Sodium
| Increased | |
| False change | Water loss from blood sample (inadequate capping) |
| Iatrogenic | Hypertonic fluids, e.g. electrolyte replacers (particularly if not given access to water), chemical diuresis (water deficits) |
| Water deficit | Excess “pure” water loss: Panting (e.g. fever, heat stroke), diabetes insipidus Inadequate intake: Water deprivation, primary adipsia or hypodipsia Hypotonic for isotonic fluid loss and inability to conserve water or drink: Renal: Causes of polyuria, such as osmotic diuresis, nonoliguric or polyuric renal failure, post-obstructive diuresis Gastrointestinal (vomiting, diarrhea) Other causes: Cutaneous, third space losses |
| Salt gain | Excess intake: Salt poisoning (with concurrent water deprivation) ↑ Renal retention: Hyperaldosteronism |
| Decreased | |
| False change | Lipemia (chylomicrons, high VLDL), hyperglobulinemia (uncommon) |
| Iatrogenic | Diuretic therapy, hypotonic fluid administration, mannitol (solvent drag from hyperosmolality) |
| Hyperosmolar states (solvent drag) | Diabetes mellitus |
| Volume overload (hypervolemic hyponatremia with inappropriate ADH release due to perceived volume depletion) | Congestive heart failure, hepatic disease, nephrotic syndrome, advanced renal failure |
| Hypotonic or isotonic fluid losses with dilution (ADH or drinking) or hypertonic fluid losses with dilution (hypovolemic hyponatremia) | Renal: Proximal renal tubule dysfunction, hypoadrenocorticism, hypoaldosteronism, osmotic diuresis (diabetes mellitus) Gastrointestinal: Vomiting and diarrhea (e.g. secretory diarrhea causes hypertonic losses) Other: Cutaneous (sweating in horses), third space losses (ruptured or obstructed urinary tract, peritonitis, repeated drainage of thoracic effusion) |
| Other | Intracellular translocation (muscle injury), decreased intake (ruminants) |
| Interpret with: | Electrolytes (K+, Cl–), urinalysis, HCT, protein, urea nitrogen, creatinine, osmolality |
Potassium
| Increased | |
| False change | 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 < 5 months of age versus adults), intravenous (IV) line contamination with potassium-containing fluids |
| Iatrogenic | IV fluids with K+ supplementation (rare unless renal disease) |
| Transcellular shifts (ICF → ECF) |
Tissue necrosis (e.g. hyperkalemic myopathy, tumor lysis syndrome), hypertonicity (diabetes mellitus), uroperitoneum (foals, small animals), primary strong ion metabolic acidosis (transient) |
| ↓ Renal excretion | Anuric or oliguric renal failure, chronic kidney disease (horses), uroabdomen, hypoaldosteronism |
| Decreased | |
| False change | 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 (transient) or metabolic alkalosis, hyperinsulinemia, catecholamine release, endotoxemia (may work via insulin) |
| ↑ Loss | Gastrointestinal: Gastric vomiting, abomasal stasis, gastric outflow obstruction or torsion, and saliva loss (e.g. choke in horses, cattle); Renal: ↑ aldosterone, ↑ distal tubular flow rate, renal tubular disease Other: Third space loss (e.g. peritonitis) or sequestration (e.g. ileus, cutaneous (e.g. sweating in horses) |
| Interpret with: | Electrolytes, UN, creatinine, urinalysis, bicarbonate, AG, blood gas analysis |
Chloride
| Increased (low strong ion difference, SID) | See changes in sodium of changes in chloride reflect those occurring in sodium or the strong ion difference is normal. |
| False change | Anticonvulsant medication (potassium bromide, zonisamide) |
| Iatrogenic | Administration of Cl–containing fluids (hypertonic saline, ammonium chloride) |
| Primary strong ion metabolic acidosis (“hyperchloremic” or normal anion gap) | Bicarbonate loss: Vomiting (biliary, pancreatic fluids), secretory diarrhea (e.g. calves), sequestration (e.g.. distal intestine in horses), loss of saliva (ruminants, horse), renal loss (proximal renal tubular acidosis) Chloride-containing acid gain: Distal renal tubular acidosis, hyperaldosteronism |
| Secondary strong ion metabolic acidosis | In compensation for a chronic respiratory alkalosis (e.g. hyperventilation from pain, fever, hypoxemia, lung disease) by decreasing renal excretion of acid (reduced ammoniagenesis) |
| Decreased (high SID) | See changes in sodium of changes in chloride reflect those occurring in sodium or the strong ion difference is normal. |
| Iatrogenic | Administration of high SID fluids (e.g. sodium bicarbonate), loop or thiazide diuretics |
| Primary metabolic alkalosis | Gastrointestinal: Loss of (H+)Cl– rich fluid (vomiting gastric contents, gastric reflux, gastroduodenal ulcers in horses), sequestration of Cl– rich fluid (displaced or torsed abomasum, abomasal atony, gastric rupture, gastric dilatation-volvulus in dogs, proximal intestinal ileus in horses) Cutaneous: Sweating in horses (loss of KCl) |
| Secondary metabolic alkalosis | In compensation for a chronic respiratory acidosis (e.g. central nervous system depression, severe pneumonia) by increasing renal excretion of acid (increased ammoniagenesis, stimulation of H+ antiporter) |
| Interpret with: | Electrolytes (Na+, K+), urinalysis, bicarbonate, AG, blood gas analysis, |
Bicarbonate
| Increased | |
| False change | Severe muscle injury (rare) |
| Iatrogenic | Administration of HCO3− containing solutions, loop or thiazide diuretics |
| Primary metabolic alkalosis | See decreased chloride with low strong ion difference above |
| Secondary metabolic alkalosis | In compensation for a chronic respiratory acidosis (e.g. central nervous system depression, severe pneumonia) by increasing renal excretion of acid (increased ammoniagenesis, stimulation of H+ antiporter) |
| Decreased | |
| False change | Aged samples (production of lactate in tube), heparin over-dilution, prolonged venous stasis |
| Iatrogenic | Ammonium chloride administration (induces a primary strong ion metabolic acidosis), sodium chloride administration, high negative dietary cation-anion diets in dairy cattle) |
| Strong ion metabolic acidosis (normal anion gap) | See increased chloride with low strong ion difference above for primary and secondary strong ion metabolic acidosis |
| Titration metabolic acidosis (high anion gap) | Accumulation of non-chloride containing non-volatile acids Endogenous: Lactic acidosis (L or D), ketoacidosis (e.g. diabetes mellitus in small animals, excess negative energy balance in camelids or ruminants), decreased excretion of renal acids (acute kidney injury or failure and less commonly chronic kidney disease), with failure of excretion of the daily acid load (decreased excretion of sulfates, hippurates, citrates, phosphates etc). Exogenous: Toxicity (ethylene glycol, salicylate, methanol) |
| Interpret with: | Blood gas analysis – Anion gap, electrolytes (corrCl–, K+), urinalysis, glucose, urea, creatinine |
Anion Gap
| Increased | |
| False change | False ↑ of sodium or potassium or ↓ chloride or bicarbonate |
| Iatrogenic | Sodium-containing drugs (e.g. penicillin, sodium salts) |
| Titration metabolic acidosis | Accumulation of non-chloride-containing non-carbonic acid (e.g. lactate, ketones, renal acids), toxins (methanol, salicylate, ethylene glycol): See low bicarbonate |
| Alkalemia (typically secondary to a chronic 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 | |
| False change | Falsely high chloride or bicarbonate, anticonvulsants (potassium bromide), muscle injury (false increase in bicarbonate from release of pyruvate and lactate dehydrogenase) |
| Iatrogenic | Bicarbonate-rich fluid administration |
| ↓ Albumin | Hypoalbuminemia (e.g. protein-losing nephropathy, negative acute phase response) |
| ↑ “Unmeasured” cations | Ionized magnesium or calcium (unlikely), neoplastic immunoglobulins (monoclonal gammopathy, e.g. multiple myeloma) |
| Interpret with: | Bicarbonate, electrolytes, blood gas analysis, urinalysis |
Glucose
| Increased | |
| Physiologic | Post-prandial, increased counter-regulatory hormones (cortisol), 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 or pituitary pars intermedia dysfunction (horses), pheochromocytoma |
| Decreased | |
| False change | Bacterial contamination of blood, serum or plasma left on cells (not separated from clot), severe hematrophic Mycoplasma infection (camelid, ruminant) |
| Iatrogenic | Insulin administration, xylitol (dogs, from increased insulin secretion) |
| ↓ Production | Glycogen storage diseases (e.g. Pompe’s disease, von Gierke’s disease), juvenile hypoglycemia, small breed hypoglycemia, hepatic synthetic dysfunction |
| ↓ Intake | Starvation, 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, paraneoplastic hypoglycemia (e.g. leiomyoma, leiomyosarcoma, hepatic and renal tumors, secrete insulin-like growth factor) |
| Interpret with: | Urinalysis, fructosamine, ketones, liver analytes |
Urea Nitrogen
| Increased | |
| ↑ Protein catabolism | Fever, burns, corticosteroid administration, starvation. |
| ↑ Protein digestion | Hemorrhage into the upper gastrointestinal tract, high protein diet, ammonia toxicity cattle (increased protein production in rumen) |
| ↓ GFR | Pre-renal, renal, post-renal causes |
| Decreased | |
| ↓ Protein intake, protein anabolism |
Low protein 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 | |
| False change | Presence of acetoacetate, glucose, vitamin C, uric acid, pyruvate, cephalosporins and amino acids in sample with Jaffe but not enzymatic reaction (latter used at Cornell) |
| Physiologic | Neonatal foals, heavily-muscled horses, Greyhounds, post-high protein meal (uncommon) |
| ↓ GFR | Pre-renal, renal, post-renal causes |
| Decreased | |
| Physiologic | Pregnancy (↑ GFR), higher in premature or newborn foals |
| ↓ Production | Starvation or cachexia (resulting in reduced muscle mass), decreased muscle mass (smaller versus larger breed dogs) |
| ↑ GFR | Portosystemic shunts |
| Interpret with: | Urea nitrogen, liver analytes, urinalysis |
Uric acid (exotics)
| Increased | |
| False change | 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 | Hemolytic anemia, also called prehepatic icterus |
| ↓ Hepatic uptake (primarily indirect) |
Hepatic injury or dysfunction. This may also occur as a consequence of cholestatic disorders (hepatic dysfunction from retained bile acids). One type of “hepatic” icterus, but primary disease can also result in increased direct or conjugated bilirubin. |
| ↓ Hepatic conjugation | Hepatic injury or dysfunction. This may also occur as a consequence of cholestatic disorders (hepatic dysfunction from retained bile acids). |
| Inherited | Southdown sheep (defect in uptake) |
| Interpret with: | Hepatocellular injury (ALT, AST, SDH, GLDH) and cholestatic enzymes (ALP, GGT), urinalysis, CBC (evidence of a hemolytic anemia) |
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) from liver or biliary disease or downregulation of transporters by inflammatory cytokines (functional cholestasis). – Structural (intra or extra-hepatic) e.g. hepatocellular swelling, extrahepatic biliary tract obstruction (cholelithiasis, gallbladder mucocele, neoplasia, parasites), bile sludging in cats (with anorexia or dehydration). This is another type of “hepatic” icterus and when it involves the biliary tree primarily, it is called “post-hepatic” icterus by some pathologists. – Functional: Bacterial sepsis, severe inflammation (downregulation of transporters) |
| 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 (look for bilirubinuria which is excessive for the urine specific gravity in dogs and abnormal in any other species regardless of the urine specific gravity), CBC, cholesterol (often goes up in cholestatic disorders in dogs) |
ALP
| Increased | |
| Physiologic | Young animals, breed-associated (Siberian Huskies – benign familial hyperphosphatasemia) |
| Iatrogenic | Liver injury: Anticonvulsants (e.g. phenobarbital, primidone), thyroxine Induction: exogenous corticosteroid (dogs) |
| Hepatobiliary | Cholestasis (structural/functional); can be localized |
| Endocrine | Hyperthyroidism (cats, bone isoform), hyperadrenocorticism, chronic stress (increased endogenous corticosteroids) and other adrenal dysfunction in dogs |
| Increased osteoblastic activity | Hyperparathyroidism, fracture healing, osteosarcoma (dogs) |
| Other | Mammary tumors in dogs (mild increase) |
| Interpret with: | Other hepatic enzymes, bilirubin |
GGT
| Increased | |
| Physiologic | Neonates, breed (donkeys, burros have higher GGT activity than horses), marker of passive transfer of immunity in cattle (not crias or foals) |
| Iatrogenic | Anticonvulsants (phenobarbital, phenytoin, mysoline), exogenous corticosteroids (dogs) |
| Hepatobiliary | Cholestasis: Usually structural in nature; many causes Biliary hyperplasia: (e.g. pyrrolizidine alkaloids such as Senecio, Crotalaria, Heliotropium in grazing animals) Been noted to be increased in hyperadrenocorticism (without ALP activity) in dogs |
| Interpret with: | Bilirubin, other hepatic enzymes |
ALT
| Increased | |
| False change | 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 | |
| False change | Moderate to severe hemolysis (in vitro) and delayed serum or plasma separation from cells (leakage from red blood 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, and is located throughout the hepatic lobule) |
| Skeletal muscle* | Myopathies (e.g. muscular dystrophy), trauma, rhabdomyolysis, other myopathies, e.g. white muscle disease (vitamin E-selenium deficiency), clostridial myositis |
| * Based on sheer mass. There is not enough smooth or cardiac muscle tissue to reliably increase AST activity when tissues with these muscle types are injured | |
| Interpret with: | Other liver analytes, hemolytic index (may be increased > 200 hemolytic units) and CK (help rule down muscle source). Does have a longer half life than CK. |
SDH
| Increased | |
| False change | Can increase if broken into subunits with storage with storage (uncommon) |
| Liver injury | Any cause (it is in a cytosolic location) |
| Interpret with: | Other liver analytes |
GLDH
| Increased | |
| Physiologic | Neonates (foals) |
| Liver | Hepatocellular injury (located in the periacinar region or zone 3 of the liver and is a mitochondrial enzyme) |
| Interpret with: | Other liver analytes |
CK
| Increased | |
| False change | In vitro or in vivo moderate to severe hemolysis (RBC constituents participate in reaction) |
| Physiologic | Age (puppies), post-exercise (horse), anorexia (cats) |
| Iatrogenic | Muscle injury: Muscle penetration during venipuncture (“muscle stick”), intramuscular injection, especially with irritant drugs (e.g. tetracycline), pentobarbitone (hamsters), post-surgery |
| CK-1(MM) isotype | Skeletal muscle isoenzyme: Any myopathy, e.g. exertional rhabdomyolysis, polymyositis, vitamin E-selenium deficiency, snake bite poisoning, trauma with shipping (horses), recumbent or “downer” cows |
| CK2-(MB) isotype | Cardiac muscle: Doxorubicin-induced cardiotoxicity |
| CK3-(BB) isotype | Brain: Thiamine deficiency (ruminants), cerebrocortical necrosis |
| Skeletal muscle injury (see comment for AST) | Various myopathies, including nutritional (e.g. white muscle disease), inherited (e.g. hyperkalemic periodic paralysis, malignant hyperthermia in dogs and pigs) and toxins (monensin, gossypol, ricin) |
| Interpret with: | Hemolytic index (may be increased > 100 hemolytic units), AST activity |
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 globulin concentrations.
| Increased | |
| Proportional (albumin and globulins) | Fluid losses (relative change) |
| 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 | |
| False change | Heparinized plasma > serum |
| Physiologic | Hemoconcentration (relative change) |
| ↑ production | Hepatocellular carcinoma, exogenous corticosteroids |
| Decreased | |
| Iatrogenic | Excessive fluid administration |
| ↓ Production | Severe malnutrition or starvation, hepatic synthetic dysfunction, 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 (proteinuria that is in excess for the urine specific gravity), urea nitrogen and creatinine, liver analytes or function tests |
Globulins
| Increased | |
| ↑ Production | α-globulins: Acute phase reactant response, corticosteroids (dogs) β-globulins: Increase in immunoglobulins from antigenic stimulation, 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 not the other globulins |
| 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) on cattle, Lawsonia in horses |
| 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 administration |
| ↑ Bone mobilization | ↑ PTH: Primary hyperparathyroidism (dogs and horses: parathyroid adenoma – more common, parathyroid hyperplasia, malignant parathyroid carcinoma – rare) ↑ PTH related peptide (PTHrP): Humoral hypercalcemia of malignancy (e.g. dogs – anal sac adenocarcinomas, lymphoma, squamous cell carcinoma in horses; lymphoma and pulmonary carcinoma in cats) 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 (particularly horses with chronic renal failure), hypoadrenocorticism, primary hyperparathyroidism, humoral hypercalcemia of malignancy |
| ↑ Protein binding | Hyperalbuminemia |
| Unknown cause | 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) |
| False change | EDTA, citrate anticoagulants |
| Iatrogenic | Sodium-phosphate enemas, exogenous calcitonin |
| ↓ Protein binding | Hypoalbuminemia |
| Abnormal PTH | Primary hypoparathyroidism, pseudohypoparathryoidism, PTH resistance, ↓ secretion (secondary to 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) Gastrointestinal disease: Horses (colic, enterocolitis, endotoxemia); protein-losing enteropathy (dogs) Hyperadrenocorticism (dogs) |
| ↑ Loss | Renal: Hypoparathyroidism, increased calcitonin (sepsis, C-cell tumors), acute kidney injury (horses), renal disease (dogs, cats) Fetus and milk: Pregnancy, parturient or lactational hypocalcemia or eclampsia Cutaneous: Excess sweating in horses |
| ↑ Binding or precipitation | Pancreatitis, ethylene glycol toxicity |
| Unknown cause | Idiopathic hypocalcemia (foals), equine myopathy, cantharidin toxicosis |
| Interpret with: | Albumin, ionized calcium, phosphate, urea nitrogen, creatinine, urinalysis |
Phosphate
| Increased | |
| False change | In vitro hemolysis especially with storage, monoclonal gammopathy |
| Physiologic | Post-prandial (mild to no increase), 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 (renal or post-renal azotemia), hypoparathyroidism, acromegaly, hyperthyroidism Reduced salivary excretion in sick ruminants |
| Decreased | |
| False change | 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, catecholamines, insulin or glucose administration |
| ↑ Loss | Renal: Renal disease, hyperparathyroidism, urolithiasis (loss via saliva in ruminants), diuresis (osmotic or solute), phosphatonins (urinary loss), hyperadrenocorticism (dogs) Gastrointestinal: Diarrhea, vomiting Fetus and milk: Post-parturient cattle |
| Unknown cause | Hepatic lipidosis (cat), hypothermia |
| Interpret with: | Calcium, urea nitrogen, creatinine |
Magnesium
| Increased | |
| False change | Severe hemolysis (>800 hemolytic index units), 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 or anuric renal failure), hypocalcemia, hypoadrenocorticism |
| Release from cells | Myopathy, soft tissue necrosis, tumor lysis syndrome |
| ↑ PTH | Hyperparathyroidism (rare) |
| Decreased | |
| False change | 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 | Gastrointestinal: 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, VLDL or chylomicrons |
| ↑ 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 (dogs) |
| Endocrine disorders | Diabetes mellitus, pancreatitis, hyperadrenocorticism |
| Decreased | |
| False change | Severe icterus |
| ↓ Absorption | Malabsorption, maldigestion (protein-losing enteropathies, exocrine pancreatic insufficiency) |
| ↓ Production | Liver synthetic dysfunction (chronic liver disease, synthetic liver failure, such as from massive necrosis), 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 syndromes (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 frequently than amylase in this condition) |
| Interpret with: | Amylase |
Iron
| Increased | |
| False change | In vitro or in vivo hemolysis with storage |
| Physiologic | Random transient variation |
| Iatrogenic | Corticosteroids (dogs, horses), iron administration, hemosiderosis from repeated blood transfusions |
| Intracellular release | Hepatocellular injury (e.g. necrosis) |
| ↑ RBC turnover | Hemolytic anemia, disordered or abnormal erythropoiesis (e.g. primary myelodysplasia and ineffective erythropoiesis, precursor-directed immune-mediated anemia) |
| ↓ Erythropoeisis | Bone marrow aplasia or hypoplasia, pure red cell aplasia |
| Hemochromataosis | Mynah birds, lemurs, Saler or Saler-cross cattle |
| Decreased | |
| False change | Anticoagulant chelation (e.g. EDTA) |
| Physiologic | Random transient fluctuation |
| 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 | |
| False change | 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 | Most common cause is inflammation (of > 24 hours duration) |
| ↓ Production | Acute phase response (most common cause), hepatic synthetic dysfunction, portosystemic shunts, ↓ protein intake |
| Loss of transferrin | Protein-losing nephropathy, protein-losing enteropathy, burns (decreases generally parallel albumin) |
| Transferrin catabolism | Negative energy states |
| 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 (mild increase; not equidae) |
| ↓ Clearance from portal circulation | Hepatic insufficiency or failure, portosystemic shunts (congenital or acquired), microvascular dysplasia |
| ↓ 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 | |
| False change | 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) |
| False change | 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 | |
| False change | Hypoalbuminemia |
| Persistent hypoglycemia | Insulinoma (dogs) |
| Idiopathic | Hyperthyroidism (cats) |
| Interpret with: | Glucose |
