biliary injury or cholestasis: Anticonvulsants (phenobarbital, phenytoin, mysoline), exogenous corticosteroids (dogs)
Hepatobiliary Biliary hyperplasia (e.g. pyrrolizidine alkaloids such as Senecio, Crotalaria, Heliotropium in grazing animals)
Cholestasis: Many causes


Interpret with: Bilirubin, other hepatic enzymes


Artifact In vitro hemolysis in some species (e.g. cats)
Iatrogenic Liver injury from drugs: Anticonvulsants (e.g. phenobarbital, phenytoin, primidone), corticosteroids, cephalosporin, cyclosporin, isoniazide
Hepatic injury Many causes (ALT is cytosolic)
Muscle Severe muscle injury: Aortic thromboembolism (cats), inherited or inflammatory myopathies (dogs), trauma (ALT < AST)


Interpret with: Bilirubin, hepatic enzymes, muscle enzymes



Artifact Hemolysis (in vitro) and delayed serum/plasma separation from cells
Iatrogenic Liver injury from drugs: Anticonvulsants, imidocarb (goats)
Physiologic Exercise (horses) from muscle (mild to moderate increase)
Liver Injury of any cause (AST is cytosolic and mitochondrial, throughout the hepatic lobule)
Muscle Myopathies, muscle trauma, rhabdomyolysis, white muscle disease (vitamin E-selenium deficiency), clostridial myositis, muscular dystrophy


Interpret with: Other liver enzymes, hemolytic index and CK (help exclude muscle source)



Artifact Can increase if broken into subunits with storage (uncommon), usually false decrease with storage (unstable)
Liver injury Any cause (cytosolic location)


Interpret with: Other liver enzymes



Physiologic Neonates (foals)
Liver Hepatocellular injury (periacinar, mitochondrial)


Interpret with: Other liver analytes



Artifact In vitro or in vivo hemolysis (RBC constituents participate in reaction), muscle penetration during venipuncture (“muscle stick”)
Physiologic Age (puppies), post-exercise (horse), anorexia (cats)
Iatrogenic Muscle injury: Intramuscular injection, especially irritant drugs (e.g. tetracycline), pentobarbitone (hamsters), post-surgery
CK-1(MM) isotype Skeletal muscle isoenzyme: Exertional rhabdomyolysis, polymyositis, vitamin E-selenium deficiency, snake bite poisoning, post-shipping, recumbent  and “downer” cows
CK2-(MB) isotype Cardiac muscle: dDxorubicin-induced cardiotoxicity
CK3-(BB) isotype Brain: Thiamine deficiency (ruminants), cerebrocortical necrosis
Muscle injury Nutritional: White muscle disease (vitamin E-selenium deficiency), polioencephalomalacia
Inherited: Muscular dystrophy, (Cavalier King Charles Spaniel dystrophin-deficient muscular dystrophy, hyperkalemic periodic paralysis, malignant hyperthermia (dogs, pigs)
Toxins: Monensin, gossypol, ricin, myotoxin (snake-bite)


Interpret with: Hemolytic index



Artifact In vitro or in vivo hemolysis (dog particularly), serum concentrations > plasma (release from cells during clotting)
Physiologic Exercise (mild increase from muscle)
Liver injury ↑ LDH1 & LDH2 (cattle, sheep), ↑ LDH5 (horse, small animals)
Muscle injury ↑ LDH5 (ruminants, horse): Exertional rhabdomyolysis, white muscle disease, cardiac muscle lesions (rats)
Neoplasia Many neoplasms


Interpret with: Hepatocellular leakage enzymes (ALT, AST, GLDH, SDH), hemolytic index, CK

Total Protein

Should not be interpreted alone – should determine if changes in albumin or globulins (disproportional) or both (proportional) are causing the altered protein concentrations. Protein may be normal despite alterations in albumin and globulins.

Proportional (albumin and globulins) Dehydration or fluid losses
Disproportional Increased albumin (uncommon)
Increased globulins (more common; see below)


Proportional (albumin and globulins) Blood loss, protein-losing enteropathy, overdilution with fluids
Disproportional Decreased albumin (common)
Decreased globulins (uncommon; see below)



Artifact Heparinized plasma > serum
Physiologic Hemoconcentration
Increased production Hepatocellular carcinoma, exogenous corticosteroids


 Iatrogenic Excessive fluid administration
 ↓ Production Malnutrition/starvation, hepatic insufficiency or failure, acute phase response, malabsorption
 ↑ Loss Protein-losing glomerulopathy, protein-losing enteropathy, severe hemorrhage, exudative dermatopathies, sequestration (third space losses), catabolism


Interpret with: Total protein, globulins, CBC, urinalysis, urea nitrogen and creatinine, liver analytes or function tests



↑ Production α-globulins: Acute phase reactant response
β-globulins: Increase in immunoglobulins from antigenic stimulation, artifact of in vitro or in vivo hemolysis (hemoglobin). 
γ-globulins: Antigenic stimulation – polyclonal gammopathy, restricted oligoclonal gammopathy (e.g. Ehrlichia canis); monoclonal gammopathy – usually neoplastic from multiple myeloma, lymphoma, chronic lymphocytic leukemia, extramedullary plasmacytoma, Waldenström’s macroglobulinemia (rare)


Decreased Only relevant for immunoglobulins
Inherited Immunodeficiency: Primary severe combined immunodeficiency (Basset hounds, Cardigan Welsh Corgis, Dachshunds and Arabian [horses]), agammaglobulinemia (foals), IgM deficiency (Dobermans, Arabians, Paso Fino, Quarterhorses and Thoroughbreds), IgA deficiency (Sharpei, Beagle, Airedale terriers, and German Shepherd Dogs), transient hypogammaglobulinemia (Arabian horses, dogs)
Physiologic Failure of passive transfer of immunity
Loss Blood loss
Protein-losing enteropathy: Many causes, e.g. lymphangiectasia in dogs Mycobacteria pseudotuberculosis (Johne’s disease)


Interpret with: Albumin, hemogram, etc



A/G Ratio

Do not interpret in isolation but with changes in albumin and globulins.



Most common causes Humoral hypercalcemia of malignancy; hypoadrenocorticism (dogs); chronic renal failure (horses); iatrogenic (cattle); hypercalcemia is uncommon in cats (idiopathic most common)
Physiologic Young animals
Iatrogenic Thiazide diuretics, calcium borogluconate administration, strontium salts
↑ Bone mobilization ↑ PTH: Primary hyperparathyroidism (parathyroid adenoma – common, parathyroid hyperplasia, malignant parathyroid carcinoma – rare)
↑ PTHrP: Humoral hypercalcemia of malignancy (e.g. dogs – anal sac adenocarcinomas, lymphoma, squamous cell carcinoma in horses; cats – lymphoma, pulmonary carcinoma)
Localized osteolysis (multiple myeloma)
↑ Intestinal absorption Hypervitaminosis D: ingestion of cholecalciferol rodenticides and plants (e.g. Cestrum diurnum, Solanum sp.), excessive dietary supplementation, granulomatous disease (e.g. fungal, parasitic), humoral hypercalcemia of malignancy (macrophage and lymphocyte origin e.g. histiocytic sarcoma, lymphoma)
Hypoadrenocorticism (dogs)
↓ Renal excretion Renal disease, hypoadrenocorticism, primary hyperparathyroidism, humoral hypercalcemia of malignancy
↑ Protein binding Hyperalbuminemia
Idiopathic Idiopathic hypercalcemia (cats), endometritis and retained fetus (dogs)


Most common causes Low albumin; renal disease (dogs, cats); pancreatitis (dogs); gastrointestinal disease (colic in horses); milk fever (cattle)
Artifact EDTA, citrate anticoagulants
Iatrogenic Sodium phosphate enemas, exogenous calcitonin
↓ Protein binding Hypoalbuminemia
Abnormal PTH Primary hypoparathyroidism, pseudohypoparathryoidism, PTH resistance, ↓ secretion (from low magnesium)
↓ Absorption Nutritional secondary hyperparathyroidism (bran disease in horses)
Hypovitaminosis D
Renal secondary hypoparathyroidism (dogs, cats, cattle)
Toxicosis: Oxalate-containing plants (e.g. Kikuku grass, rhubarb, purslane, sorrel, dock, foxtail grass)
GI disease: Horses (colic, enterocolitis, endotoxemia); protein-losing enteropathy (dogs)
Hyperadrenocorticism (dogs)
↑ Loss Renal loss
↑ calcitonin: Sepsis, pancreatitis, hypercalcitonism, ethylene glycol toxicosis
Pregnancy, parturient or lactational hypocalcemia/eclampsia
Excess sweating (horses)
Idiopathic Idiopathic hypocalcemia (foals), equine myopathy, cantharidin toxicosis


Interpret with: Albumin, ionized calcium, phosphate, urea nitrogen, creatinine, urinalysis



Artifact In vitro hemolysis especially with storage, anticoagulants (EDTA, oxalate, citrate), monoclonal gammopathy
Physiologic Post-prandial, young animals
Iatrogenic Phosphate enemas (especially cats)
↑ Intake Hypervitaminosis D: ingestion of cholecalciferol rodenticides and plants (e.g. Cestrum diurnum, Solanum sp.), excessive dietary supplementation, granulomatous disease (e.g. fungal, parasitic), humoral hypercalcemia of malignancy (macrophage and lymphocyte origin e.g. histiocytic sarcoma)
Excessive dietary phosphate: Nutritional secondary hyperparathyroidism
Transcellular shifts Acute tumor lysis syndrome, severe skeletal muscle injury
↓ Excretion ↓ GFR (of any cause), hypoparathyroidism, acromegaly, hyperthyroidism


Artifact Monoclonal immunoglobulins (causing precipitation out of solution)
Iatrogenic Diuretics, corticosteroids (diuresis), phosphate-binding antacids
↓ intestinal absorption Enteral tube feeding (cats), hypovitaminosis D (rare cause)
Transcellular shifts Alkalemia due to respiratory alkalosis, insulin, hypothermia
↑ Loss Renal: Renal disease, hyperparathyroidism, urolithiasis (loss via saliva in ruminants), diuresis (osmotic or solute), phosphatonins (urinary loss), hyperadrenocorticism (dogs)
GI: Diarrhea, vomiting
Unknown cause Hepatic lipidosis (cat)


Interpret with: Calcium, urea nitrogen, creatinine



Artifact Severe hemolysis, prolonged storage with hemolysis, postmortem blood samples
Physiologic Post-partum (cattle)
Iatrogenic Excessive supplementation of fluids, diet and oral supplements (e.g. antacids)
↑ Absorption Exogenous magnesium administration, intestinal hypomotility
↓ Excretion Moderate to severe ↓ GFR (e.g. chronic kidney disease, urinary tract obstruction, oliguric/anuric renal failure), hypocalcemia, hypoadrenocorticism
Release from cells Myopathy, soft tissue necrosis, tumor lysis syndrome
↑ PTH Hyperparathyroidism (rare)


Artifact Citrate, oxalate, fluoride anticoagulants
Physiologic Age (Mg absorption ↓ after 6 weeks of age)
Iatrogenic Administration of Mg-poor fluids or total parenteral without adequate Mg supplementation (small animals)
↓ Albumin Hypoalbuminemia
↓ Intake Anorexia (especially lactating dairy cows), high potassium diet, pastures fertilized with nitrates, ammonia, sulphates and potassium
Translocation into cells Insulin, hypothermia, sepsis (horses)
Excess loss GI: Malabsorption, chronic diarrhea, saliva loss (e.g. choke, rabies), hyperaldosteronism (rare)
Renal: Diuresis, hyperthyroidism, primary hypoparathyroidism, ketonuria, renal tubular injury
Cutaneous: sweating (horses)


Interpret with: Calcium, phosphate, potassium, albumin, glucose, urinalysis



Increased  Increased LDL
↑ Production Post-prandial (mild to minimal), nephrotic syndrome (amyloidosis, immune-complex glomerulonephritis)
↓ Lipolysis, abnormal processing Nephrotic syndrome, hypothyroidism
Inherited Familial hypercholesterolemia (Briards, Rottweilers, Shetland Sheepdogs, Dobermans), hyperlipidemia of Miniature Schnauzers, hyperchylomicronemia of cats
Decreased excretion Cholestasis
Endocrine disorders  Diabetes mellitus, pancreatitis, hyperadrenocorticism


Artifact Severe icterus
↓ Absorption Malabsorption, maldigestion (protein-losing enteropathies, exocrine pancreatic insufficiency)
↓ Production Chronic liver disease, synthetic liver failure, hypoadrenocorticism
Altered metabolism Inflammatory cytokines
↑ Lipoprotein uptake Upregulation of LDL-receptors on cells (peripheral tissues and liver) from rapidly proliferating tumor cells, e.g. acute myeloid leukemia, multiple myeloma


Interpret with: Glucose, urinalysis, urea nitrogen, creatinine, hepatic analytes, triglycerides, lipemic index or gross lipemia



Increased Increased chylomicrons or VLDL
Most common causes Post-prandial
Fasting: Diabetes mellitus, hyperadrenocorticism, hyperlipidemia (miniature horses, ponies, donkeys)
Physiologic Post-prandial
Iatrogenic Corticosteroids
Inherited Hypertriglyceridemia in Miniature Schnauzers, inherited hyperchylomicronemia (young cats)
↑ Lipolysis Excessive negative energy imbalance: Metabolic syndrome (obesity plus insulin resistance), pregnancy, stress (e.g. transport) and lactation (horses); pregnancy toxemia, ketosis (camelids)
↓ Lipoprotein lipase activity Pancreatitis


Interpret with: Cholesterol, NEFA, BHB (latter two in ruminants and camelids)



Pancreatic cell injury Acute pancreatitis
↓ Renal excretion ↓ GFR (usually renal azotemia)
Unclear mechanism Intestinal disease or obstruction


Interpret with: Lipase



Iatrogenic Corticosteroids
Pancreatic cell injury Acute pancreatitis (more sensitive than amylase)
Gastrointestinal disease Peritonitis, gastritis, bowel obstruction, visceral manipulation (laparotomy)
Unclear mechanism ↓ GFR from renal disease (not invariably increased and increased less than amylase in this condition)


Interpret with: Amylase



Artifact In vitro or in vivo hemolysis (likely with storage)
Physiologic Random transient variations
Iatrogenic Corticosteroids (dogs, horses), iron administration, hemosiderosis from repeated blood transfusions
Intracellular release Necrotizing hepatitis
↑ RBC turnover Hemolytic anemia, disordered/abnormal erythropoiesis (e.g. primary myelodysplasia and ineffective erythropoiesis, precursor-directed immune-mediated anemia)
↓ Erythropoeisis Bone marrow aplasia/hypoplasia, pure red cell aplasia
Hemochromataosis Mynah birds, lemurs, Saler/Saler-cross cattle


Artifact Anticoagulant chelation (e.g. EDTA)
Physiologic Random transient fluctuations
Iatrogenic Dexamethasone (cattle)
↓ Absorption/Intake Acid pH in intestine, inflammatory cytokine-mediated upregulation of hepcidin, copper deficiency, zinc excess, inadequate dietary content, intestinal disease, malnutrition (cattle)
Sequestration (most common) Mild transient injury/trauma, inflammation, portosystemic shunts, neoplasia (inflammatory cytokines upregulate hepcidin)
Loss Chronic external hemorrhage with depletion of stores, e.g. gastrointestinal hemorrhage from intestinal parasites (e.g. hookworms, whipworms, Haemonchus contortus),  gastrointestinal neoplasia, and vascular ectasia or angiodysplasia, urinary (e.g. persistent hematuria), reproductive (e.g. menstruation in primates, respiratory (hemotypsis, uncommon)


Interpret with: TIBC, % Saturation, hemogram (indices, smear evidence of hypochromasia), protein panel (proportional decreases in albumin and globulin due to chronic blood loss) etc



This is an indirect measure of transferrin, the iron transport protein

Artifact Anticoagulants with chelating agents (e.g. EDTA, oxalate, fluoride), in vitro or in vivo hemolysis
Iron deficiency anemia Pigs, horses and cattle; unreliable in dogs, cats or camelids
Release of ferritin Necrotizing hepatitis (uncommon)


↓ Production Acute phase response (most common cause), hepatic insufficiency or failure, portosystemic shunts, ↓ protein intake
Loss of transferrin Protein-losing nephropathy, protein-losing enteropathy, burns (decreases generally parallel albumin)
Transferrin catabolism Negative energy states
Most common cause Acute inflammation


Interpret with: Iron, % Saturation, Albumin



Changes can be due to iron or TIBC so interpret as an iron panel (iron, TIBC, % saturation). Can be normal if concurrent decreases in iron concentration and TIBC (e.g. longer-standing inflammation).

↓ Transferrin Loss or decreased production (e.g. protein-losing states)
Secondary to increased iron See above (TIBC normal or rarely decreased)


Secondary to decreased iron See iron above (TIBC usually normal)


Interpret with: Iron panel, CBC (inflammation, anemia),  protein (albumin, globulin)


Bile Acids

Physiologic ↓ feed intake (horses, mild); postprandial (gall bladder contraction); spontaneous gallbladder contraction during fast in species with a gallbladder (not equidaae)
↓ Clearance from portal circulation Hepatic insufficiency or failure, portosystemic shunts (congenital/acquired)
↓ Excretion Cholestasis: Obstructive or functional


Physiologic Prolonged fasting (dogs, cats)
Enterohepatic Intestinal malabsorption, rapid gastrointestinal transit


Interpret with: Urea nitrogen and creatinine, bilirubin (don’t run if cholestatic), liver analytes, hemogram (e.g. microcytosis seen with shunts)



Artifact In vitro or in vivo hemolysis, citrate anticoagulant


Iatrogenic Physostigmine
Toxins Organophosphate or carbamate toxicity, cyanotoxins


B-hydroxybutyrate (BHB)

Increased At risk of hepatic lipidosis due to increased lipolysis
Negative energy balance with excess lipolysis Cattle: Negative energy balance (e.g. lactation demands, pregnancy, illness), alimentary ketosis (spoiled silage with excess butyric acid)
Small ruminants: Negative energy balance, e.g. pregnancy toxemia 
Camelids: Negative energy balance (e.g. stress, anorexia, pregnancy, lactation
Small animals: Diabetes mellitus (small animals), negative energy balance (lactating bitches, starvation), can become ketotic


Interpret with: Glucose, NEFA, triglycerides, liver analytes



Increased Increased lipolysis (increased risk of hepatic lipidosis)
Artifact Serum separator tubes, non-cooled samples, delayed sample testing
Physiologic Exercise, stress, collection before daily feeding
Negative energy balance Food deprivation, stress etc, pregnant dairy cows or dairy cows in early lactation
Endocrine Diabetes mellitus


Interpret with: BHB, Glucose



Persistent hyperglycemia Diabetes mellitus


Artifact Hypoalbuminemia
Persistent hypoglycemia Insulinoma (dogs)
Idiopathic Hyperthyroidism (cats)


Interpret with: Glucose
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