Biochemistry

The term “total protein” covers a large group of all blood plasma proteins and interstitial fluid. This concerns more than 100 structurally known proteins. Their key functions include maintenance of oncotic pressure, transportation of many substances, defence against infection, enzyme activity, hemocoagulation, buffering and anti-oxidation effects. The liver synthesises most of these proteins, but lymphocytes are also involved in their production. Sufficient intake of proteins in food, as a source of amino acids (particularly essential amino acids, which our body is unable to produce) also plays an important role in synthesis. Synthesis is regulated by hormones. 

Metabolic products are amino acids, which are subsequently used for synthetic reactions or are metabolised further. The final product of protein degradation is urea, which is mainly excreted in urine. A small amount of protein molecules are excreted directly in the urine and faeces. 

Testing the concentration of total serum protein provides us with approximate information about biosynthesis, utilisation and excretion of proteins.  

Reference limits: 

0 - 1 week 44 - 76 g/l
1 week - 1 rok 51 - 73 g/l
1 - 2 years 56 - 75 g/l
2 - 3 years 58 - 78 g/l
3 - 15 years 60 - 80 g/l
> 15 years 64 - 83 g/l

Albumin makes up the greatest fraction (55 - 65%) of all plasma proteins. The colloid osmotic pressure of the plasma depends on its concentration, it binds and transports a number of blood components, it serves as a reserve of amino acids for producing proteins and is also the main plasma antioxidant. Concentrations depend mainly on its distribution, less on production defects, increased catobolism, or increased losses. Measuring albumin is essential for understanding and interpreting calcium and magnesium levels.

Reference limits: 

0 - 3 m: 28,0 - 44,0 g/l
3 m - 49 y: 35,0 - 52,0 g/l
49 + t: 35,0 - 53,0 g/l

Globulin is the name of the serum protein fraction that moves slower than albumin during serum electrophoresis (a system of separation methods that separates substances depending on their different motion in a direct current electrical field). The term “globulin” is a general term, which encompasses a number of proteins, it is less soluble in water and has larger molecules than albumin. 

Electrophoresis proteins are used to categorise globulins and are divided into 4 categories (Alpha 1 globulins, Alpha 2 globulins, Beta globulins - these have a transportation function and Gamma globulins - this group chiefly includes immunoglobulins, which function as antibodies. )

Globulins are the product of specialised cells of the body’s defence system  - the lymphatic tissue. 

When determining total proteins, the total amounts of two classes of proteins are measured: albumin and globulin. 

The A/G ratio is calculated on the basis of the values obtained by direct measurement of total proteins and albumin. This expresses the relative albumin and globulin numbers in total protein.  Under normal circumstances, there are more albumins than globulins. Many pathological conditions cause changes to albumin and globulin concentrations in various ways. 

We use this parameter to determine the nutritional condition or when looking for some liver, kidney or other diseases.

Reference limits: 

Reference range: of the A/G coefficient is 1.5 - 2

Total proteins are the total concentration of all blood plasma proteins. When determining total proteins, the total amounts of two classes of proteins are measured: albumin and globulin. 

Albumin transports many small molecules in the body, but its main role is to retain fluid within the bloodstream and prevent it from leaking. 

Globulins include enzymes, antibodies and more than 500 other proteins. 

The A/G ratio is calculated on the basis of the values obtained by direct measurement of total proteins and albumin. This expresses the relative albumin and globulin numbers in total protein. 

Under normal circumstances, there are more albumins than globulins. Many pathological conditions cause changes to albumin and globulin concentrations in various ways. 

We use this parameter to determine the nutritional condition or when looking for some liver, kidney or other diseases. 

Reference limits: 

The reference range: 1.5 – 2 

Bilirubin is a bile pigment of a hydrophobic nature, which results from the breakdown of heme.

Its synthesis is chiefly concentrated in the spleen, bone marrow, liver and in the skin. 

Total bilirubin consists of unconjugated and conjugated components. 

Erythrocytes breakdown to release hemoglobin, which breaks down further into heme and globin. The heme is subsequently transformed into biliverdin and this produces unconjugated bilirubin.  This is bound to blood protein (albumin) and transported to the liver, where it is conjugated with glucorunic acid to produce conjugated bilirubin. Conjugated bilirubin is water soluble and is excreted through the bile ducts as a component of bile, into the intestine where it is converted into stercobilinogen by intestinal bacteria and causes the brown colour of the stool. Some of the bilirubin is broken down by bacteria into urobilinogen, which is reabsorbed into the circulatory system and excreted in the urine (so-called enterohepatic circulation). 

Hyperbilirubinemia is the main symptom of bilirubin metabolism disorders. If levels increase to over 30 μmol/l, we can observe yellow skin and mucous membrane pigmentation, which is caused by bilirubin being deposited in the tissues. 

Bilirubin levels are determined for diagnosis of hepatopathy, for diagnosis of congenital disorders of bilirubin metabolism, conditions with intra/extravascular hemolysis, ineffective hematopoiesis.

Reference limits: 

The reference range: 3 – 17 μmol/l

Bilirubin, a bile pigment of a hydrophobic nature, originates through breakdown of heme (erythrocytes break down to release hemoglobin, which breaks down further into heme and globin). The heme is subsequently transformed into biliverdin and this produces unconjugated bilirubin. This is bound to blood protein (albumin) and transported to the liver, where it is conjugated with glucorunic acid to produce conjugated bilirubin. Conjugated bilirubin is water soluble and is excreted through the bile ducts as a component of bile, into the intestine where it is converted into stercobilinogen by intestinal bacteria and causes the brown colour of the stool. Some of the bilirubin is broken down by bacteria into urobilinogen, which is reabsorbed into the circulatory system and excreted in the urine. 

This means that conjugated bilirubin levels inform us of liver damage or decreased bile flow. 

Reference limits: 

Reference range: <5 μmol/l  

Bilirubin, a bile pigment originating through the breakdown of heme (erythrocytes break down to release hemoglobin, which breaks down further into heme and globin). The heme is subsequently transformed into biliverdin and this produces unconjugated bilirubin. This is bound to blood protein (albumin) and transported to the liver, where it is conjugated with glucorunic acid to produce conjugated bilirubin. Conjugated bilirubin is water soluble and is excreted through the bile ducts as a component of bile, into the intestine where it is converted into stercobilinogen by intestinal bacteria and causes the brown colour of the stool. Some of the bilirubin is broken down by bacteria into urobilinogen, which is reabsorbed into the circulatory system and excreted in the urine. 

This means that the level of unconjugated bilirubin informs us of increased breakdown of red blood cells. 

Reference limits: 

Reference range: < 12 μmol/l  

Is an enzyme that is present specifically in liver tissue in the cytosol of hepatocytes. Enzyme activity is a sensitive indicator of the extent of liver damage. The half-life of this enzyme in plasma is 47 hours. Increased levels, along with the cytoplasmic isoenzyme AST, indicates a lesion in the membrane, particularly in the hepatocytes. Simultaneous determination of AST and determination of the AST/ALT ratio is important. Levels below 1 are usually present during slight liver impairment, often of an inflammatory nature. Levels over 1  or possibly 2, are present during more serious, chronic disease, often necrotic.

Reference limits: 

0 - 1 months: 0,06 – 1,27 μkat/l 

1 months – 1 year: 0,06 - 0,97 μkat/l 

1 year – 15 years: 0,06 - 0,65 μkat/l 

MALE: 

15 years - >50 years: 0,06 - 0,67 μkat/l 

FEMALE: 

15 years - >50 years: 0,06 - 0,58 μkat/l

Is an enzyme that is present specifically in liver tissue in the cytosol of hepatocytes. Enzyme activity is a sensitive indicator of the extent of liver damage. The half-life of this enzyme in plasma is 47 hours. Increased levels, along with the cytoplasmic isoenzyme AST, indicates a lesion in the membrane, particularly in the hepatocytes. Simultaneous determination of AST and determination of the AST/ALT ratio is important. Levels below 1 are usually present during slight liver impairment, often of an inflammatory nature. Levels over 1 or possibly 2, are present during more serious, chronic disease, often necrotic.

Reference limits: 

1 - 1 months: 0,06 – 1,27 μkat/l 

1 months – 1 year: 0,06 - 0,97 μkat/l 

1 year – 15 years: 0,06 - 0,65 μkat/l 

MALE: 

15 years - >50 years: 0,06 - 0,67 μkat/l 

FEMALE: 

15 years - >50 years: 0,06 - 0,58 μkat/l

Is an important enzyme present in all tissues, but particularly in the liver, biliary tract, kidneys, pancreas and intestine. Increased serum levels are the result of increased synthesis of this enzyme, caused by induction of alcohol or drugs. Levels may also be increased during malfunction of cellular membranes or release of the enzyme from the surface of cells. GMT levels are considered a sensitive, but not specific marker, mainly of liver damage with bile excretion disorders. GMT levels can increase substantially in patients with liver cirrhosis caused by alcohol. Increased levels are also present with acute or chronic hepatitis, fatty liver, cholestasis, liver tumours, possibly hormonal contraceptives. The amount of drugs also affects the increase in GMT levels, which react quite sensitively. (This applies to anti-epileptic drugs, anti-convulsants, thyreostatic drugs, steroids with anabolic effect, thiazide diuretics, meprobomate, phenothyiazine, tuberculostatic agents, antirheumatics, cytostatic agents, etc.) 

Reference limits: 

CHILDREN: 0 - 1 day: 0,10 – 2,52 μkat/l 1 day - 1 year: 0,10 – 1,68 μkat/l 

1 year – 15 years: 0,10 – 0,34 μkat/l 

FEMALE: 

15 years – >50 years: 0,10 - 0,67 μkat/l 

MALE: 

15 years – >50 years: 0,10 - 1,07 μkat/l

Alkaline phosphatase is an enzyme consisting of a number of isoenzymes catalysing hydrolysis of phosphate monoesters during increased alkaline pH: hepatobiliary diseases and acute pancreatitis, liver and bone disease (cirrhosis, Crohns diseases, DM, etc.)

Reference limits: 

CHILDREN: 0 - 1 months: 0,80 - 6,77 μkat/l (female), 1,25 - 5,32 μkat/l (male) 1 months – 1 year: 2,07 - 5,68 μkat/l (female), 1,37 - 6,38 μkat/l (male) 

1 year – 3 years: 1,80 - 5,28 μkat/l (female), 1,73 - 5,75 μkat/l (male) 

3 years – 6 years: 1,60 - 4,95 μkat/l (female), 1,55 - 5,15 μkat/l (male) 

6 years – 9 years: 1,15 - 5,42 μkat/l (female), 1,43 - 5,25 μkat/l (male) 

9 years – 12 years: 0,85 - 5,53 μkat/l (female), 0,70 - 6,03 μkat/l (male) 12 years – 15 years: 0,83 - 2,70 μkat/l (female), 1,23 - 6,50 μkat/l (male) 

15 years – 18 years: 0,78 - 1,98 μkat/l (female), 0,87 - 2,85 μkat/l (male) 

MALE: 

18 years - 50 years: 0,88 - 2,13 μkat/l 

50 years - >50 years: 0,93 - 1,98 μkat/l 

FEMALE: 

18 years - 50 years: 0,70 - 1,63 μkat/l 

50 years - >50 years: 0,88 - 2,35 μkat/l

Creatinase is an enzyme that is mainly localised in the skeletal muscles and in the cardiac muscle. Total CK consist of multiple isoenzymes. Total CK levels increase especially during damage to the skeletal muscles, cardiac muscle and brain. It is used as a  marker to confirm acute myocardial infarction when more appropriate tests are not available. This assay is suitable when treating patients with cardiotoxic drugs and also as an early marker for rhabdomyolosis during treatment with statins.

Reference limits: 

CHILDREN: 0 – 1 year: 0,20 – 2,44 μkat/l 1 year - 15 years: 0,20 - 2,27 μkat/l FEMALE: 15 years - 30 years: 0,20 - 2,50 μkat/l 

30 years - 40 years: 0,20 - 2,22 μkat/l 

40 years - 50 years: 0,20 - 3,10 μkat/l 

50 years - 60 years: 0,20 - 2,90 μkat/l 

60 years - >50 years: 0,20 – 1,90 μkat/l 

MALE: 15 years - 30 years: 0,20 - 3,80 μkat/l 

30 years - 40 years: 0,20 - 2,85 μkat/l 

40 years - 50 years: 0,20 - 3,60 μkat/l 

50 years - 60 years: 0,20 - 4,30 μkat/l 

60 years - >50 years: 0,20 - 2,60 μkat/l

Creatinase is an enzyme that catalyses phosphate transfer from ATP to creatine. It plays an important role in ATP synthesis. It occurs in 3 forms: CK BB (B = brain), CK MM (M = muscle), CK MB (myocardial).

Most CK-MB is therefore found in the cardiac muscle. Its concentration increases during damage to cardiac muscle cells, which is why we measure its levels (along with other cardiac markers) in patients with chest pain, in order to determine whether they have suffered a myocardial infarction. CK-MB levels increase over a period of 3-6 hours from the time myocardial ischemia begins. 

If myocardial infarction has occurred, we can subsequently monitor the effectiveness of treatment using CK-MB. 

Increased levels can also be detected in other heart diseases, such as myocarditis, angina pectoris, post heart surgery conditions...and, because it is not fully cardiac specific, we can also use it to detect an increase in damage to skeletal muscles (trauma, muscular dystrophy, intramuscular injections, resuscitation, defibrillation), during extreme exercise and chronic renal insufficiency.

Reference limits: 

Reference range: Men 0,2–3,6 μkat/l         

Women 0,2–3,1 μkat/l

Lactate dehydrogenase is NAD + oxidoreductase catalysing oxidation of lactate into pyruvate. The reaction is reversible and it reduces pyruvate to lactate at physiological pH. There are 5 isoforms of LD in serum consisting of 4 sub-units (peptide chains) of two types - H and M. We distinguish LD-1 (H4) in the heart, erythrocytes, kidneys and testicular tumours; LD-2 (H3M) in the cardiac muscle, erythrocytes and kidneys; (LD-3 (H2M2) in the spleen, lymph nodes and thrombocytes; LD-4 (HM3) and LD-5 (M4) both in the liver and skeletal muscles. LDH is used for differential diagnosis of haemolytic anaemia and as a tumour marker for some cancerous tumours, e.g. germ-cell tumours. With regard to the fact that LDH is a non-specific marker, it is used during diagnosis and treatment of the patient in combination with other markers. 

Reference limits: 

CHILDREN: 0 – 1 day: 5,43 – 11,20 μkat/l 1 day – 1 months: 2,08 - 12,75 μkat/l

1 month c – 1 year: 2,83 – 7,50 μkat/l

1 year – 3 years: 2,58 – 6,58 μkat/l

3 years – 6 years: 2,25 – 5,75 μkat/l

6 years – 9 years: 2,33 - 5,00 μkat/l

9 years – 12 years: 2,00 - 5,42 μkat/l

12 years – 15 years: 1,67 – 4,83 μkat/l

15 years – 18 years: 1,75 – 3,92 μkat/l FEMALE:

18 years - >50 years: 2,25 – 3,58 μkat/l

MALE:

18 years - >50 years: 2,25 - 3,75 μkat/l

Lactate dehydrogenase (LD or LH) is an oxidoreductive enzyme catalysing reversible conversion of lactate into pyruvate. It occurs as a tetramer, consisting of one or two various types of sub-unit. Various combinations of H and M sub-unit produce 5 isoenzymes (LD1-5). The individual tissues are distinguished by their presence. 

Alpha-HBDH is not an separate specific enzyme, but is a general term for LD1 and LD2. Alpha-HBDH levels, which actually reflect the activity of LDH1 and 2 isoenzymes, are measured for the purpose of diagnosing myocardial disease and liver disease. 

For example, higher levels can be detected during acute myocardial infarction, lymphoma, leukaemia and haemolytic anaemia. On the contrary, lower levels will be detected in patients being treated with immunosuppressive therapy or anti-tumour therapy. 

Reference limits: 

Reference range: 90 – 220 U/l

Use: for monitoring TAG levels, determining cardiovascular risk, monitoring hypolipidemic treatment, monitoring the patient when giving parenteral nutrition in intensive care, as part of the Friedewald equation and Planell calculation for LDL

Clinical data: TAG are glycerides consisting of one molecule of glycerol combined with fatty acid molecules from all three OH groups (the fatty acids can be all different or all the same or two of them the same). Ester bonds are formed between each of the fatty acids and the glycerol. The pancreatic lipase enzyme acts on these and hydrolyses these bonds to release the fatty acids.  Lipids in the form of TAG cannot be absorbed in the duodenum. Fatty acids, monoglycerides (one glycerol molecule, one fatty acid molecule) and some diglycerides, can be absorbed.   

These form most of the fats in the food humans eat. They are the main component of vegetable oil and animal fat. 

TAG are the main element in very low density lipoproteins (VLDL) and chylomicrons.  They play an important role in the metabolism as a source of energy and carrier of nutritional fat. They contain more than twice the energy of carbohydrates and proteins. They breakdown into monoacylglycerols and free fatty acids in the intestine during a process called lipolysis. These substances are then transferred into cells in the intestinal walls where they are used to produce TAG again, which are converted to chylomicrons along with cholesterol and proteins. These are excreted from the cells, collected by the lymph system and transported to the large veins. Chylomicrons may be captured by various tissues and release TAG for use as a source of energy. 

They are endogenously synthesised chiefly in the liver, fatty tissue and small intestine. 

Increased serum TAG levels are a risk factor for atherosclerosis and extremely high TAG levels can lead to pancreatitis. 

 Slightly higher TAG levels, low HDL levels and slightly higher cholesterol levels form the atherogenic triad. This lipoprotein phenotype is typical for diabetics and patients with metabolic syndrome. TAG must always be evaluated in the context of the overall lipid profile). 

Sources: https://www.cskb.cz/res/file/KBM-pdf/2010/2010-1/dop-lipidy.pdf 

https://cs.wikipedia.org/wiki/Triacylglycerol

Reference limits: 

Reference range: 0.45 – 1.70 mmo/l (upper and lower limits)

Cholesterol is present in all animal tissues, in bile and in the blood. It is an essential and important component of the cellular membranes and is used to produce important substances (steroid hormones, bile acids, etc.). The body produces it independently and also receives it in animal-based food products. It is not present in plant-based food products. Its intake with food has only a small effect on blood cholesterol levels. One quarter of increased cholesterol levels is caused by genetic factors. Increased cholesterol levels are one of the risk factors for atherosclerosis.

Reference limits: 

2,90 - 5,00 mmol/l

These are high-density lipoprotein particles, which transport around 25% of total cholesterol. They are produced in the liver and small intestine. These particles pick up free cholesterol from the peripheral tissues,  partially esterify it, convert to other types of particle and metabolise it. Measuring HDL levels is very important in relation to assessing atherogenic risk. A so-called atherogenic index, or the total cholesterol to HDL cholesterol ratio, is calculated.

Reference limits: 

CHILDREN: 

0 – 15 years: 1,03 - 1,81 mmol/l 

FEMALE: 

15 years – >50 years: 1,20 – 2,70 mmol/l 

MALE: 

15 years – >50 years: 1,00 - 2,10 mmol/l

These are low-density lipoprotein particles, which enable cholesterol, triacylglycerols to be dissolved and transported through the bloodstream.  They are produced in the liver from VLDL.  Lipoprotein lipase in skeletal muscle and adipose tissue depletes the VLDL of TAG, which  is enriched by esterified cholesterol through the effects of cholesteryl ester transfer protein. This produces IDL, which can be used to produce LDL. These are also partially produced in the liver. These particles are broken down in all cells with the respective receptor, but mainly in the liver.  LDL cholesterol is identified as a key factor during pathogenesis of atherosclerosis and coronary cardiac disease.

Increased levels are the result of a defect in LDL-receptor formation or apoprotein B-100 defect. 

Reference limits: 

1,20 - 3,00 mmol/l

Glucose is a simple sugar (saccharide), which is used by our body as the main source of energy for all cells. We usually ingest polysaccharides (carbohydrates consisting of simple sugars) in our food, which are broken down into glucose (and other simple sugars), subsequently absorbed in the small intestine and transported.  

Under physiological conditions, blood glucose levels (glycaemia) are maintained within a narrow range of values (a significant decline or increase in these levels is pathological). These levels are strictly regulated by a number of mechanisms: insulin, which lowers glycaemia, as well as anti-insulin hormones - glucagon, catecholamine, glucocorticoids and growth hormone, which elevates glycaemia. The liver has a crucial effect on regulation of glucose homeostasis. 

Glucose level tests are used to prove both hyperglycaemia and hypoglycaemia.  These tests mainly help to  diagnose diabetes mellitus and are then used to monitor this disease if diagnosed. 

Reference limits: 

Reference range:  3.9 – 5.6 mmol/l

(Confirmation of diabetes mellitus diagnosis if test results on an empty stomach are >7.00 mmol/l. and random results are  >11.1 mmol/l

If blood glucose levels remain elevated for a specific period, then the glucose molecules attach to blood protein molecules. This process is called glycation (it particularly concerns albumin, as well as other proteins and hemoglobin to a lesser degree). The higher the blood glucose level, the more glycated proteins and glycated hemoglobin is produced. These linked molecules subsequently persist in the circulatory system until the end of their lifespan.  The lifespan of erythrocytes is 120 days, which is why glycated hemoglobin reflects average glycaemia values for the last 2-3 months, whereas serum proteins have a shorter lifespan of approximately 14-21 days and therefore represent the average glucose level for 2-3 weeks. 

Glycated hemoglobin and glycated protein tests are therefore used to control diabetes mellitus and to diagnose chronic hyperglycaemia.  Elevated glycated derivative levels indicate that the patient experienced predominant elevated blood glucose levels in the elapsed weeks and that diabetes mellitus was not compensated sufficiently.   

Reference limits: 

Reference range: Glycated protein men: 1.5– 2.1 mmol/l, women: 1.4– 1.9 mmol/l 

An amino acid that is produced during normal metabolism from the amino acid methionine, which is one of the 11 essential amino acids, which must be obtain from food, because our body is unable to produce it. 

Homocystein is broken down into cystein by means of B vitamins (particularly B6, B12 and folic acid). A lack of these vitamins in food, or a rare congenital disorder (homozygous homocystinuria) may lead to elevated blood homocystein levels. 

A number of studies have proven an increased risk of myocardial infarction in people with elevated homocystein, compared to people with average levels. Elevated homocystein levels are linked to an increased tendency to form unnecessary blood clots. 

This means we can test for homocystein levels as part of assessment of the risk of origin of atherosclerosis depending on age and other risk factors. This test can also be used as an auxiliary factor for monitoring treatment following myocardial infarction. Detection is appropriate in persons with a suspected deficit of vitamin B12 or folic acid and in children with suspected homocystinuria.  

Reference limits: 

Reference range: 3 – 15 μmol/l   

An enzyme secreted in the acinar cells in the pancreas and released into the small intestine in the form of pancreatic secretion (pancreatic juice) along with other digestive enzymes. AMS is excreted from the circulatory system through glomerular filtration. 

For clinical diagnosis, AMS levels in the serum and urine are measured and the amylase/creatine index clearance is calculated. 

Increased serum p-AMS activity is typical for pancreatic disease, such as acute pancreatitis, pancreatic cancer, etc. Elevated levels can also be detected in relation to non-pancreatic disease (intestinal perforation, gall bladder colic, liver disease, diabetic coma, ulcer, etc....). 

Reference limits: 

S-AMS total serum amylase 0.30–1.67 μkat/l

U-AMS total urine amylase < 7.67 μkat/l

S-pAMS serum pancreatic amylase 0.22–0.88 μkat/l

U-pAMS urine pancreatic amylase < 5.83 μkat/l

A cyclic amide or creatin lactam secreted in the muscles. The body produces creatinine at a relatively stable rate. Its production is a reflection of muscle mass (which is why the production rate is a little higher in men).

It is stable at physical rest and if a meat-free diet is maintained.  it is excreted by the kidneys, mostly by glomerular filtration, the kidney tubules excrete it in more considerable volumes only if blood levels are increased. 

Measuring serum creatinine levels is a good indicator of glomerular filtration and is used especially for monitoring the progress of kidney disease (including patients undergoing dialysis). 

Reference limits: 

Serum creatinine in women: 44– 104 μmol/l.

Serum creatinine in men: 44– 110 μmol/l

An organic compound containing nitrogen, which is the end metabolite of proteins - amino acids. The blood levels of this compound chiefly reflect kidney activity. It is produced in the liver. Ammonium is produced during protein catabolism and is converted to urea in the urea cycle.  Serum levels also partially depend on dietary protein content. Levels are lower during pregnancy (increased nitrogen amino acid requirements for protein synthesis). In adults, 90% of ingested amino acids are converted to urea (approx. 16 g per day). Urea levels increase substantially if glomerular filtration falls to below 0.5 ml/s.

Reference limits: 

CHILDREN: 

0 – 15 years: 2,6 – 7,5 mmol/l 

adults: 15 years - 90 years: 2,6 – 8,3 mmol/l 90 years - >50 years: 3,6 – 11,1 mmol/l

Urea is quantitatively the most important product of amino acid and protein breakdown. It is produced in the liver from ammonia. It passes easily through cellular membranes, so its levels are identical in plasma and in intracellular fluid. it is excreted mainly by the kidneys by glomerular filtration and tubular resorption. Minor amounts are also excreted in sweat and some seeps into the intestine. 

Blood urea levels depend on dietary protein content, kidney excretion and liver metabolic function. Urea level tests are mainly used to assess kidney function and protein catabolism levels. 

Reference limits: 

0 – 6 weeks - 0.7 – 5.0 mmol/l

6 weeks – 1 year - 0.4 – 5.4 mmol/l

1 – 15 years- 1.8 – 6.7 mmol/l

women 15 – 60 years - 2.0 – 6.7 mmol/l

men 15 – 60 years - 2.8 – 8.0 mmol/l

60 – 90 years - 2.9 – 8.2 mmol/l

> 90 years - 3.6 – 11.1 mmol/l

A colourless gas, flavourless, odourless, heavier than air. Its molecule consists of one carbon atom and two oxygen atoms. 

CO2 is a by-product of oxidative metabolism and released from tissue into the blood on the basis of the pressure gradient. It is transported in the blood as physically dissolved and bound to proteins, or as a bicarbonate molecule. 

Most  CO2 produced in the tissues is transported to the lungs in the form of HCO3-. The bicarbonate anion (HCO3-) is mainly produced in the erythrocytes (red blood cells) and also, to a limited degree, in the plasma. 

In the lungs, oxygen is attached to the hemoglobin, which reduces CO2 affinity, and it is therefore released in the lungs and exhaled. 

CO2 is measured as part of the blood gas test (so-called Astrup). This test is one of the basic methods used during ventilatory and respiratory disorders (e.g. asthma bronchiale, CHOPD...), and also during cardiac disorders and internal diseases - kidney and liver disease, some types of poisoning, etc.)  

Reference limits: 

Reference range: pCO2 (partial CO2 pressure) 5.3 +/- 0.5 kPa

Parathormone is a single-chain polypeptide secreted by the parathyroid glands. Intact PTH is excreted into the bloodstream where it is extensively proteolytically modified. On the contrary to the levels of its degradation products, its levels are independent of glomerular filtration and correspond to the biologically active level of  this hormone. Its key function is to regulate blood calcium levels. Synthesis and secretion of PTH is stimulated within several minutes CA2+ levels are low. Its biological effect consists of increasing calcium absorption from food; reducing kidney clearance and release reserves of skeletal calcium. 

Reference limits: 

2 years – 20 years: 0,95 – 5,51 pmol/l 

20 years – >50 years: 1,59 – 7,24 pmol/l

An element that is part of bones and teeth, along with calcium. It plays a very important role in cellular energy management (ATP) and during synthesis of important compounds, including nucleic acids for example. Parathormone, calcitonin and vitamin D manage phosphor exchange in the bones. These compounds also influence its storage if calcium levels are sufficient. A fall in phosphate levels leads to an ATP deficit, which manifests as reduced erythrocyte and thrombocyte lifespan. This is followed by muscular weakness in the limbs, loss of appetite, disorders of articulation and muscles of mastication and hyperventilation.

Reference limits: 

CHILDREN: 0 - 1 months: 1,60 – 3,10 mmol/l 1 months - 1 year: 1,60 - 2,60 mmol/l 1 year - 15 years: 1,10 - 2,00 mmol/l 

adults: 

15 years - >50 years: 0,85 – 1,45 mmol/l

The potassium ion is an important element in the human body. It forms the cation in the cell core. It is crucial for electrical activity in cell membranes, particularly in the heart, muscles and nerves. Potassium disorders may have serious effects, particularly on heart rhythm. Reduced potassium levels are nearly always accompanied by lowered magnesium levels. Potassium level reduction is caused by use of diuretics and laxatives, renal function disorders, sweating, vomiting, diarrhoea, leukaemia, intestinal and gall bladder fistula, anorexia and various types of syndrome. Potassium levels rise in the case of reduced kidney excretion during chronic renal insufficiency, when potassium is transferred from the cells into the serum during tissue breakdown (burns, injury, etc.).

Reference limits: 

CHILDREN: 0 – 1 months: 3,70 – 5,90 mol/l 1 months - 2 years: 4,10 – 5,30 mol/l 2 years - 15 years: 3,30 – 5,40 mol/l adults: 15 years – >50 years: 3,50 – 5,10 mol/l

Sodium is the main extracellular cation. It is involved in osmotic mechanisms for maintenance of body fluid volume. It also affects electric activity in cell membranes. Increased sodium loss is prevented by the hormone aldosterone. Increased sodium intake in the form of rock or kitchen salt increases blood pressure and this is also inappropriate during cardiac, kidney or liver disease linked to swelling. Sodium is crucial for maintaining the acid-base balance and maintaining blood osmolality.

Reference limits: 

CHILDREN: 0 - 18 years: 130 - 145 mmol/l 

adults: 

18 years – >50 years: 134 - 148 mmol/l

An element involved in nerve and muscle activity and production of a number of enzymes in the body. Leafy vegetables are the main source. It is applied intravenously in the case of treatment for spasms and is also contained in drugs reducing stomach acidity. Along with the potassium cation, Mg is one of the most important intracellular cations. Mg deficiency results in serious proteosynthesis disorder. It also plays an important role in phagocytosis, capillary permeability and hemocoagulation. Vitamin D and its metabolites activate Mg absorption, and Ca absorption to a lesser degree. Magnesium influences bone mineralisation, acts as an aggregation and crystallisation inhibitor and thereby prevents formation of urine concrements, reduces muscle tone, and affects heart rhythm and blood pressure.

Reference limits: 

CHILDREN: 0 – 1 months: 0,70 - 1,15 mmol/l 1 months - 1 year: 0,66 - 0,95 mmol/l 1 year - 15 years: 0,78 - 0,99 mmol/l 

adults: 

15 years – 149 years: 0,70 – 1,10 mmol/l 

149 years – >50 years: 0,80 – 1,00 mmol/l

This is the most abundant anion in the body and is strongly dissociated under physiological conditions. 88% of this element is found in the body extracellularly. Intake and loss of this element corresponds to physiological intake and loss of sodium. It is involved in maintaining osmotic pressure and the acid-base balance. Chlorides are important during secretion of hydrochloric acid in the stomach. Increased levels are present during NaCl infusion, nephropathy, dehydration, congenital kidney disorders, etc. Reduced levels are present during diarrhoea, vomiting, sweating, use of diuretics, chronic laxative use, hyperaldosteronism, etc.

Reference limits: 

95 - 112 mmol/l

This is a colourless, pungent gas with the formula NH3. 

Its peripheral blood levels are very low, its production may increase during metabolic alkalosis for example (ammonia is involved in regulating the acid-base balance and retention of some cations).  Ammonia may be produced in most tissue. In the human body, it is mainly produced by breakdown of proteins - it is a waste product of amino-nitrogen, amino acids and is a gut bacteria product. This is a neurotoxic substance that, under physiological conditions, is detoxified primarily in the liver by conversion to urea (which is not toxic). 

In the case of liver damage, it may accumulate in the blood and cause typical symptoms of its increased concentration (these are tremors, blurred vision, slurred speech and even coma and death during serious poisoning). It is also partially produced extrahepatically, but it them occurs in the blood plasma in non-toxic form, bound in glutamine and alanine molecules. 

Reference limits: 

Reference range: 18– 72 μmol/l