Sodium
| Increased | |
| 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 |
| Decreased | |
| 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 |
Potassium
| Increased | |
| 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 (ICF → ECF) |
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 |
| Decreased | |
| 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 |
Chloride
| Increased | |
| Artifact | Lipemia (chylomicrons, high VLDL), anticonvulsant medication (KBr, zonisamide) |
| Iatrogenic | Administration of Cl–containing 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) |
| Decreased | |
| 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, |
Bicarbonate
| Increased | |
| 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) |
| Decreased | |
| 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
| Increased | |
| 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) |
| Decreased | |
| 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 |
Glucose
| Increased | |
| 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 |
| Decreased | |
| 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
| Increased | |
| ↑ 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 |
| Decreased | |
| ↓ 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 |
Creatinine
| Increased | |
| 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 |
| Decreased | |
| Physiologic | Pregnancy (↑ GFR) |
| ↓ Production | Starvation, cachexia, decreased muscle mass |
| ↑ GFR | Portosystemic shunts |
| Interpret with: | Urea nitrogen, liver analytes |
Uric acid
| Increased | |
| Artifact | Dehydation, fecal urate contamination |
| Physiologic | Post-prandial |
| Renal disease | ↓ GFR, Loss of >70% functional renal capacity |
| ↑ Deposition | Articular gout |
Bilirubin (indirect, unconjugated)
| Increased | |
| 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)
| Increased | |
| ↓ 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) |
ALP
| Increased | |
| 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 |
GGT
| Increased | |
| 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 |
ALT
| Increased | |
| 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 |
AST
| Increased | |
| 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) |
SDH
| Increased | |
| 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 |
GLDH
| Increased | |
| Physiologic | Neonates (foals) |
| Liver | Hepatocellular injury (periacinar, mitochondrial) |
| Interpret with: | Other liver analytes |
CK
| Increased | |
| 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 |
LDH
| Increased | |
| 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.
| Increased | |
| Proportional (albumin and globulins) | Dehydration or fluid losses |
| Disproportional | Increased albumin (uncommon) Increased globulins (more common; see below) |
| Decreased | |
| Proportional (albumin and globulins) | Blood loss, protein-losing enteropathy, overdilution with fluids |
| Disproportional | Decreased albumin (common) Decreased globulins (uncommon; see below) |
Albumin
| Increased | |
| Artifact | Heparinized plasma > serum |
| Physiologic | Hemoconcentration |
| Increased production | Hepatocellular carcinoma, exogenous corticosteroids |
| Decreased | |
| 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 |
Globulins
| Increased | |
| ↑ 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.
Calcium
| Increased | |
| 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) |
| Decreased | |
| 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 |
Phosphate
| Increased | |
| 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 |
| Decreased | |
| 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 |
Magnesium
| Increased | |
| 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) |
| Decreased | |
| 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 |
Cholesterol
| 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 |
| Decreased | |
| 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 |
Triglycerides
| 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) |
Amylase
| Increased | |
| Pancreatic cell injury | Acute pancreatitis |
| ↓ Renal excretion | ↓ GFR (usually renal azotemia) |
| Unclear mechanism | Intestinal disease or obstruction |
| Interpret with: | Lipase |
Lipase
| Increased | |
| 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 |
Iron
| Increased | |
| 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 |
| Decreased | |
| 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 |
TIBC
This is an indirect measure of transferrin, the iron transport protein
| Increased | |
| 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) |
| Decreased | |
| ↓ 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 |
Saturation
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).
| Increased | |
| ↓ Transferrin | Loss or decreased production (e.g. protein-losing states) |
| Secondary to increased iron | See above (TIBC normal or rarely decreased) |
| Decreased | |
| Secondary to decreased iron | See iron above (TIBC usually normal) |
| Interpret with: | Iron panel, CBC (inflammation, anemia), protein (albumin, globulin) |
Bile Acids
| Increased | |
| 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 |
| Decreased | |
| 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) |
Cholinesterase
| Increased | |
| Artifact | In vitro or in vivo hemolysis, citrate anticoagulant |
| Decreased | |
| 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 |
NEFA
| 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 |
Fructosamine
| Persistent hyperglycemia | Diabetes mellitus |
| Decreased | |
| Artifact | Hypoalbuminemia |
| Persistent hypoglycemia | Insulinoma (dogs) |
| Idiopathic | Hyperthyroidism (cats) |
| Interpret with: | Glucose |
