Residual blood nitrogen. Fractions of residual nitrogen

An increased content of residual nitrogen in the blood occurs with azotemia, but reduced values ​​\u200b\u200bare no less dangerous, this is a possible sign of hypoazotemia.

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Anna Poniaeva. She graduated from the Nizhny Novgorod Medical Academy (2007-2014) and residency in clinical laboratory diagnostics (2014-2016).

When carried out with a diagnostic purpose, many different parameters and indicators are comprehensively evaluated. One of them is residual blood nitrogen.

When carrying out, the total indicators of all blood substances, which include nitrogen, are evaluated after all proteins have been extracted from it. This sum of data is called residual nitrogen in the blood. It is recorded after the removal of all proteins, as they are the substances containing the most nitrogen in the human body.

Residual nitrogen is determined in , creatinine, creatine, amino acids, ergotianine, indican and ammonia. It can also be contained in substances of non-protein origin, for example, in peptides and some other compounds.

Obtaining data on residual nitrogen can give an idea of ​​the general state of health of the patient, as well as draw conclusions about the presence of a number of acute and, mainly related to the filtering and excretory function.

Diagnostics

A blood test for residual nitrogen requires proper preparation for a reliable result!

Since the test for residual nitrogen in the blood is part of the biochemical analysis, the preparation for it is exactly the same as for other components of this type of diagnosis.

There are certain rules that are recommended to be followed in order to obtain correct and accurate results:

• Since different laboratories may use different types of diagnostic specimens and use different systems for scoring results, it is better to perform the analysis in the same laboratory as before in case of a repeat analysis.
• A blood sample is taken from a vein, as an exception, they can also be taken from a finger if the veins are damaged or inaccessible.
• The analysis is carried out on an empty stomach, the fasting period takes at least 8-12 hours. All this time only pure water without gas and additives is allowed.
• The ideal time for the test is from 7 am to 11 am.
• It is advisable to maintain the usual type and diet for about three days before blood sampling, but exclude spicy, fried and fatty foods from it.
• It is also recommended to cancel sports activities for three days, especially if they are associated with large overloads.
• The test requires prior discontinuation of the medications taken. This must be discussed with the attending physician.
• Stress, excitement, increased excitability can affect the test result, so you need to sit quietly for about half an hour before performing the test.

With proper preparation, the sample readings should give accurate and reliable results. The interpretation of the analysis data should be carried out by specially trained medical personnel, but not on their own, since the sample indicators may fluctuate slightly relative to the standard.

Decryption: norm

In the normal state, residual nitrogen in the blood fits into the range from 14.3 to 26.8 mmol / l.

However, a rise in nitrogen levels even up to 35 mmol / l cannot be interpreted as a manifestation of pathology, since such indicators can be caused by a number of natural causes, for example, when using a large amount of nitrogen-containing food, eating dry food (dry food with a lack of extractive substances), before childbirth , after intense physical exertion and so on.

If the indicators are strikingly different from normal data, this may indicate the presence of a number of diseases in the patient's body.

Moreover, both strongly reduced figures of residual nitrogen and very high rates relative to the norm are pathological.

Reasons for the increase

The condition in which elevated numbers of residual nitrogen are recorded is called azotemia.

It can be of two types:

1. Retention azotemia is a condition in which excretory function is impaired, that is, renal failure occurs. The following diseases can be the cause of the development of retention azotemia: glomerulonephritis, polycystic, tuberculosis or hydronephrosis of the kidneys, nephropathy during pregnancy, arterial hypertension with the development of kidney disease, the presence of mechanical or biological obstacles to the natural outflow and excretion of urine (accumulation of sand, stones, benign or malignant neoplasms in the kidneys and urinary tract).
2. Production azotemia is recorded with an excess of nitrogen-containing substances that enter the bloodstream due to the accelerated breakdown of tissue proteins. Kidney function in this type of azotemia usually does not suffer. Production azotemia most often appears with severe fevers, during the decay of a tumor of any kind.

In some cases, a mixed type of azotemia may occur. Most often, it occurs when poisoning with toxic substances such as mercury salts, dichloroethane and other dangerous compounds, as well as injuries associated with prolonged squeezing and / or crushing of tissues. In this case, necrosis of the kidney tissues occurs, in which retention azotemia occurs along with production.

There may also be a sharp increase in residual nitrogen - up to 20 times above normal levels. This condition is called hyperazotemia and is the highest stage of manifestation of mixed azotemia. It can also be recorded in extremely severe kidney damage.

More information about kidney failure can be found in the video:

Nitrogen levels in the blood increase not only with kidney diseases, but also with impaired adrenal function (Addison's disease), with symptoms of heart failure, with extensive burns, especially serious degrees, with severe dehydration, if there are severe infectious diseases of a bacterial nature, gastric bleeding , severe stress.

Elimination of these manifestations is possible upon detection and treatment of the underlying cause of such a condition. For this, the doctor prescribes a number of additional tests and, based on the results of which, a conclusion is made and the necessary medications or other methods of treatment are prescribed.Timely delivery of tests will help to find the disease in time and cure it before the occurrence of complications or the transition to a chronic condition.

Residual nitrogen is plasma or serum nitrogen-containing compounds that are not proteins or polypeptides and remain in the supernatant after protein precipitation with trichloroacetic acid. Normally, residual nitrogen components are filtered in the glomeruli and some of them are not reabsorbed in the tubules. On this basis, the determination of the components of residual nitrogen in the blood serum is traditionally used to monitor kidney function.

Useful clinical information is obtained by determining the individual components of the residual nitrogen fraction. The residual nitrogen fraction includes 15 compounds representing the products of protein and nucleic acid metabolism. Clinically significant residual nitrogen compounds are shown in the table.

Table - Clinically significant components of residual nitrogen

Urea is the main component of residual nitrogen

The largest fraction of residual nitrogen is urea, the main end product of protein metabolism. It is synthesized in the liver from CO 2 and ammonia, which is formed during the deamination of amino acids. Urea is excreted by the kidneys, while 40% of it is reabsorbed in the tubules;<10% от общего содержания в крови выводятся через желудочно-кишечный тракт и с потом.

The concentration of urea is determined in order to assess the function of the kidneys,

assessing the degree of hydration, determining the nitrogen balance and to check the adequacy of dialysis. In sports medicine, the adequacy and digestibility of power loads are assessed by the level of urea.

Elevated concentrations of urea in the blood are called azotemia. A very high plasma urea concentration that accompanies kidney failure is called uremia, or the uremic syndrome.

There are the following reasons for the elevation of urea in plasma:

• prerenal,
• renal,
• postrenal.

Prerenal azotemias:

1) a decrease in the functional volume of blood filtered by the kidneys:

• congestive heart failure,
• shock,
• hemorrhage,
• dehydration.

2) high protein diet or increased protein catabolism (fever, severe illness, stress, exercise).

Renal azotemias- a decrease in the filtration function of the kidneys leads to an increase in urea in the blood:

• acute and chronic renal failure,
• glomerular nephritis,
• tubular necrosis,
• other kidney diseases.

Post-renal azotemias- obstruction of the outflow of urine:

• stones in the kidneys,
• tumors of the bladder or prostate,
• severe infections.

Reducing the content of urea nitrogen s:

• low protein in the diet;
• liver disease (reduced urea synthesis);
• severe vomiting and/or diarrhea (urea loss);
• increase in protein synthesis.

Reference values ​​for urea nitrogen: in serum or plasma from 6 to 20 mg / dl; in daily urine - 12 - 20 g.

Creatinine/creatine as residual nitrogen fraction

Creatine is synthesized in the liver from arginine, glycine and methionine.

In muscles, it is converted into creatine phosphate - an energy source for muscle work. Creatinine is formed as a by-product of creatine and creatine phosphate

1) Creatine phosphate - phosphoric acid = creatine;

2) Creatine - water = creatinine.

Creatinine is released from the muscles into the bloodstream at a constant rate proportional to muscle mass. It is filtered by the glomerulus and excreted in the urine. Does not undergo reabsorption in the kidneys .

Plasma creatinine concentration is a function of relative muscle mass, creatine turnover rate, and kidney function.

The daily excretion of creatinine is quite stable, which allows it to be used as a very good test for assessing kidney function.

Measurement of creatinine concentration is used to

• assessment of kidney function;
• severity of kidney damage;
• control of the course of kidney disease.

To assess kidney function, creatinine clearance is determined - the amount of creatinine eliminated per unit time by the kidneys from the blood. Plasma creatinine concentration is inversely proportional to clearance. Therefore, an increase in plasma creatinine reflects a decrease in filtration rate (GFR) . GFR is the volume of plasma (V) filtered by the glomeruli per unit time.

Table - Reference intervals for plasma or serum creatinine (mg / dl, µmol / l)

Creatine Increases in plasma and urine in muscular dystrophy, hyperthyroidism and trauma.

Samples were analyzed for creatine content before and after heating the acidic sample solutions using the Jaffe method.

Heating converts the creatine to creatinine and the difference between the two samples is the creatine concentration.

Uric acid as a component of residual nitrogen

Uric acid is the end product of the breakdown of purine bases (adenine/guanine) in the human liver.

Uric acid is filtered by the kidneys (70%); 98% of primary urine uric acid is reabsorbed in the proximal tubules, some is secreted in the distal tubules. With urine, 6-12% of the initial content in the blood is excreted; 30% is excreted through the intestines.

It is present in plasma as monosodium urate, which is relatively insoluble at plasma pH.

A plasma uric acid concentration > 6.8 mg/dl is saturating. Under saturation conditions, uric acid forms urate crystals, which precipitate in the tissues.

• assessment of hereditary disorders of purine metabolism,
• confirming the diagnosis and monitoring the treatment of gout,
• to assist in the diagnosis of the nature of kidney stones,
• to detect kidney dysfunction.

Gout. First of all, men are ill, the onset of the disease is 30-50 years. A disease marker is a uric acid concentration above 6.0 mg/dL. It is clinically manifested by pain and inflammation of the joints due to the deposition of sodium urate crystals in the tissues.

An increased risk is in 25-30% the formation of kidney stones.

Reference values ​​for uric acid: men - 0.5-7.2, women - 2.6-6.0 mg / dl.

Ammonia as a component of residual nitrogen

The concentration of ammonia in the blood ranges from 11 to 78 mmol/l. The main cause of hyperammonemia is acute and chronic liver disease (acute hepatitis, acute fatty degeneration) or portosystemic shunting (liver cirrhosis, surgical portosystemic shunts). The main amount of ammonia is produced in the large intestine with the participation of microflora, from where ammonia enters the portal system by passive diffusion and is normally taken up by the liver. In addition, a certain amount of ammonia is formed in the kidneys, small intestine, muscles. Ammonia is utilized by the synthesis of urea or non-toxic glutamine. Most ammonia is converted to urea in the liver with the participation of ornithine in the urea cycle, the rest is converted to glutamine in the liver, brain and skeletal muscles. Only a small amount of ammonia can be excreted in the form of an ammonium ion with urine and feces, as well as in a gaseous state - with exhaled air through the lungs. In tissues and fluids, ammonia exists in the form of ammonium ions NH 4+ in equilibrium with a small concentration of non-ionized ammonia NH 3 . Ammonia is a substance toxic to the human body, especially to the brain, the damaging effect of which is manifested by hepatic encephalopathy, which is a complex of syndromes of potentially reversible mental and neurological changes. When impaired consciousness reaches a severe degree, the term "hepatic coma" is used.

The concentration of ammonia in the blood ranges from 11 to 78 mmol/l. The main cause of hyperammonemia is acute and chronic liver disease (acute hepatitis, acute fatty degeneration) or portosystemic shunting (liver cirrhosis, surgical portosystemic shunts).

Widely used in diagnosis, they help to identify serious diseases such as diabetes, cancerous growths, various anemias, and take timely measures in treatment. Residual nitrogen is present in amino acids, indican. Its level can also indicate any pathological changes in the human body.

Blood chemistry

The indicative composition of the blood makes it possible with a high degree of probability to determine various changes in tissues and organs in the early stages. Preparation for biochemistry is carried out in the same way as with a regular blood test. For research, blood is taken from the cubital vein. The important criteria are:

The presence of protein
. nitrogenous fractions - residual nitrogen, creatinine, urea content, inorganic compounds;
. bilirubin content;
. the level of fat metabolism.

Residual blood nitrogen - what is it?

In conducting blood, the total indicators of the content of blood substances, which include nitrogen, are evaluated only after all proteins have already been extracted. The sum of the data is called the residual blood nitrogen. This indicator is recorded only after the proteins are removed, for the reason that they have the most nitrogen in the human body. Thus, the residual nitrogen of urea, amino acids, creatinine, indican, uric acid, ammonia is determined. Nitrogen may also be contained in other substances of non-protein origin: peptides, bilirubin, and other compounds. Residual nitrogen analysis data give an idea of ​​the patient's health, indicate chronic diseases, most often associated with problems in the excretory and filtering functions of the kidneys. Normally, residual nitrogen is from 14.3 to 28.5 mmol / liter. The increase in this indicator occurs against the background of:

Polycystic;
. chronic kidney disease;
. hydronephrosis;
. stones in the ureter;
. tuberculosis of the kidneys.

Diagnostics

Since the test for residual nitrogen is included in the biochemical analysis, preparation is carried out according to the same principles as before passing on other components of this diagnostic. To get more correct results, you need to follow a number of rules when donating blood for biochemistry:

If you have to take a second analysis, it is better to do it in the same laboratory as the first time. Since all laboratories have their own diagnostic samples, they differ in systems for evaluating the result.
. A blood sample is taken from the cubital vein, possibly from a finger if the vein is not accessible or damaged.
. It is necessary to carry out the analysis on an empty stomach, not less than 9-12 hours after the last meal. You can drink water, but without gas.
. The ideal time for blood sampling is considered to be 7-10 am.
. Three days before the analysis, it is better to maintain the usual diet, you only need to remove fatty, spicy and fried foods.
. For three days, sports activities should be excluded, especially if they are associated with body overloads.
. If you have to take an analysis for residual blood nitrogen, biochemistry requires the abolition of medication. This point must be discussed with the attending physician.
. The results may be affected by stress, anxiety, so at least half an hour before the test you need to sit in a calm atmosphere.
If the preparation for biochemistry was correct, then the test results will be more reliable. Only medical specialists should deal with decoding. Indicators often fluctuate relative to the standard, so they can be misinterpreted on their own.

The rate of residual nitrogen in the blood

Normal readings in the blood of residual nitrogen fit into the numbers from 14.3 to 26.8 mmol / l. It should be noted that the rise in the indicator even to 30-36 mmol / l is not immediately interpreted as a manifestation of pathology. Residual nitrogen, the norm of which is much less, can rise when eating nitrogen-containing foods, when eating dry food, and when there is a deficiency of emergency substances. A jump in the indicator can also occur before childbirth, after enhanced sports training, and for a number of other reasons. That is why it is necessary to carefully prepare for the delivery of samples for blood biochemistry. If the tests dramatically overestimate or underestimate the norm and at the same time there was proper preparation before blood sampling, this may indicate a number of diseases in the body.

The fraction of residual nitrogen includes:

Urea nitrogen (46-60%);
. creatine (2.5-2.7%);
. amino acid nitrogen (25%);
. uric acid (4%);
. creatinine (2.6-7.5%);
. other products of protein metabolism.

Residual nitrogen is the difference between residual nitrogen and urea nitrogen. Here, the free fraction is free amino acids.

Pathologies

Residual nitrogen pathologies include:

• hyperazotemia - when the level of residual nitrogen in the blood is too high;
• hypoazotemia - residual nitrogen in the blood is underestimated.

Hypoazotemia is most commonly seen with poor nutrition or, rarely, during pregnancy.

Hyperazotemia is divided into retention and production.

With retention hyperazotemia, violations of the excretory function of the kidneys occur, in this case, renal failure is diagnosed. The most common causes of the development of retention hyperazotemia are the following diseases:

Glomerulonephritis;
. pyelonephritis;
. hydronephrosis or tuberculosis of the kidneys;
. polycystic;
. nephropathy during pregnancy;
. arterial hypertension in the development of kidney disease;
. the presence of biological or mechanical obstacles to the outflow of urine (stones, sand, malignant or benign formations in the kidneys, urinary tract).

Production hyperazotemia

Elevated residual blood nitrogen may indicate production hyperazotemia, when the pathological condition is accompanied by a syndrome of endogenous intoxication. It is also observed with prolonged stress in the postoperative period. Production hyperazotemia is noted in infectious diseases that occur with fever, when progressive tissue breakdown occurs, these include diseases: diphtheria, scarlet fever. Production hyperazotemia is characterized by an increase in residual nitrogen from the first day of the disease to the last manifestation of fever.

Relative can be observed with increased sweating, thickening of the blood, as well as profuse diarrhea, when the water balance in the body is disturbed.

Mixed type of hyperazotemia

There are cases when residual nitrogen is increased and mixed hyperazotemia is determined. It often occurs when poisoned by toxic substances: dichloroethane, mercury salts, and other dangerous compounds. The cause may be injuries associated with prolonged tissue compression. In such cases, necrosis of the renal tissues may occur, while retention hyperazotemia begins along with production. At the highest stage of hyperazotemia, residual nitrogen in some cases exceeds the norm by twenty times. Such indicators are recorded in extremely severe cases of kidney damage.

Indicators of residual nitrogen are overestimated not only with kidney damage. In Addison's disease (adrenal dysfunction), the norms are also exceeded. This also happens with heart failure, with burns of a high severity, with dehydration, with severe infections of a bacterial nature, with severe stress and with gastric bleeding.

cure

It is possible to eliminate the manifestations of elevated residual nitrogen by detecting the cause of this condition in time. For further treatment, the doctor must prescribe a number of additional studies, based on the results of which he will make a conclusion, establish the correct diagnosis and prescribe the necessary medication or other treatment. In order to detect the disease in time and cure it, it is necessary to undergo examinations and pass all tests in a timely manner. If any pathology is found, proper treatment will not allow complications to develop, the disease will go into exacerbation and chronic form.

The biological role of creatine.to reatin is an important component of muscles, the brain. In the form of creatine phosphate, it serves as a high-energy phosphate. This is the only reserve macroerg.

Creatinine synthesis. Creatinine is formed as a result of non-enzymatic dephosphorylation of creatine phosphate.

7. Ammonia.

formation of ammonia.

1. Due to the deamination of amino acids

2. With the breakdown of purine and pyrimidine nucleotides.

3. Inactivation of biogenic amines with the participation of monoamine oxidase enzymes.

4. In the intestines & as a waste product of microbial microflora (during the decay of proteins in the intestines

Mechanism safe transport of ammonia.

Ammonia, which is formed in the cells of various organs and tissues in a free state, cannot be transported by the blood to the liver or kidneys due to its high toxicity. It is transported to these organs in a bound form in the form of several compounds, but predominantly in the form of dicarboxylic acid amides, namely glutamine and aspartine. glutamine - is formed in the cells of peripheral organs and tissues from ammonia and glutamate in an energy-dependent reaction catalyzed by the enzyme glutamine synthetase. In the form of glutamine, ammonia is transported to the liver or kidneys where it is broken down to ammonia and glutamate in a reaction catalyzed by glutaminase.

The main organ where ammonia is detoxified is undoubtedly the liver. In its hepatocytes, up to 90% of the formed ammonia is converted into urea, which enters the bloodstream from the liver to the kidneys and is then excreted in the urine. Normally, 20-35 g of urea is excreted in the urine per day. A small part of the ammonia formed in the body (about 1g per day) is excreted by the kidneys in the urine in the form of ammonium salts. Ammonia is formed everywhere.

Causes of changes in the content of ammonia in the urine.

Ammonia is excreted; with urine In the form of ammonium salts. With acidosis, their amount in the urine increases, and with alkalosis it decreases. The amount of ammonium salts in the urine can be reduced if: in the kidneys, the processes of formation of ammonia from glutamine.

Causes of changes in the content of ammonia in the blood. In plasma (7.1-21.4 μM / l) Ammonia entering the portal system or into the general circulation quickly turns into urea in the liver. Liver failure can lead to elevated blood ammonia levels, especially if accompanied by high protein intake or intestinal bleeding. Ammonia rises in the blood with liver failure or with shunting of blood flow in the liver due to portacaval anastomosis, especially against the background of a high protein content in food or with intestinal bleeding.

8. Residual blood nitrogen.

Residual nitrogen - non-protein nitrogen of the blood, i.e. remaining in the filtrate after protein precipitation. In the blood - 14.3-28.6 mmol/l

The content of non-protein nitrogen in whole blood and plasma is almost the same and is 15 - 25 mmol / l in the blood. The composition of non-protein nitrogen in the blood includes mainly nitrogen of the end products of the metabolism of simple and complex proteins (urea nitrogen (50% of the total amount of non-protein nitrogen), amino acids (25%), ergothioneine (8%), uric acid (4%) , creatine (5%), creatinine (2.5%), ammonia and indican (0.5%)

Non-protein blood nitrogen is also called residual nitrogen, i.e., remaining in the filtrate after protein precipitation. In a healthy person, fluctuations in the content of non-protein, or residual, nitrogen in the blood are insignificant and mainly depend on the amount of proteins ingested with food. In a number of pathological conditions, the level of non-protein nitrogen in the blood increases. This state is called azotemia. Azotemia, depending on the causes that cause it, is divided into retention and production.

With renal retention azotemia, the concentration of residual nitrogen in the blood increases due to a weakening of the cleansing (excretory) function of the kidneys. A sharp increase in the content of residual nitrogen in retention renal azotemia occurs mainly due to urea. In these cases, the share of urea nitrogen accounts for 90% of non-protein blood nitrogen instead of 50% in the norm. Extrarenal retention azotemia may result from severe circulatory failure, decreased blood pressure, and decreased renal blood flow. Often, extrarenal retention azotemia is the result of an obstruction to the outflow of urine after it has been formed in the kidney.

Production azotemia is observed with excessive intake of nitrogen-containing products into the blood, as a result of increased breakdown of tissue proteins during extensive inflammation, wounds, burns, cachexia, etc.

As already noted, quantitatively, the main end product of protein metabolism in the body is urea. It is generally accepted that urea is 18 times less toxic than other nitrogenous substances. In acute renal failure, the concentration of urea in the blood reaches 50 - 83 mmol / l (the norm is 3.3 - 6.6 mmol / l). An increase in the content of urea in the blood up to 16 - 20.0 mmol / l is a sign of impaired renal function of moderate severity, up to 35 mmol / l - severe and over 50 mmol / l - a very severe violation with an unfavorable prognosis.