ACTH is a polypeptide hormone of the anterior lobe of the pituitary gland (hypophysis) that stimulates growth of the adrenal cortex or secretion of its hormones. Indicator used in the differential diagnosis of hypercortisolism and adrenocortical insufficiency.

Increased: central Cushing syndrome—pituitary ACTH secreting adenoma (usually microadenomas), hypothalamic hyperfunction (increased corticotropin-releasing hormone), ACTH therapy, Addison’s disease, ectopic ACTH syndrome

Decreased: adrenal Cushing syndrome (adrenal adenoma, adrenal hyperplasia, adrenal carcinoma), iatrogenic hypercortisolism (long-term glucocorticoid therapy)

Albumin is a transport protein for small molecules, including bilirubin, calcium, magnesium, progesterone, and various medications. Its oncotic pressure serves to keep the fluid in the blood and avoid it leaking out into the tissues. The test helps assess protein absorption or malnutrition of the body and determine whether the patient has liver or kidney disease.

Increased: dehydration, shock

Decreased: cystic fibrosis, proteinuric glomerular kidney disease, cirrhosis, Hodgkin’s disease, malnutrition, nephrotic syndrome, multiple myeloma, inflammatory bowel disease, leukemia, collagen-vascular diseases

Normal:

<30 mg/g

<17 mg/g (men)

<25 mg/g (women)

<30 mg/24 hr

Microalbuminuria:

30–300 mg/g (either sex)

17–300 mg/g (men)

25–300 mg/g (women)

30–300 mg/24 hr

Macroalbuminuria:

>300 mg/24 hr

It is used to measure albuminuria as a sign of kidney disease, or in diabetes and hypertension as a marker which may lead to kidney disease and/or cardiovascular risk.

Microalbuminuria: chronic kidney disease, diabetes mellitus, congestive cardiac failure, acute or chronic obstructive airways disease, hypertension, malignancy

Plasma: supine 2–9 ng/dL [SI units: 55–250 pmol/L]

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  Standing: 7–20 ng/dL [SI units: 195–555 pmol/L]

Urine: 5–19 mcg/day [SI units: 14–53 nmol/day]

Adrenal glands release the hormone aldosterone which maintains blood volume and pressure. Blood pressure increases when aldosterone increases the tubular reabsorption of sodium by the kidneys. It also causes renal excretion of potassium. Renin levels should usually be measured simultaneously to assess whether a high aldosterone is primary (with low renin) or secondary (with high renin).

Increased: primary hyperaldosteronism, secondary hyperaldosteronism, very low-sodium diet

Decreased: Addison’s disease, very high-sodium diet, hyporeninemic hypoaldosteronism

This is a group of enzymes that hydrolyze many orthophosphoric monoesters and are present ubiquitously (liver, kidney, bones, intestine, and placenta).

Increased: physiological—during growth, last trimester of pregnancy, rickets, osteomalacia, ulcerative colitis, bowel perforation, fatty liver, hepatitis, hyperparathyroidism, bone resorption, hyperthyroidism

Decreased: vitamin D intoxication, pernicious anemia, hypothyroidism, celiac sprue, malnutrition, fibrate therapy

30–110 U/L [SI units: 0.4–1.4 μkat/L]

Enzyme amylase is generated in the pancreas and salivary glands. It is released into the blood on injury to the pancreas (diseased or inflamed), or less commonly, the parotid gland. It helps in assimilation of carbohydrates.

Increased: acute pancreatitis, pancreatic duct obstruction, alcohol ingestion, mumps, parotitis, renal disease, cholecystitis, peptic ulcers, intestinal obstruction, mesenteric thrombosis, postoperative abdominal surgery

Decreased: liver damage, pancreatic destruction (pancreatitis, cystic fibrosis)

This is an important enzyme in the renin-angiotensin-aldosterone system and the kallikrein-kinin system. ACE’s effects are based on the direct vasoconstrictive effect of angiotensin II conversion from angiotensin I as well as increased catabolism of the vasodilatory bradykinins. ACE is found in the endothelial cells of the vascular system, particularly in the lungs and kidneys. It is an indicator in the diagnosis and course of sarcoidosis.

Increased: sarcoidosis (Besnier-Boeck-Schaumann disease), silicosis, asbestosis, tuberculosis, alcoholic liver disease, Gaucher disease, kidney diseases, hyperparathyroidism, hyperthyroidism, diabetes mellitus

8–12 mEq/L [SI units: 8–12mmol/L]

The anion gap is the difference between the major positive and negative ions in serum, plasma, and urine.

Calculate: Anion gap = (Na ⁺ ) – (HCO ₃ ^– + Cl ^– )

Increased: lactic acidosis, high anion gap metabolic acidosis (e.g., DR. MAPLES mnemonic: Diabetic ketoacidosis, Renal failure, Methanol, Aspirin, Paraldehyde/Propylene glycol/Pyroglutamic acid, Lactic acid, Ethylene glycol/Ethanol ketoacidosis, Starvation ketoacidosis)

Decreased: hypoalbuminemia, multiple myeloma, increased potassium, calcium or magnesium, lithium or bromide toxicity

The ANA detects antibodies to all nuclear antigens present in serum by an indirect immunofluorescence assay. Since the test is nonspecific, it may be positive in many autoimmune conditions and at low titers (1:40–1:80) in up to 20%–25% of normal persons. When positive at higher titers, autoimmune or connective tissue diseases are more likely, but more specific antibody testing is needed for better differentiation (shown below).

Positive: connective tissue disease—systemic lupus erythematosus (anti-dsDNA; anti-Sm), drug-induced lupus (anti-histone), Sjögren’s syndrome (anti-Ro/La), rheumatoid arthritis (rheumatoid factor; anti-CCP), scleroderma or systemic sclerosis (anti-Scl-70; anti-centromere), mixed connective tissue disease (anti-RNP), polymyositis or dermatomyositis (anti-PM-1; anti-Jo-1). Other conditions: autoimmune hepatitis, primary biliary cirrhosis (antimitochondrial), chronic hepatitis C, ulcerative colitis, Crohn’s disease, subacute bacterial endocarditis

Negative: negative predictive value for lupus

ANCA tests for autoantibodies to antigens in neutrophil cytoplasm; c-ANCA staining diffusely in the cytoplasm and p-ANCA in a perinuclear pattern.

Positive: c-ANCA, usually anti-proteinase 3 (PR3)—granulomatosis with polyangiitis (formerly Wegener’s), pauci-immune glomerulonephritis, Churg-Strauss syndrome; p-ANCA, usually anti-myeloperoxidase (MPO)—microscopic polyangiitis, pauci-immune necrotizing “renal-limited vasculitis” glomerulonephritis (may be positive in anti-GBM nephritis also), Churg-Strauss syndrome, drug-induced vasculitis, other connective tissue diseases, ulcerative colitis, Crohn’s disease, autoimmune hepatitis, sclerosing cholangitis

Total: 0.3–1.2 mg/dL [SI units: 5–20 µmol/L]

Direct: 0–0.3 mg/dL [SI units: 0–5.1 µmol/L]

Indirect: 0.2–0.6 mg/dL [SI units: 3.4–10.2 µmol/L]

Bile is produced by the liver and contains yellowish pigment bilirubin.

Increased total: hepatic damage (hepatitis, toxins, cirrhosis), biliary obstruction, hemolysis, fasting, Gilbert’s syndrome, hemolytic anemia

Increased direct (conjugated): biliary obstruction/cholestasis, drug-induced cholestasis

Arterial: 22–27 mEq/L [SI units: 22–27 mmol/L]

Venous: 23–29 mEq/L [SI units: 23–29 mmol/L]

Bicarbonate is a buffer that maintains the pH of the blood from getting too acidic or too alkaline (basic).

Increased: severe vomiting, pulmonary insufficiency, Cushing syndrome, hyperaldosteronism, metabolic alkalosis, respiratory acidosis (compensatory)

Decreased: Addison’s disease, chronic diarrhea, diabetic ketoacidosis, kidney failure, salicylate toxicity, ethylene glycol or methanol poisoning, metabolic acidosis, respiratory alkalosis (compensatory)

7–20 mg/dL [SI units: 2.5–7.14 mmol/L]

The test evaluates the amount of urea nitrogen in the blood to evaluate kidney function. Urea is a by-product of protein breakdown produced by the liver.

Increased: acute kidney injury, renal failure, prerenal azotemia (hypotension, septic shock, volume depletion), postrenal (obstruction), gastrointestinal (GI) bleeding, catabolic states, drugs (corticosteroids, amino acid infusions), high protein intake

Decreased: starvation, liver failure, pregnancy, infancy, overhydration

Between 10:1 and 20:1

Increased: prerenal failure, GI bleeding, catabolic states, postrenal obstruction, steroids, tetracycline

Decreased: hepatic insufficiency, rhabdomyolysis (creatinine rises more than BUN), malnutrition

Calcium, total serum

8.5–10.2 mg/dL [SI units: 2.0–2.6 mmol/L]

Calcium, ionized serum

4.8–5.3 mg/dL [SI units: 1.2–1.4 mmol/L]

Calcium is essential for the proper contraction of the muscles and blood vessels and for the efficient conduction of impulses through the nervous system and in the secretion of hormones by the endocrine system. Bones and teeth act as the chief stores of calcium in the body along with blood and other tissues of the body. Serum calcium is approximately 50% ionic and 50% bound to albumin and anions.

Increased: malignancies—non-Hodgkin’s lymphoma, multiple myeloma, breast and other cancers, primary hyperparathyroidism, tertiary hyperparathyroidism, hyperthyroidism, adrenal insufficiency, Paget’s disease, 1, 25 dihydroxy vitamin D overproduction (tuberculosis, sarcoidosis, fungal diseases, berylliosis); drugs–hypervitaminosis of A or D, calcitriol, lithium, thiazides, theophylline toxicity, tamoxifen, milk-alkali syndrome

Decreased: hypoparathyroidism, insufficient vitamin D, hypomagnesemia, renal tubular acidosis, hypoalbuminemia, chronic renal failure (phosphate retention), acute pancreatitis, alcoholism

Males <19 pg/mL [SI units: <19 ng/L]

Females <14 pg/mL [SI units: <14 ng/L]

Calcitonin is a hormone produced in the C cells of the thyroid gland that downregulates blood calcium, opposing the action of parathyroid hormone (PTH) and vitamin D.

Increased: malignant diseases—medullary thyroid cancer, lung cancer, insulinomas, VIPomas; nonmalignant diseases—newborns, pregnancy, renal failure, Zollinger-Ellison syndrome (associated with men), pernicious anemia