1 ANA [ < 80 titre Immunofluorescence / < or = 1.0 IU/mL ELISA (negative) ]

Although many methods are available for ANA detection, the indirect immunofluorescence antinuclear antibody test (IF-ANA) and enzyme immunoassay (EIA)/enzyme linked immunosorbent assay (ELISA) are commonly used.

For the ANA test, 1 part of the serum is diluted into 40 parts of diluent (called a “1:40” titre). This diluted sample is tested for the presence of ANA antibodies. If the test is positive, a new sample is made at half the strength (1:80) and tested for the presence of ANA. The test is repeated every time it is positive by diluting the sample to 1:160, 1:320, 1:640, 1:1280, and finally 1:2560.

The lowest dilution is 1:2560. When antibodies are present at the lowest dilution, this indicates that there is a very high number of antibodies in the blood, and that the body has mounted a substantial immune response against nuclear proteins.

25-30% of the population will have a titer positive at 1:40
10% of the population will have a titer positive at 1:80
5% of the population will have a titer positive at 1:160
3% of the population will have a titer positive at 1:320

1:1280 for a strongly positive ANA, or 1:160 for a weaker, borderline positive ANA. An alternative method involves reporting the intensity of fluorescence, in international units per millilitre (IU/mL), at a pre-determined dilution.

< or = 1.0 IU/mL (negative)
1.1-2.9 IU/mL (weakly positive)
3.0-5.9 IU/mL (positive)
> or = 6.0 IU/mL (strongly positive)

A positive ANA may prompt additional serologic testing targeted to the suspected Connective Tissue Disease:

SLE: anti-dsDNA, anti-Sm, anti-RNP, anti-Ro
Scleroderma: anti-Scl-70, anticentromere
Sjögren’s syndrome: anti-Ro, anti-La
Polymyositis / Dermatomyositis: anti-Jo-1
Drug induced lupus: antihistone
MCTD (Mixed Connective Tissue Disease): anti-RNP
CREST (calcinosis, Raynaud disease, esophageal motility disorder, sclerodactyly, and telangiectasia): anticentromere

Intermediate or high ANA titers can be seen in unaffected relatives of patients with connective tissue disease, elderly patients, pregnant women, patients with chronic infections, malignancy, and as noted above, in healthy individuals.

2 Anti-dsDNA [ < 30.0 IU/mL (negative) ]

Double-stranded DNA (dsDNA) antibodies are systemic lupus erythematosus (SLE)-specific antibodies and are part of the immunology domain of the 2019 European League Against Rheumatism (EULAR) / American College of Rheumatology (ACR) classification criteria for SLE.

< 30.0 IU/mL (negative)
30.0-75.0 IU/mL (borderline)
> 75.0 IU/mL (positive)

A positive result for double-stranded DNA (dsDNA) IgG antibodies in the appropriate clinical context is highly suggestive of systemic lupus erythematosus (SLE). The presence of dsDNA IgG antibodies detected using the Crithidia Luciliae Indirect Immunofluorescence Test (CLIFT) is highly specific for SLE with moderate sensitivity. A negative result does not rule out a diagnosis of SLE.

The levels of antibodies to dsDNA may fluctuate with SLE disease activity. Increasing antibody levels may be associated with flares while decline or negative results may indicate response to treatment or disease remission.

3 Anti-RNP [ < 1.0 IU/mL (negative) ]

RNP (also called nRNP and U1RNP) is a small nuclear ribonucleoprotein that contains 3 protein autoantigens (called A, C, and 68 kD). Antibodies to RNP occur in approximately 50% of patients with lupus erythematosus (LE) and in patients with other connective tissue diseases, notably mixed connective tissue disease (MCTD). MCTD is characterized by high levels of RNP antibodies without detectable Sm (Smith) or double-stranded DNA (dsDNA) antibodies. MCTD resembles LE but is not accompanied by renal involvement.

< 1.0 IU/mL (negative)
> or =1.0 IU/mL (positive)

A positive result for RNP antibodies is consistent with a connective tissue disease. Although strongly associated with connective tissue diseases, RNP antibodies are not considered a “marker” for any particular disease except in the following situation: when found in isolation (ie, dsDNA antibodies and Sm antibodies are not detectable), a positive result for RNP antibodies is consistent with the diagnosis of mixed connective tissue disease.

4 Anti-Sm [ < 1.0 IU/mL (negative) ]

Anti-Smith (Sm) Antigen is a small nuclear ribonucleoprotein composed of several protein autoantigens designated B, B1, D, E, F, and G, which range in size from 11 kD to 26 kD. The levels of Sm antibodies remain relatively constant over time in patients with lupus erythematosus LE and are usually found in patients that also have RNP (ribonucleoprotein) antibodies.

< 1.0 IU/mL (negative)
> or =1.0 IU/mL (positive)

Sm antibodies are specific for lupus erythematosus (LE) and occur in approximately 30% of LE patients.

5 Anti-La [ < 1.0 IU/mL (negative) ]

Serum Autoantibodies to SS-B/La is an extractable nuclear antigen (ENA) composed of a 48-kD protein combined with RNA species. SS-B/La antibodies are found primarily in patients with Sjogren syndrome or lupus erythematosus (LE), where they occur with frequencies of approximately 60% and 15%, respectively.

< 1.0 IU/mL (negative)
> or =1.0 IU/mL (positive)

A positive result for SS-B/La antibodies is consistent with connective tissue disease, including Sjogren syndrome and lupus erythematosus.

6 Anti-Ro [ < 1.0 IU/mL (negative) ]

Autoantibodies to SS-A/Ro is an extractable nuclear antigen (ENA) composed of protein antigens of 52 kD and 60 kD combined with cytoplasmic RNA species. SS-A/Ro antibodies occur in patients with several different connective tissue diseases including Sjogren syndrome (up to 90% of cases); lupus erythematosus (LE) (40%-60% of cases); and rheumatoid arthritis.

SS-A/Ro antibodies are also associated with childhood LE, neonatal LE, and with congenital heart block in infants born to mothers with LE. SS-A/Ro antibodies have also been reported to be associated with features of extraglandular inflammation in patients with LE including vasculitis, purpura, cytopenias, and adenopathy.

< 1.0 IU/mL (negative)
> or =1.0 IU/mL (positive)

A positive result for SS-A/Ro antibodies is consistent with connective tissue disease, including Sjogren syndrome, lupus erythematosus (LE), or rheumatoid arthritis.

A positive result for SS-A/Ro antibodies in a woman with LE prior to delivery indicates an increased risk of congenital heart block in the neonate.

7 Anti-centromere [ < 1.0 IU/mL (negative) ]

Anti-centromere [ < 1.0 U (negative) ]

Anticentromere Antibodies occur primarily in patients with the calcinosis, Raynaud phenomenon, esophageal dysfunction, sclerodactyly, and telangiectasis (CREST) syndrome variant of systemic sclerosis (scleroderma).

< 1.0 IU/mL (negative)
> or =1.0 IU/mL (positive)

A positive test for centromere antibodies is strongly associated with CREST syndrome. In various reported clinical studies, centromere antibodies occur in 50% to 96% of patients with CREST syndrome.

Centromere antibodies have also been described in some patients with primary biliary cirrhosis, and may occur in patients with rheumatoid arthritis or lupus erythematosus.

8 Anti-Scl-70 [ < 1.0 IU/mL (negative) ]

Anti-Scl-70 antibodies are considered to be specific for scleroderma (systemic sclerosis) and are found in up to 60% of patients with this connective tissue disease. Anti-Scl-70 antibodies are more common in patients with extensive cutaneous involvement and interstitial pulmonary fibrosis, and are considered a poor prognostic sign. Evaluating patients with signs and symptoms of scleroderma and other connective tissue diseases in whom the test for antinuclear antibodies ANA is positive. Testing for Anti-Scl70 antibodies are not useful in patients without demonstrable antinuclear antibodies.

< 1.0 IU/mL (negative)
> or =1.0 IU/mL (positive)

A positive test result for Scl 70 antibodies is consistent with a diagnosis of scleroderma.

9 Anti-Scl-75 [ < 20 IU/mL (negative) ]

Anti-PM/Scl antibodies are present in sera from patients with polymyositis (PM), systemic sclerosis (SSc), and PM/SSc overlap syndromes. Among anti-PM/Scl-positive SSc patients, 10.4% and 7.1% were positive for anti-Scl-75 and anti-Scl-100 antibodies, respectively. The highest prevalences of reactivity to PM/Scl were detected in diffuse SSc (19.8%) and overlap syndromes (17.6%). Patients with diffuse SSc showed mainly an anti-PM/Scl-75 response, whereas most cases of overlap syndromes were characterized by reactivity to both PM/Scl antigens. The presence of anti-PM/Scl-75/100 antibodies was associated with muscular and lung involvements as well as with digital ulcers; pulmonary arterial hypertension was found less frequently. Anti-PM/Scl-75 antibodies were detected more frequently in younger and more active patients with joint contractures. Anti-PM/Scl-100 antibodies were associated with creatine kinase elevation; however, gastrointestinal involvements were observed less frequently.

< 20 IU/mL (negative)
20 – 39 IU/mL (weak positive)
40 – 80 IU/mL (moderate positive)
> 80 IU/mL (strong positive)

The anti-PM/Scl-75 antibody is specifically associated with calcinosis, ILD, pulmonary hypertension, gastrointestinal symptoms, as well as more active disease and joint contractures.

10 Anti-Scl-100 [ < 20 IU/mL (negative) ]

Anti-PM/Scl antibodies are present in sera from patients with polymyositis (PM), systemic sclerosis (SSc), and PM/SSc overlap syndromes. Among anti-PM/Scl-positive SSc patients, 10.4% and 7.1% were positive for anti-Scl-75 and anti-Scl-100 antibodies, respectively. The highest prevalences of reactivity to PM/Scl were detected in diffuse SSc (19.8%) and overlap syndromes (17.6%). Patients with diffuse SSc showed mainly an anti-PM/Scl-75 response, whereas most cases of overlap syndromes were characterized by reactivity to both PM/Scl antigens. The presence of anti-PM/Scl-75/100 antibodies was associated with muscular and lung involvements as well as with digital ulcers; pulmonary arterial hypertension was found less frequently. Anti-PM/Scl-75 antibodies were detected more frequently in younger and more active patients with joint contractures. Anti-PM/Scl-100 antibodies were associated with creatine kinase elevation; however, gastrointestinal involvements were observed less frequently.

< 20 IU/mL (negative)
20 – 39 IU/mL (weak positive)
40 – 80 IU/mL (moderate positive)
> 80 IU/mL (strong positive)

The anti-Scl-100 antibody is associated with younger age, calcinosis and has lower rates of gastrointestinal symptoms, interstitial lung disease ILD and pulmonary hypertension. There is also evidence of a possibly better survival compared to the presence of either anti-Scl-75 or anti-Scl-70 antibodies.

11 Anti-Jo-1 [ < 1.0 IU/mL (negative) ]

Jo 1 (histidyl tRNA synthetase) is a member of the amino acyl-tRNA synthetase family of enzymes found in all nucleated cells. Jo 1 antibodies evaluate patients with signs and symptoms compatible with a connective tissue disease, especially those patients with muscle pain and limb weakness, concomitant pulmonary signs and symptoms, Raynaud phenomenon, and arthritis.

Jo 1 antibodies are a marker for the disease polymyositis, and occur most commonly in myositis patients who also have interstitial lung disease. The antibodies occur in up to 50% of patients with interstitial pulmonary fibrosis and symmetrical polyarthritis.

< 1.0 IU/mL (negative)
> or =1.0 IU/mL (positive)

A positive result for Jo 1 antibodies is consistent with the diagnosis of polymyositis and suggests an increased risk of pulmonary involvement with fibrosis in such patients.

12 Anti-Mi-2 [ Negative ]

Anti-Mi-2 antibodies are found in 10-20% of adult dermatomyositis (DM) and <10% of juvenile DM. They are associated with classic DM features: mild to moderate weakness with shawl rash, heliotrope rash, V-sign, Gottron’ s papules and have good response to therapy, with lower incidence of cancer compared to Mi-2 negative DM.


13 Anti-TIF1 gamma [ < 20 IU/mL (negative) ]

Anti-TIF-1(P155) antibodies are present in 15-38% of adult dermatomyositis DM and 20-30% in juvenile DM. Highly associated with malignancy which is found in 50-75% of positive adult patients; 89% specificity and 78% sensitivity for diagnosing cancer associated DM; no cancer association in children.

< 20 IU/mL (negative)
20 – 39 IU/mL (weak positive)
40 – 80 IU/mL (moderate positive)
> 80 IU/mL (strong positive)

14 Anti-MDA-5 [ < 20 IU/mL (negative) ]

Anti-MDA5 antibodies are present in 7-35% of adult dermatomyositis (DM). Clinical features consist of absent or mild muscle symptoms (CADM), rapidly progressive interstitial lung disease (ILD), specific mucocutaneous features of skin ulcerations and papules, oral ulcerations and arthritis.

< 20 IU/mL (negative)
20 – 39 IU/mL (weak positive)
40 – 80 IU/mL (moderate positive)
> 80 IU/mL (strong positive)

15 Anti-SAE1 [ < 20 IU/mL (negative) ]

Anti-SAE 1 IgG autoantibody can be used to assist in the diagnoses and characterization of a subset of dermatomyositis (DM). It is highly specific for DM (>95%) and is present in 5-8% of the European DM population.

Initial disease onset may consist of mild myopathic features with severe skin involvement; however, extensive myalgia and muscle disease with weakness can appear as the disease progresses. It is associated with dysphagia and systemic symptoms (i.e. fevers, weight loss, increased inflammatory markers). In one cohort, an association with interstitial lung disease ILD and cancer had been found.

< 20 IU/mL (negative)
20 – 39 IU/mL (weak positive)
40 – 80 IU/mL (moderate positive)
> 80 IU/mL (strong positive)

16 Anti-NXP2 [ < 20 IU/mL (negative) ]

Anti-NXP-2 antibodies are present in 2-30% of adult DM and 18-25% of JDM. In JDM, they are associated with cutaneous calcinosis cutis. In adult DM, they are significantly associated with the presence of cancer (cancer was found in 13.6% of Anti-NXP-2 positive DM patients).

< 20 IU/mL (negative)
20 – 39 IU/mL (weak positive)
40 – 80 IU/mL (moderate positive)
> 80 IU/mL (strong positive)

17 Anti-Ku [ negative ]

Anti-Ku antibodies are found in about 20% of idiopathic inflammatory myopathies IIM; associated with overlap syndromes such as PM/SSc (most common), SLE/PM and other autoimmune disorders such as PM, SS, SSc, SLE, UCTD, MCTD, RA; common clinical features include arthralgias / arthritis, myositis, Raynaud’s, esophageal dysmotility and ILD.


18 Anti-SRP [ negative ]

SRP is considered a Myositis-specific antibody. It is commonly found in Polymyositis, ILD and arthritis, and occasionally in dermatomyositis. Anti-SRP was first described in a polymyositis patient in 1986. Anti-SRP antibodies are rare, in only about 4% of myositis patients, and are often found in African American females with an acute, severe onset of polymyositis, with poor response to therapy.


19 Anti-PL-7 [ negative ]

Anti-histidyl-tRNA synthetase autoantibodies are the most common MSA, comprising 30-40% of Idiopathic Inflammatory Myopathies (IIM), although PL-7 specifically is seen in less than 5% of IIM. Anti-Synthetase antibodies can be found in polymyositis, dermatomyositis or overlap myositis. Symptoms associated with these antibodies include nonerosive arthritis, ILD, fever, mechanic’s hands and Raynaud’s.


20 Anti-PL-12 [ negative ]

Anti-histidyl-tRNA synthetase autoantibodies are the most common MSA, comprising 30-40% of Idiopathic Inflammatory Myopathies (IIM), although PL-12 specifically is seen in less than 5% of IIM. Anti-Synthetase antibodies can be found in polymyositis, dermatomyositis or overlap myositis. Symptoms associated with these antibodies include non-erosive arthritis, ILD, fever, mechanic’s hands and Raynaud’s.


21 Anti-EJ [ negative ]

Anti-histidyl-tRNA synthetase autoantibodies are the most common Myositis Specific Antibodies (MSA), comprising 30-40% of Idiopathic Inflammatory Myopathies (IIM), although EJ specifically, is seen in less than 5% of IIM. Anti-Synthetase antibodies can be found in polymyositis, dermatomyositis or overlap myositis. Symptoms associated with these antibodies include non-erosive arthritis, ILD, fever, mechanic’s hands and Raynaud’s.


22 Anti-OJ [ negative ]

Anti-histidyl-tRNA synthetase autoantibodies are the most common Myositis Specific Antibodies (MSA), comprising 30-40% of Idiopathic Inflammatory Myopathies (IIM), although OJ specifically is seen in less than 5% of IIM. Anti-Synthetase antibodies can be found in polymyositis, dermatomyositis or overlap myositis. Symptoms associated with these antibodies include non-erosive arthritis, ILD, fever, mechanic’s hands and Raynaud’s.


23 Anti-histone [ < 1.0 IU/mL (negative) ]

Anti-histidyl-tRNA synthetase autoantibodies are the most common MSA, comprising 30-40% of Idiopathic Inflammatory Myopathies (IIM), although PL-12 specifically is seen in less than 5% of IIM. Anti-Synthetase antibodies can be found in polymyositis, dermatomyositis or overlap myositis. Symptoms associated with these antibodies include non-erosive arthritis, ILD, fever, mechanic’s hands and Raynaud’s.

< 1.0 IU/mL (negative)
1.0 – 1.5 IU/mL (weak positive)
1.6 – 2.5 IU/mL (moderate positive)
> 2.5 IU/mL (strong positive)

24 ANCA [ < 20 titre (negative) ]

cytoplasmic antineutrophil cytoplasmic antibodies (cANCA); perinuclear antineutrophil cytoplasmic antibodies (pANCA) evaluate patients suspected of having autoimmune vasculitis (both Wegener granulomatosis [WG] and microscopic polyangiitis).

Antineutrophil cytoplasmic autoantibodies (ANCA) are a serological marker associated with vasculitis and glomerulonephritis. Specifically, ANCA have been found (at frequencies ranging from 70% to 90%) in patients with active Wegener granulomatosis, microscopic polyarteritis nodosa, and idiopathic crescentic glomerulonephritis (with manifestations ranging from kidney-limited disease to extrarenal systemic disease, including pulmonary-renal syndromes). Glomerular lesions in patients with ANCA-associated systemic vasculitis or renal-limited disease are virtually identical. Normal controls are negative for ANCA and <10% of patients with other renal diseases are positive. ANCA may be directly involved in the pathogenesis of the vascular injury that causes the clinical manifestations in ANCA-associated disease.

Cytoplasmic (c−ANCA) titre
Perinuclear (p−ANCA) titre
< 1:20 titre (negative)
> 1:20 tire (positive)

Positive results for antineutrophil cytoplasmic antibodies (cANCA or pANCA) are consistent with the diagnosis of Wegener granulomatosis (WG), either systemic WG with respiratory and renal involvement or limited WG with more restricted end-organ involvement. Positive results for pANCA are consistent with the diagnosis of autoimmune vasculitis including microscopic polyangiitis (MPA) or pauci-immune necrotizing glomerulonephritis. Sequential measurements of titers of cANCA may be useful to indicate the clinical course of patients with WG. Changes in titer of 2 or more serial dilutions are considered significant. In patients with very low levels of cANCA, the immunofluorescent staining pattern may mimic the pANCA pattern. In patients with MPA, monitoring of disease activity may be performed by measuring MPO ANCA (MPO / Myeloperoxidase Antibodies, IgG, Serum).

24 Anti-Desmoglein 1&3 Antibody [ < 20 RU/ml (negative) ]

Pemphigus has been associated with autoantibodies to desmoglein (Dsg) dermal cell adhesion molecules. These autoantibodies cause epithelial blistering, which may lead to potentially severe malnutrition, dehydration, and infection. There are two major subtypes of pemphigus: pemphigus vulgaris and foliaceus characterized by autoantibodies to Dsg3 and Dsg1, respectively.

Method: Enzyme-Linked Immunosorbent Assay (ELISA)
Specimen Type: Serum

<20 RU/mL (negative)
≥20 RU/mL (positive)

<20 RU/mL (negative)
≥20 RU/mL (positive)

Anti-Desmoglein 1 Antibody: Postive –
Anti-Desmoglein 3 Antibody: Postive -> Pemphigus  vulgaris

Anti-Desmoglein 1 Antibody: Postive –
Anti-Desmoglein 3 Antibody: Negative -> Pemphigus folicaceus

Anti-Desmoglein 3 Antibody: Positive –
Anti-Desmoglein 1 Antibody: Negative -> Pemphigus vulgaris

Anti-Desmoglein 3 Antibody: Negative –
Anti-Desmoglein 1 Antibody: Negative -> Healthy or other diseases

25 Indirect immunofluorescence IMF

Indirect immunofluorescence, or secondary immunofluorescence, is a technique used in laboratories to detect circulating IgA autoantibodies in patient serum.

METHOD: Indirect Immunofluorescence Assay (IFA)

Indirect IMF is used to diagnose the following autoimmune blistering diseases:

  • Pemphigus vulgaris
  • Pemphigus foliaceus
  • Paraneoplastic pemphigus
  • Immunoglobulin (Ig)A pemphigus
  • Linear IgA bullous dermatosis and chronic bullous disease of childhood
  • Dermatitis herpetiformis
  • Bullous pemphigoid
  • Pemphigoid gestationis
  • Mucous membrane pemphigoid
  • Epidermolysis bullosa acquisita
  • Bullous systemic lupus erythematosus


1 BUN / Urea [ 2.8-7.7 mmol/L, or 7.84-21.56 mg/dL ]

Serum Blood Urea Nitrogen (BUN) or Urea is the final degradation product of protein and amino acid metabolism. In protein catabolism, the proteins are broken down to amino acids and deaminated. The ammonia formed in this process is synthesized to urea in the liver. This is the most important catabolic pathway for eliminating excess nitrogen in the human body.

1-17 years: 7-20 mg/dL
> or =18 years: 8-24 mg/dL
Reference values have not been established for patients who are <12 months of age.

1-17 years: 7-20 mg/dL
> or =18 years: 6-21 mg/dL
Reference values have not been established for patients who are <12 months of age.

High BUN may be due to prerenal causes (cardiac decompensation, water depletion due to decreased intake and excessive loss, increased protein catabolism, and high protein diet), renal causes (acute glomerulonephritis, chronic nephritis, polycystic kidney disease, nephrosclerosis, and tubular necrosis), and postrenal causes (eg, all types of obstruction of the urinary tract, such as stones, enlarged prostate gland, tumors).

Low BUN occurs in normal pregnancy, decreased protein intake, with intravenous fluids, with some antibiotics, and in some but not all instances of liver disease.

BUN determinations are considerably less sensitive than BUN clearance (and creatinine clearance) tests, and levels may not be abnormal until the BUN clearance has diminished to less than 50%. With creatinine, BUN is used to monitor patients on dialysis.

2 Creatinine [ 35-97 umol/L, or 0.40-1.10 mg/dL ]

Creatinine is a chemical compound left over from energy-producing processes in your muscles. Healthy kidneys filter creatinine out of the blood. Creatinine exits your body as a waste product in urine. A creatinine test is a measure of how well your kidneys are performing their job of filtering waste from your blood.

35-97 umol/L, or 0.40-1.10 mg/dL

High creatinine:
Renal diseases and insufficiency with decreased glomerular filtration, urinary tract obstruction, reduced renal blood flow including congestive heart failure, shock, and dehydration; rhabdomyolysis can cause elevated serum creatinine.

Low creatinine:
Small stature, debilitation, decreased muscle mass; some complex cases of severe hepatic disease can cause low serum creatinine levels. In advanced liver disease, low creatinine may result from decreased hepatic production of creatinine and inadequate dietary protein as well as reduced muscle mass.

3 eGFR [ > or = 60 mL/min/1.73 square metres ]

The serum estimated glomerular filtration rate (eGFR) provides an assessment of the filtering capacity of the kidney. The eGFR is calculated from a serum creatinine using the CKD EPI equation. In muscle metabolism, creatinine is synthesized endogenously from creatine and creatine phosphate. Creatinine is removed from plasma by glomerular filtration into the urine without being reabsorbed by the tubules to any significant extent. Renal tubular secretion also contributes a small quantity of creatinine to the urine. As a result, creatinine clearance often overestimates the true glomerular filtration rate (GFR) by 10% to more than 20%.

eGFR used for diagnosing and monitoring treatment of acute and chronic renal diseases, adjusting dosage of renally excreted medications, monitoring renal transplant recipients. Among patients with chronic kidney disease (CKD), the eGFR is instrumental in determining the stage of disease according to the K/DOQI CKD classification.

While a normal GFR in young adults is approximately 120−130 mL/minute/1.73 m2, it declines with age, and values <60 mL/minute/1.73 m2 for three months or more is defined as CKD. To determine the presence of proteinuria, low eGFR results may be followed up with albumin:creatinine ratio. An albumin:creatinine ratio >30 mg/g would be indicative of kidney damage.

4 Sodium [ 135-150 mmol/L ]

Serum sodium is assessing acid-base balance, water balance, water intoxication, and dehydration.

Sodium is the primary extracellular cation. Sodium is responsible for almost one-half the osmolality of the plasma and, therefore, plays a central role in maintaining the normal distribution of water and the osmotic pressure in the extracellular fluid compartment. The amount of sodium in the body is a reflection of the balance between sodium intake and output.

Hypernatremia (high sodium) occurs in dehydration. For instance, nasogastric protein feeding with insufficient fluids may cause hypernatremia. Hypernatremia without obvious cause may relate to Cushing syndrome, central or nephrogenic diabetes insipidus with insufficient fluids, primary aldosteronism, and other diseases. Severe hypernatremia may be associated with volume contraction, lactic acidosis, azotemia, weight loss, and increased hematocrit as evidence of dehydration.

Hyponatremia (low sodium) occurs with nephrotic syndrome, cachexia, hypoproteinemia, intravenous glucose infusion, in congestive heart failure, and other clinical entities. Serum sodium is a predictor of cardiovascular mortality in patients in severe congestive heart failure.

Hyponatremia without congestive failure or dehydration may occur with hypothyroidism, the syndrome of inappropriate secretion of antidiuretic hormone (SIADH), renal failure, or renal sodium loss.

5 Potassium [ 3.3-5.0 mmol/L ]

Serum potassium used for evaluation of electrolyte balance, cardiac arrhythmia, muscular weakness, hepatic encephalopathy, and renal failure.

Potassium is the major cation of the intracellular fluid. Disturbance of potassium homeostasis has serious consequences. Decreases in extracellular potassium are characterized by muscle weakness, irritability, and eventual paralysis. Cardiac effects include tachycardia, other cardiac conduction abnormalities that are apparent by electrocardiographic examination, and eventual cardiac arrest.

Hyperkalemia (high potassium) reflects generally inadequate renal excretion, mobilization of potassium from the tissues, or excessive intake or administration. High potassium produce symptoms of mental confusion; weakness, numbness, and tingling of the extremities; weakness of the respiratory muscles; flaccid paralysis of the extremities; slowed heart rate; and eventually peripheral vascular collapse and cardiac arrest. Hyperkalemia may be seen in end-stage renal failure, hemolysis, trauma, Addison disease, metabolic acidosis, acute starvation, dehydration, and with rapid potassium infusion.

Hypokalemia (low potassium) occurs with vomiting, diarrhea, alcoholism, folic acid deficiency, fistulas, laxatives, diuretics, burns, excessive perspiration, Bartter syndrome, some cases of alcoholism and folic acid deficiency, in alkalosis and in renal tubular acidosis. Additionally, more than 90% of hypertensive patients with aldosteronism have hypokalemia. Low potassium occurs with endogenous or exogenous increase in other corticosteroids, including that in Cushing syndrome as well as with dietary or parenteral deprivation of potassium (eg, parenteral therapy without adequate potassium replacement).

6 Chloride [ 96-108 mmol/L ]

Serum chloride is the major anion in the extracellular water space; its physiological significance is in maintaining proper body water distribution, osmotic pressure, and normal anion-cation balance in the extracellular fluid compartment.

Used for evaluation of water, electrolyte, and acid-base status.

High Chloride occurs in dehydration, renal tubular acidosis (hyperchloremia metabolic acidosis), acute renal failure, metabolic acidosis associated with prolonged diarrhea and loss of sodium bicarbonate, diabetes insipidus, adrenocortical hyperfunction, salicylate intoxication, and with excessive infusion of isotonic saline or extremely high dietary intake of salt. Hyperchloremia acidosis may be a sign of severe renal tubular pathology.

Low Chloride occurs in overhydration, chronic respiratory acidosis, salt-losing nephritis, metabolic alkalosis, congestive heart failure, Addisonian crisis, certain types of metabolic acidosis, persistent gastric secretion and prolonged vomiting, aldosteronism, bromide intoxication, syndrome of inappropriate antidiuretic hormone secretion, and conditions associated with expansion of extracellular fluid volume.

7 Bicarbonate [ 21-32 mmol/L ]

Serum or plasma Bicarbonate is the second largest fraction of the anions in plasma. Included in this fraction are the bicarbonate (HCO3[-]) and carbonate (CO3[-2]) ions, carbon dioxide in physical solution, as well as the carbamino compounds.

Used for Diagnosis and treatment of acid-base imbalance in respiratory and metabolic systems.

High results may represent respiratory acidosis with CO2 retention, or metabolic alkalosis (eg, prolonged vomiting).

Low value may indicate respiratory alkalosis as in hyperventilation or metabolic acidosis (eg, diabetes with ketoacidosis).


1 Bilirubin Total [ 0-26 umol/L, or 0-1.52 mg/dL ]

Bilirubin is one of the most commonly used tests to assess liver function. Approximately 85% of the total bilirubin produced is derived from the heme moiety of hemoglobin, while the remaining 15% is produced from the red blood cell precursors destroyed in the bone marrow and from the catabolism of other heme-containing proteins. After production in peripheral tissues, bilirubin is rapidly taken up by hepatocytes where it is conjugated with glucuronic acid to produce mono- and diglucuronide, which are excreted in the bile.

High Bilirubin:

Liver disease: hepatitis, cholangitis, cirrhosis, other types of liver disease (including primary or secondary neoplasia); alcoholism (usually with high AST (SGOT), GGT, MCV, or some combination of these findings); biliary obstruction (intrahepatic or extrahepatic); infectious mononucleosis (look also for increased LD (LDH), lymphocytosis); Dubin-Johnson syndrome; Gilbert disease (familial hyperbilirubinemia) is encountered as a moderate elevation with otherwise unremarkable chemistries.

Anorexia or prolonged fasting: 36 hours or more may cause moderate rise.

Pernicious anemia, hemolytic anemias, erythroblastosis fetalis, other neonatal jaundice, hematoma, and following a blood transfusion, especially if several units are given in a short time.

Pulmonary embolism and/or infarct, congestive heart failure.

2 Alkaline Phosphatase [ 35-120 mu/ml, 35-120 U/L ]

serum alkaline phosphatase (ALP) is for diagnosing and monitoring treatment of liver, bone, intestinal, and parathyroid diseases.

Alkaline phosphatase in serum consists of 4 structural genotypes: the liver-bone-kidney type, the intestinal type, the placental type, and the variant from the germ cells. It occurs in osteoblasts, hepatocytes, leukocytes, the kidneys, spleen, placenta, prostate, and the small intestine. The liver-bone-kidney type is particularly important.

High alkaline phosphatase include bone growth, healing fracture, acromegaly, osteogenic sarcoma, liver or bone metastases, leukemia, myelofibrosis, rarely myeloma, Hypervitaminosis D, Paget disease. Hyperthyroidism, Hyperparathyroidism, Chronic alcohol ingestion (in chronic alcoholism, alkaline phosphatase may be normal or increased, but often with high AST (SGOT) and/or high bilirubin and especially with high GT; MCV may be high), Biliary obstruction, Cirrhosis, Gilbert syndrome, Hepatitis, Fatty metamorphosis of liver (moderate increase occurs in acute fatty liver), Diabetes mellitus, diabetic hepatic lipidosis, Infiltrative liver diseases (eg, sarcoid, TB, amyloidosis, abscess), Sepsis. Certain viral diseases: infectious mononucleosis; cytomegalovirus infections, Postoperative cholestasis. Pancreatitis, carcinoma of pancreas, cystic fibrosis, Tumors, especially hypernephroma; neoplastic ectopic production (Regan, Nagao isoenzymes), Fanconi syndrome, Congestive heart failure.

Drugs − estrogens (large doses), birth control agents, methyltestosterone, phenothiazines, oral hypoglycemic agents, erythromycin, or any drug producing hypersensitivity or toxic cholestasis. Many commonly and uncommonly used drugs elevate alkaline phosphatase, and tenfold increases may be seen with drug cholestasis.

Low alkaline phosphatase: Hypothyroidism − but most hypothyroid patients have normal alkaline phosphatase.

Pernicious anemia − in very few patients.

Hypophosphatasia: Very low alkaline phosphatase values are found in the presence of normocalcemia or hypocalcemia. This diagnosis may be confirmed by quantitation of urinary phosphoethanolamine.

Malnutrition has been reported to relate to low values, but in practice, diseases causing malnutrition relate often to high alkaline phosphatase results (eg, disseminated neoplasia).

Some drugs (clofibrate, azathioprine, estrogens and estrogens in combination with androgens) lower serum ALP activity.

3 Total Protein [ 62-82 g/L, or 6.20-8.20 g/dL ]

Plasma proteins are synthesized predominantly in the liver; immunoglobulins are synthesized by mononuclear cells of lymph nodes, spleen and bone marrow. The two general causes of alterations of serum total protein are a change in the volume of plasma water and a change in the concentration of one or more of the specific proteins in the plasma.

Total Protein test measures two types of proteins: globulin and albumin. Low protein levels may signal liver or kidney disease.

High total protein (Hyperproteinemia): dehydration; some cases of chronic liver disease, including chronic active hepatitis and cirrhosis; neoplasms, especially myeloma; macroglobulinemia of Waldenström; tropical diseases (eg, kala-azar, leprosy, and others); granulomatous diseases, such as sarcoidosis; diseases in which total protein is sometimes high include collagen disease (eg, systemic lupus erythematosus (SLE), and other instances of chronic infection/inflammation).

Low total protein (Hypoproteinemia): pregnancy; intravenous fluids; cirrhosis or other liver disease, including chronic alcoholism; prolonged immobilization; heart failure; nephrotic syndromes; glomerulonephritis; neoplasia; protein losing enteropathies; Crohn’s disease and chronic ulcerative colitis; starvation, malabsorption or malnutrition; hyperthyroidism; burns; severe skin disease; and other chronic diseases.

Very low total protein (<4 g/dL) and low albumin cause edema (eg, the nephrotic syndromes).

4 Albumin [ 37-51 g/L, or 3.70-5.0 g/dL ]

Albumin is a carbohydrate-free protein, which constitutes 55% to 65% of total plasma protein. It maintains oncotic plasma pressure, is involved in the transport and storage of a wide variety of ligands, and is a source of endogenous amino acids. Albumin binds and solubilizes various compounds, including bilirubin, calcium, long-chain fatty acids, toxic heavy metal ions, and numerous pharmaceuticals.

High albumin (Hyperalbuminemia) may indicate dehydration. Look for increase in hemoglobin, hematocrit in such patients.

Low albumin (Hypoalbuminemia) is found with use of I.V. fluids, rapid hydration, overhydration; cirrhosis, other liver disease, including chronic alcoholism; in pregnancy and with oral contraceptive use; many chronic diseases including the nephrotic syndromes, neoplasia, protein-losing enteropathies (including Crohn’s disease and ulcerative colitis), peptic ulcer, thyroid disease, burns, severe skin disease, prolonged immobilization, heart failure, chronic inflammatory diseases such as the collagen diseases and other chronic catabolic states.

Starvation, malabsorption, or malnutrition: In the absence of I.V. fluid therapy and in patients without liver or renal disease, low albumin may be regarded as an indication of inadequate body protein reserves. It is described as the most common nutrition-related abnormality in patients with infection.malnutrition. Low albumin values are associated with longer hospital stay.

5 Globulin [ 19-39 g/L, or 1.90-3.90 g/dL ]

Globulins are a group of proteins in your blood. They are made in your liver by your immune system. Globulins play an important role in liver function, blood clotting, and fighting infection. There are four main types of globulins. They are called alpha 1, alpha 2, beta, and gamma. The gamma globulin band as seen in conventional serum protein electrophoresis consists of 5 immunoglobulins. In normal serum, about 80% is immunoglobulin G (IgG), 15% is immunoglobulin A (IgA), 5% is immunoglobulin M (IgM), 0.2% is immunoglobulin D (IgD), and a trace is immunoglobulin E (IgE).

Total protein test measures two types of proteins: globulin and albumin. Low protein levels may signal liver or kidney disease.

The serum protein electrophoresis measures gamma globulin and other proteins in the blood. Doctors can use this test to diagnose immune system disorders and other conditions.

Normal value ranges are:
Serum globulin: 2.0 to 3.5 grams per deciliter (g/dL) or 20 to 35 grams per liter (g/L)
IgM component: 75 to 300 milligrams per deciliter (mg/dL) or 750 to 3,000 milligrams per liter (mg/L)
IgG component: 650 to 1,850 mg/dL or 6.5 to 18.50 g/L
IgA component: 90 to 350 mg/dL or 900 to 3,500 mg/L

High Globulin may indicate: Acute viral and bacterial infections, Dehydration, Blood and bone marrow cancers including multiple myeloma, and some lymphomas and leukemias, Immune deficiency disorders, chronic inflammatory disease (for example, rheumatoid arthritis and systemic lupus erythematosus), Waldenström macroglobulinemia. Certain drugs, such as amiodarone (Cordarone, Nexterone), used to treat and prevent irregular heartbeat.

Low Globulin may indicate Kidney disease (nephrotic syndrome), which can cause protein loss, Liver disease, Inborn (Congenital) immune deficiency, which decreases globulin production, Malnutrition or lack of nutrients from the diet, which decreases globulin production, Acromegaly, a disorder which results from excess growth hormone, Lung cancer, Oxidative stress in women with pregnancy-induced hypertension (limited evidence)

6 Alb/Glo Ratio [ 1.2-2.5 ]

There are two major types of protein in the blood:

Albumin, which helps keep blood from leaking out of blood vessels. It also helps move hormones, medicines, vitamins, and other important substances throughout the body. Albumin is made in the liver.

Globulins, which help fight infection and move nutrients throughout the body. Some globulins are made by the liver. Others are made by the immune system.

Albumin/Globulin (A/G) ratio compares the amount of albumin in your blood to the amount of globulin.

Low A/G ratio may occurs in autoimmune disease, such as lupus, Liver disease, including cirrhosis, Kidney disease

Hight A/G ratio  may occurs in certain types of genetic disorders, Leukemia.

7 AST / SGOT [ 0-40 U/L ]

Aspartate aminotransferase (AST / SGOT) is found in high concentrations in liver, heart, skeletal muscle, and kidney. AST is present in both cytoplasm and mitochondria of cells. In cases involving mild tissue injury, the predominant form of AST is that from the cytoplasm. Severe tissue damage results in more of the mitochondrial enzyme being released.

High AST can be found in cases such as myocardial infarction, acute liver cell damage, viral hepatitis, earlier stages of hemochromatosis and chemical injury (eg, necrosis related to toxins such as carbon tetrachloride). Some instances of cholecystitis cause increased AST. Slight to moderate elevation of AST is seen in muscular dystrophy, dermatomyositis, acute pancreatitis, and crushed muscle injuries.

Chronic alcohol ingestion, not limited to overt chronic alcoholism; cirrhosis. In alcoholic hepatitis, AST values usually are <300 units/L. In hepatitis, look for a high AST:LD (LDH) ratio, >3, and very high AST peaking at 500−3000 units/L in acute viral hepatitis (ie, in clinical acute viral hepatitis the transaminases may be increased 10 times or more above their upper limits of normal).

AST and ALT (SGPT) are increased in Reye syndrome. In infectious mononucleosis, LD (LDH) is commonly considerably higher than AST. Trauma (including head trauma and including surgery) and other striated muscle diseases, including dystrophy, dermatomyositis, trichinosis, polymyositis, and gangrene cause AST increases. Both AST and ALT elevations are found with Duchenne muscular dystrophy. Look for high CK in myositis, high LD5 (or isomorphic pattern in some instances of polymyositis) on LD isoenzymes.

In myocardial infarction AST peaks about 24 hours after infarct and returns to normal three to seven days later. In acute MI without shock or heart failure, ALT is not apt to increase significantly. AST increases in congestive failure with centrilobular liver congestion, in which high LD5 on LD isoenzymes is found, and in pericarditis, myocarditis, pancreatitis, and other inflammatory states including Legionnaires’ disease. In renal infarction LD is usually high, out of proportion to AST. Lung infarction and other disease entities leading to necrosis including large, necrotic tumors cause increased AST; LD is commonly also increased in such instances. Shock (LD also usually increased); hypothyroidism (LD and/or CK not infrequently increased in myxedema); hemolytic anemias (LD high with increased LD1) and certain CNS diseases may increase AST.

Drugs: A large number of commonly used drugs have been reported to elevate AST: isoniazid, phenothiazines, erythromycin, progesterone, anabolic-androgenic steroids, halothane, methyldopa, opiates, indomethacin, salicylates in children, and other drugs. Hepatotoxicity from drugs may cause high aminotransferase activity with elevation of AST:ALT ratio. Acetaminophen (Paracetamol) hepatotoxicity deserves special mention. In alcoholics, apparently moderate doses of the analgesic have caused severe hepatotoxicity.

8 ALT / SGPT [ 3-40 U/L ]

Alanine aminotransferase (ALT) is present primarily in liver cells. In viral hepatitis and other forms of liver disease associated with hepatic necrosis, serum ALT is elevated even before the clinical signs and symptoms of the disease appear. Although serum levels of both aspartate aminotransferase (AST) and ALT become elevated whenever disease processes affect liver cell integrity, ALT is more specific for liver injury than AST (SGOT). Useful for hepatic cirrhosis, other liver disease. Increased in Reye syndrome, with AST. Test for hepatitis. Acute hepatitis A or B or C can be confirmed serologically. Negative serological findings in the presence of hepatitis-like chemistry abnormalities may also suggest acute drug-induced hepatitis, an impression supported by resolution after removal of the offending drugs. The combination of increased AST and ALT with negative hepatitis markers occurs in a number of other entities including infectious mononucleosis. Sensitive to heart failure.

9 GGT [ 0-50 U/L ]

Gamma-Glutamyl Transferase (GGT) is primarily present in kidney, liver, and pancreatic cells. Small amounts are present in other tissues. Even though renal tissue has the highest level of GGT, the enzyme present in the serum appears to originate primarily from the hepatobiliary system, and GGT activity is elevated in any and all forms of liver disease. Elevated values can also indicate alcoholic cirrhosis or individuals who are heavy drinkers.

It is highest in cases of intra- or posthepatic biliary obstruction, reaching levels some 5 to 30 times normal. GGT is more sensitive than alkaline phosphatase (ALP), leucine aminopeptidase, aspartate transaminase (AST), and alanine aminotransferase (ALT) in detecting obstructive jaundice, cholangitis, and cholecystitis; its rise occurs earlier than with these other enzymes and persists longer. Only modest elevations (2-5 times normal) occur in infectious hepatitis, and in this condition, GGT determinations are less useful diagnostically than are measurements of the transaminases. High elevations of GGT are also observed in patients with either primary or secondary (metastatic) neoplasms. Elevated serum values are also seen in patients receiving drugs such as phenytoin and phenobarbital, and this is thought to reflect induction of new enzyme activity.


1 Total Cholesterol [ < 200 mmol/L, or <200 mg/dL ]

Cholesterol is a steroid with a secondary hydroxyl group in the C3 position, a waxy, fat-like substance that’s found in your blood and every cell of your body. It is synthesized in many types of tissue but particularly in the liver and intestinal wall. You need some cholesterol to keep your cells and organs healthy. Your liver makes all the cholesterol your body needs. But you can also get cholesterol from the foods you eat, especially meat, eggs, poultry, and dairy products. Foods that are high in dietary fat can also make your liver produce more cholesterol. Approximately 75% of cholesterol is newly synthesized and 25% originates from dietary intake. Normally, the cholesterol in the plasma or serum is 60% to 80% esterified.

There are two main types of cholesterol: low-density lipoprotein (LDL), or “bad” cholesterol, and high-density lipoprotein (HDL), or “good” cholesterol. A cholesterol test is a blood test that measures the amount of each type of cholesterol and certain fats in your blood. Approximately 50% to 75% of the plasma cholesterol is transported by low-density lipoproteins (LDL) and 15% to 40% by high-density lipoproteins (HDL).

<200 mg/dL, Desirable
200-239 mg/dL, Borderline High
> or =240 mg/dL, High

Hight Cholesterol (hyperlipoproteinemia) may occurs in various metabolic diseases. Moderate-to-markedly elevated values are also seen in cholestatic liver disease. Hypercholesterolemia is a risk factor for cardiovascular disease.

Low Cholesterol (hypolipoproteinemia) may occurs in hyperthyroidism, malabsorption, and deficiencies of apolipoproteins.

2 HDL Cholesterol [ > 59 mmol/L, or >59 mg/dL ]

A lipoprotein test measures the level of lipoprotein in your blood. Lipoproteins are substances made of protein and fat that carry cholesterol through your bloodstream. There are two main types of cholesterol:

High-density lipoprotein (HDL), or “good” cholesterol
Low-density lipoprotein (LDL), or “bad” cholesterol.

High-density lipoprotein (HDL) is the smallest of the lipoprotein particles and comprises a complex family of lipoprotein particles that exist in a constant state of dynamic flux as the particles interact with other HDL particles and with low-density lipoprotein particles and very-low-density lipoprotein particles. HDL has the largest proportion of protein relative to lipid compared to other lipoproteins (>50% protein).

<40 mg/dL, Low HDL
40-45 mg/dL Borderline Low
>45 mg/dL, Acceptable

Total cholesterol levels have long been known to be related to coronary heart disease (CHD). high-density lipoprotein (HDL) cholesterol is also an important tool used to assess an individual’s risk of developing CHD since a strong negative relationship between HDL cholesterol concentration and the incidence of CHD has been reported. In some individuals, exercise increases the HDL cholesterol level; those with more physical activity have higher HDL cholesterol values.

Low high-density lipoprotein (HDL) cholesterol levels correlate with increased risk for coronary heart disease (CHD). Values greater than or equal to 80 to 100 mg/dL may indicate metabolic response to certain medications such as hormone replacement therapy, chronic liver disease, or some form of chronic intoxication, such as with alcohol, heavy metals, or industrial chemicals including pesticides.

3 LDL Cholesterol [ < 100 mmol/L, or <100 mg/dL ]

A lipoprotein test measures the level of lipoprotein in your blood. Lipoproteins are substances made of protein and fat that carry cholesterol through your bloodstream. There are two main types of cholesterol:

High-density lipoprotein (HDL), or “good” cholesterol
Low-density lipoprotein (LDL), or “bad” cholesterol.

Low-density lipoprotein cholesterol (LDL cholesterol) is acknowledged as being causally related with atherosclerotic cardiovascular disease. LDL Cholesterol remains the primary focus for cardiovascular risk assessment and effectiveness of risk reduction interventions including diet, physical activity and pharmacologic therapies.

<100 mg/dL, Desirable
100-129 mg/dL, Above desirable
130-159 mg/dL, Borderline high
160-189 mg/dL, High
> or =190 mg/dL, Very High

4 Total Cholesterol/HDL Ratio [ < 4.6 ]

ratio of HDL compared to the total cholesterol.

5 Triglycerides [ < 150 mmol/L, or <150 mg/dL ]

Triglycerides is type of fat found in your blood, are esters of the trihydric alcohol, glycerol, with 3 long-chain fatty acids. They are partly synthesized in the liver and partly derived from the diet. According to some studies, high levels of triglycerides may increase the risk of heart disease, especially in women.

<150 mg/dL, Normal
150-199 mg/dL, Bordeline Hight
200-499 mg/dL, High
> or =500 mg/dL, Very High

Increased plasma triglyceride levels are indicative of a metabolic abnormality and, along with elevated cholesterol, are considered a risk factor for atherosclerotic disease. Hyperlipidemia may be inherited or be associated with biliary obstruction, diabetes mellitus, nephrotic syndrome, renal failure, or metabolic disorders related to endocrinopathies. Increased triglycerides may also be medication-induced (eg, prednisone). Since cholesterol and triglycerides can vary independently, measurement of both is more meaningful than the measurement of cholesterol only.


1 Calcium [ 2.10-2.60 mol/L, or 8.0-10.0 mg/dL ]

The calcium content of an adult is somewhat over 1 kg (about 2% of the body weight). Of this, 99% is present as calcium hydroxyapatite in bones and less than 1% is present in the extra-osseous intracellular space or extracellular space (ECS). The calcium level in the ECS is in dynamic equilibrium with the rapidly exchangeable fraction of bone calcium. In serum, calcium is bound to a considerable extent to proteins (approximately 40%), 10% is in the form of inorganic complexes, and 50% is present as free or ionized calcium.

Calcium ions affect the contractility of the heart and the skeletal musculature, and are essential for the function of the nervous system. In addition, calcium ions play an important role in blood clotting and bone mineralization.

High Calcium (Hypercalcemia) may occurs in primary hyperparathyroidism (pHPT) or bone metastasis of carcinoma of the breast, prostate, thyroid gland, or lung. Patients who have pHPT and bone disease, renal stones or nephrocalcinosis, or other signs or symptoms are candidates for surgical removal of the parathyroid glands, myeloma, leukemia and lymphoma, dehydration, sarcoidosis, prolonged immobilization, in patient with increased bone turnover (eg, Paget disease of bone, malignancy, children), Milk-alkali syndrome. Severe hypercalcemia may result in cardiac arrhythmia.

Low Calcium (Hypocalcemia) may occurs in chronic renal failure is also frequently associated with hypocalcemia due to decreased vitamin-D synthesis as well as hyperphosphatemia and skeletal resistance to the action of parathyroid hormone (PTH). Characteristic symptoms of hypocalcemia are latent or manifest tetany and osteomalacia.  High phosphorus: renal insufficiency, hypoparathyroidism, pseudohypoparathyroidism, Vitamin D deficiency, rickets, osteomalacia, Milkman syndrome, Malabsorption or malnutrition with interference with vitamin D and/or calcium absorption, Renal tubular acidosis, acute ancreatitis, Bacteremia, Hypomagnesemia

Anticonvulsants and other common drugs, most by in vivo action, can depress calcium. Barbiturates in elderly may cause calcium decrease. Other drugs, including calcitonin, corticosteroids, gastrin, glucagon, glucose, insulin, magnesium salts, methicillin and tetracycline in pregnancy.

2 Phosphate [ 0.77-1.42 mol/L, 2.5-4.5 mg/dL ]

Phosphate is an electrically charged particle that contains the mineral phosphorus. Phosphorus works together with the mineral calcium to build strong bones and teeth.

High phosphate/phosphorus levels (Hyperphosphatemia), may occurs in Kidney disease, Hypoparathyroidism, a condition in which your parathyroid gland doesn’t make enough parathyroid hormone, Too much vitamin D in your body, Too much phosphate in your diet, Diabetic ketoacidosis, a life-threatening complication of diabetes. May due to exercise; dehydration and hypovolemia; high phosphorus content enema; acromegaly; hypoparathyroidism; pseudohypoparathyroidism; bone metastases; hypervitaminosis D; sarcoidosis; milk-alkali syndrome; liver disease, such as portal cirrhosis; catastrophic events such as cardiac resuscitation, pulmonary embolism, renal failure; diabetes mellitus with ketosis; serum artifact−sample not refrigerated; overheated, hemolyzed sample, or serum allowed to remain too long on the clot.

Low phosphate/phosphorus (Hypophosphatemia) may occurs in Hyperparathyroidism, a condition in which your parathyroid gland produces too much parathyroid hormone, Malnutrition, Alcoholism, Osteomalacia, condition that causes bones to become soft and deformed. It’s caused by a vitamin D deficiency. When this condition happens in children, it’s known as rickets.

3 Uric Acid [ 147-400 umol/L, 2.50-6.80 mg/dL ]

Uric acid is the final product of purine metabolism in humans. Purines, compounds that are vital components of nucleic acids and coenzymes, may be synthesized in the body or they may be obtained by ingesting foods rich in nucleic material (eg, liver, sweetbreads). Approximately 75% of the uric acid excreted is lost in the urine; most of the remainder is secreted into the gastrointestinal tract where it is degraded to allantoin and other compounds by bacterial enzymes.

High Uric Acid (Hyperuricemia) is increased purine synthesis, inherited metabolic disorder, excess dietary purine intake, increased nucleic acid turnover, malignancy, cytotoxic drugs, and decreased excretion due to chronic renal failure or increased renal reabsorption. Long-term follow-up of these patients is undertaken because many are at risk of developing renal disease; few of these patients ever develop the clinical syndrome of gout.

Low Uric Acid (Hypouricemia), often defined as serum urate below 2.0 mg/dL, is much less common than hyperuricemia. It may be secondary to severe hepatocellular disease with reduced purine synthesis, defective renal tubular reabsorption, overtreatment of hyperuricemia with allopurinol, as well as some cancer therapies (eg, 6-mercaptopurine).


1 Glucose (Fasting) [ 3.9-6.0 mmoll/L, 70-100 mg/dL ]

A blood glucose test is a blood test that screens for diabetes by measuring the level of glucose (sugar) in a person’s blood. Normally, your pancreas releases insulin when your blood sugar, or “blood glucose,” gets high – after a meal, for example. That signals your body to absorb glucose until levels get back to normal.

If you have diabetes, your body doesn’t make insulin (type 1 diabetes) or doesn’t respond to it normally (type 2 diabetes). That can leave your blood sugar too high for too long. Over time, that can damage nerves and blood vessels and lead to heart disease and other problems.

2 HBA1C [ 4.5-6.4 % ]

Hemoglobin A1c (HbA1c) level reflects the mean glucose concentration over the previous period (approximately 8-12 weeks, depending on the individual) and provides a much better indication of long-term glycemic control than blood and urinary glucose determinations. Diabetic patients with very high blood concentrations of glucose have from 2 to 3 times more HbA1c than normal individuals.

4.5-6.4 %, Ideal
6.5-7.0 %, Optimal
7.1-8.0 %,. Suboptimal
> 8.0 %, Unacceptable


1 Urine Microalbumin Creatinine Ratio ACR [ < 2.5 mg/mmoL (male), < 3.5 mg/mmoL (female) ]

Albumin accounts for approximately 50% of the protein in plasma. The kidney works to prevent the loss of albumin into the urine through active resorption, but a small amount of albumin can be measured in urine of individuals with normal renal function.

If there is any albumin in your urine, the amount can vary greatly throughout the day. But creatinine, a normal waste product found in urine, is released as a steady rate. Because of this, your health care provider can more accurately measure the amount of albumin by comparing it to the amount of creatinine in your urine. If albumin is found in your urine, it may mean you have a problem with your kidneys.

The prognostic value of consistently elevated albumin levels is particularly well established in diabetic patients. Renal disease is a common microvascular complication of diabetes. Without specific interventions, 80% of type I diabetics with repeatedly elevated albumin levels will go on to end-stage renal disease. Twenty percent to 40% of type II diabetics with sustained albuminuria will progress to overt nephropathy.

< 2.5 mg/mmoL (male), < 3.5 mg/mmoL (female), Normal
2.5-30 mg/mmoL (male), 3.5-30 mg/mmoL (female), Microalbuminuria
>30 mg/mmoL (male/female), Macroalbuminuria

2 Protein [ Negative ]

Protein is normally found in the blood. If there is a problem with your kidneys, protein can leak into your urine. While a small amount is normal, a large amount of protein in urine may indicate kidney disease.

If a large amount of protein is found in your urine sample, it doesn’t necessarily mean that you have a medical problem needing treatment. Strenuous exercise, diet, stress, pregnancy, and other factors can cause a temporary rise in urine protein levels.

If your urine protein levels are consistently high, it may indicate kidney damage or other medical condition. These include: Urinary tract infection, Lupus, High blood pressure, Preeclampsia, a serious complication of pregnancy, marked by high blood pressure. If it is not treated, preeclampsia can be life-threatening to the mother and baby, Diabetes, Certain types of cancer.

3 Blood [ Negative ]

There are a variety of factors that can cause red or white blood cells to be present in the urine. Many are not cause for concern. Small amounts of blood in the urine may be due to certain medicines, intense exercise, sexual activity, or menstruation.

Increased red blood cells in urine may indicateA viral infection, Inflammation of the kidney or bladder, A blood disorder, Bladder or kidney cancer

Increased white blood cells in urine may indicate: A bacterial urinary tract infection. This is the most common cause of a high white blood cell count in urine, Inflammation of the urinary tract or kidneys.

4 Glucose [ Negative ]

Glucose is not normally found in urine. If results show glucose (glycosuria or glucosuria), it may be a sign of: Diabetes, Pregnancy. As many half of all pregnant women have some glucose in their urine during pregnancy. Too much glucose may indicate gestational diabetes, A kidney disorder.

5 Ketones [ Negative ]

The test measures ketone levels in your urine. Normally, your body burns glucose (sugar) for energy. If your cells don’t get enough glucose, your body burns fat for energy instead. This produces a substance called ketones, which can show up in your blood and urine. High ketone levels in urine may indicate diabetic ketoacidosis (DKA), a complication of diabetes that can lead to a coma or even death. A ketones in urine test can prompt you to get treatment before a medical emergency occurs.

If you have diabetes, ketones in urine can mean that you are not getting enough insulin.

If you don’t have diabetes, you may still be at risk for developing ketones if you: Experience chronic vomiting and/or diarrhea, Have a digestive disorder, Participate in strenuous exercise, Are on a very low-carbohydrate diet, Have an eating disorder, Are pregnant.

6 Bilirubin [ Negative ]

Bilirubin is a yellowish substance made during the body’s normal process of breaking down red blood cells. Bilirubin is found in bile, a fluid in your liver that helps you digest food. If your liver is healthy, it will remove most of the bilirubin from your body. If your liver is damaged, bilirubin can leak into the blood and urine. Bilirubin in urine may be a sign of liver disease.

7 Urobilinogen [ Normal ]

A urobilinogen in urine test measures the amount of urobilinogen in a urine sample. Urobilinogen is formed from the reduction of bilirubin. Bilirubin is a yellowish substance found in your liver that helps break down red blood cells. Normal urine contains some urobilinogen. If there is little or no urobilinogen in urine, it can mean your liver isn’t working correctly. Too much urobilinogen in urine can indicate a liver disease such as hepatitis or cirrhosis.


1 ESR [ < 0-10 mm/hr ]

Erythrocyte Sedimentation Rate or Westergren Sedimentation Rate, is a type of blood test that measures how quickly erythrocytes (red blood cells) settle at the bottom of a test tube that contains a blood sample. Normally, red blood cells settle relatively slowly. A faster-than-normal rate may indicate inflammation in the body. Inflammation is part of your immune response system. It can be a reaction to an infection or injury. Inflammation may also be a sign of a chronic disease, an immune disorder, or other medical condition.

High ESR may be related to an inflammatory condition, such as: Infection, Rheumatoid arthritis, Rheumatic fever, Vascular disease, Inflammatory bowel disease, Heart disease, Kidney disease, Certain cancers

Low ESR may indicate a blood disorder, Polycythemia, Sickle cell anemia, Leukocytosis, an abnormal increase in white blood cells

2 CRP [ < or = 9.9 mg/L ]

C-reactive protein (CRP) is produced by the liver. It’s sent into your bloodstream in response to inflammation. Inflammation is your body’s way of protecting your tissues if you’ve been injured or have an infection. It can cause pain, redness, and swelling in the injured or affected area. Some autoimmune disorders and chronic diseases can also cause inflammation. The level of CRP rises when there is inflammation throughout the body. It is one of a group of proteins, called acute phase reactants, that go up in response to inflammation. The levels of acute phase reactants increase in response to certain inflammatory proteins called cytokines. These proteins are produced by white blood cells during inflammation.

CRP is an acute phase reactant, which can be used as a test for inflammatory diseases, infections, and neoplastic diseases. Progressive increases correlate with increases of inflammation/injury. CRP is a more sensitive, rapidly responding indicator than ESR. CRP may be used to detect early postoperative wound infection and to follow therapeutic response to anti-inflammatory agents.

3 Haemoglobin [ 13.5-18.0 g/dL ]

Hemoglobin is a protein in your red blood cells that carries oxygen from your lungs to the rest of your body. If your hemoglobin levels are abnormal, it may be a sign that you have a blood disorder.

High hemoglobin levels may be a sign of: Lung disease, Heart disease, Polycythemia vera, a disorder in which your body makes too many red blood cells. It can cause headaches, fatigue, and shortness of breath.

Low hemoglobin levels may be a sign of:, Different types of anemia, Thalassemia, Iron deficiency, Liver disease, Cancer.

4 RBC [ 14.5-6.5 x 10^12 /L, or 4.5-6.5 x 10^6 /microliter ]

Red blood cell (RBC),or erythrocytes, carry oxygen from your lungs to every cell in your body. Your cells need oxygen to grow, reproduce, and stay healthy. An RBC count that is higher or lower than normal is often the first sign of an illness. So the test may allow you to get treatment even before you have symptoms.

High RBC (polycythemia)

  • Dehydration
  • Lung (pulmonary) disease
  • Kidney or other tumor that produces excess erythropoietin
  • Smoking
  • Living at high altitude
  • Genetic causes (altered oxygen sensing, abnormality in hemoglobin oxygen release)
  • Polycythemia vera—a rare disease

Low RBC (anemia)

  • Acute or chronic bleeding
  • RBC destruction (e.g., hemolytic anemia, etc.)
  • Nutritional deficiency (e.g., iron deficiency, vitamin B12 or folate deficiency)
  • Bone marrow disorders or damage
  • Chronic inflammatory disease
  • Chronic kidney disease

5 WBC [ 4.0-11.1 x 10^9 /L, or 4500-11,100 cells/mcL ]

A white blood count measures the number of white cells in your blood. White blood cells are part of the immune system. They help your body fight off infections and other diseases. When you get sick, your body makes more white blood cells to fight the bacteria, viruses, or other foreign substances causing your illness. This increases your white blood count.

Other diseases can cause your body to make fewer white blood cells than you need. This lowers your white blood count. Diseases that can lower your white blood count include some types of cancer and HIV/AIDS, a viral disease that attacks white blood cells. Certain medicines, including chemotherapy, may also lower the number of your white blood cells.

There are five major types of white blood cells:, Neutrophils, Lymphocytes, Monocytes, Eosinophils, Basophils

A white blood count measures the total number of these cells in your blood. Another test, called a blood differential, measures the amount of each type of white blood cell.

High WBC (leukocytosis):

  • Infection, most commonly bacterial or viral
  • Inflammation
  • Leukemia, myeloproliferative neoplasms
  • Allergies, asthma
  • Tissue death (trauma, burns, heart attack)
  • Intense exercise or severe stress

Low WBC (leukopenia):

  • Bone marrow disorders or damage
  • Autoimmune conditions
  • Severe infections (sepsis)
  • Lymphoma or other cancer that spread to the bone marrow
  • Dietary deficiencies
  • Diseases of immune system (e.g., HIV/AIDS)

6 Neutrophils [ 2.00-7.50 x 10^9 /L, 45-75% ]

High (neutrophilia)

  • Acute bacterial infections
  • Inflammation
  • Trauma, heart attack, or burns
  • Stress, rigorous exercise
  • Certain leukemias (e.g., chronic myeloid leukemia)
  • Cushing syndrome
  • Corticosteroids

Low (neutropenia)

  • Severe, overwhelming infection (sepsis)
  • Autoimmune disorders
  • Dietary deficiencies
  • Reaction to drugs
  • Immunodeficiency
  • Myelodysplasia
  • Bone marrow damage (e.g., chemotherapy, radiation therapy)
  • Cancer that spreads to the bone marrow
  • Congenital neutropenia

7 Lymphotcytes [ 1.5-4.0 x 10^9 /L , 18-45 % ]

High (lymphocytosis)

  • Acute viral infections (e.g., chicken pox, cytomegalovirus (CMV), Epstein-Barr virus (EBV), herpes, rubella)
  • Certain bacterial infections (e.g., pertussis (whooping cough), tuberculosis (TB))
  • Toxoplasmosis
  • Chronic inflammatory disorder (e.g., ulcerative colitis)
  • Lymphocytic leukemia, lymphoma
  • Stress (acute)

Low (lymphocytopenia)

  • Autoimmune disorders (e.g., lupus, rheumatoid arthritis)
  • Infections (e.g., HIV, viral hepatitis, typhoid fever, influenza, Covid-19)
  • Bone marrow damage (e.g., chemotherapy, radiation therapy)
  • Corticosteroids

8 Monocytes [ 0.2-0.8 x 10^9 /L , 1-10 % ]


  • Chronic infections (e.g., tuberculosis, fungal infection)
  • Infection within the heart (bacterial endocarditis)
  • Collagen vascular diseases (e.g., lupus, scleroderma, rheumatoid arthritis, vasculitis)
  • Monocytic or myelomonocytic leukemia (acute or chronic)


  • Bone marrow damage or failure
  • Hairy cell leukemia
  • Aplastic anemia

8 Eosinophils [ 0.04- 0.40 x 10^9 /L , 0-7 % ]


  • Asthma, allergies such as hay fever
  • Drug reactions
  • Parasitic infections
  • Inflammatory disorders (celiac disease, inflammatory bowel disease)
  • Some cancers, certain acute or chronic leukemias or lymphomas
  • Addison disease
  • Connective tissue disorders


  • usually not medically significant

9 Basophils [ < 0.21 x 10^9 /L , 0-0.5 % ]


  • Rare allergic reactions (hives, food allergy)
  • Inflammation (rheumatoid arthritis, ulcerative colitis)
  • Some leukemias
  • Uremia


  • usually not medically significant

10 Platelets [ 140-440 x 10^9 /L, or 140-440 x 10^3 /mcL ]

Platelets, or thrombocytes, are tiny fragments of cells that are essential for normal blood clotting. They are formed from very large cells called megakaryocytes in the bone marrow and are released into the blood to circulate. Clotting is the process that helps you stop bleeding after an injury.

A lower than normal platelet count is called thrombocytopenia. This condition can cause you to bleed too much after a cut or other injury that causes bleeding. A higher than normal platelet count is called thrombocytosis. This can make your blood clot more than you need it to. Blood clots can be dangerous because they can block blood flow.

High (thrombocytosis)

  • Cancer, most commonly lung cancer, gastrointestinal cancer, ovarian cancer, breast cancer, or lymphoma
  • Anemia, in particular, iron-deficiency anemia and hemolytic anemia
  • Inflammatory conditions such as inflammatory bowel disease (IBD) or rheumatoid arthritis
  • Infectious diseases such as tuberculosis
  • If you have had your spleen removed surgically
  • Use of birth control pills (oral contraceptives)
  • Recovery from significant blood loss, such as from trauma or major surgery
  • After physical activity or exertion
  • Recovery from excess alcohol consumption and vitamin B12 and folate deficiency

Low (thrombocytopenia)

  • Idiopathic thrombocytopenia (ITP), also known as immune thrombocytopenic purpura, is the result of antibody production against platelets.
  • Viral infections such as mononucleosis, hepatitis, HIV, or measles
  • Use of certain drugs, such as aspirin and ibuprofen, some antibiotics (including those containing sulfa), colchicine and indomethacin, H2-blocking agents, hydralazine, isoniazid, quinidine, thiazide diuretics, and tolbutamide; these are just a few that have been associated with drug-induced decreased platelet counts.
  • Heparin-induced thrombocytopenia (HIT) results in low platelets when you are or have been treated with heparin and you develop an antibody.
  • Leukemia, lymphoma, or another cancer that has spread (metastasized) to the bone marrow—people with cancers often experience excessive bleeding due to a significantly decreased number of platelets. As the number of cancer cells increases in the bone marrow, normal bone marrow cells are crowded out, resulting in fewer platelet-producing cells.
  • Aplastic anemia—a condition in which the production of all blood cells is significantly reduced
  • Sepsis, especially sepsis caused by a serious Gram-negative bacterial infection
  • Cirrhosis
  • Autoimmune disorders, such as lupus, where the body’s immune system produces antibodies that attack its own organs or tissues, causing increased destruction of platelets
  • Chemotherapy or radiation therapy, which may affect the bone marrow’s ability to produce platelets
  • Platelets may be used up quickly in serious conditions, such as disseminated intravascular coagulation (DIC), thrombocytopenic purpura (TTP), and hemolytic uremic syndrome (HUS).
  • Bone marrow damage caused by exposure to toxic chemicals, such as certain pesticides or benzene
  • Excessive alcohol drinking, especially in heavy drinkers who are low in iron, vitamin B12 or folate
  • A number of congenital (genetic) syndromes that result in a decreased number of platelets


There is no universally applicable reference value

The reference values provided herewith should be used as guidelines only. Reference values vary based on several factors, including the demographics of the healthy population from which specimens were obtained and the specific methods and/or instruments used to assay these specimens. Laboratories are required to establish and/or validate their own reference values at least annually. Thus, any given result should be interpreted based on the reference value of the laboratory in which the test was done; the laboratory typically provides these values with the test result.

Therefore, there is no universally applicable reference value!  A normal result in one lab may be abnormal in another: You must use the range supplied by the laboratory that performed your test to evaluate whether your results are “within normal limits.” While accuracy of laboratory testing has significantly evolved over the past few decades, some lab-to-lab variability can occur due to differences in testing equipment, chemical reagents used, and analysis techniques.

A normal result does not promise health

While having all test results within normal limits is certainly a good sign, it’s not a guarantee. For many tests, there is a lot of overlap among results from healthy people and those with diseases, so there is still a chance that there could be an undetected problem. Lab test results in some people with disease fall within the reference range, especially in the early stages of a disease.

An abnormal result does not mean you are sick

A test result outside the reference range may or may not indicate a problem. Since many reference values are based on statistical ranges in healthy people, you may be one of the healthy people outside the statistical range, especially if your value is close to the expected reference range. However, the abnormal value does alert your healthcare provider to a possible problem, especially if your test result is far outside the expected values.