Recent evidence from urine porphyrin testing. Porphyrins (7 indicators) in urine Urine for porphyrins in vitro

Porphyrinuria- this is an increase in porphyrins in the urine, which may be a symptom of porphyria or liver disease, intoxication, cytostatic therapy, infection, iron deficiency and hemolytic anemia, lymphogranulomatosis, leukemia.

Porphyrins are intermediate products of heme synthesis (the non-protein part of hemoglobin). They are formed from the amino acid glycine and a derivative of succinic acid - succinyl-coenzyme A. The main quantities of porphyrins are synthesized in the bone marrow (for the formation of hemoglobin heme) and liver (for the synthesis of redox enzymes, myoglobin heme, myelin, bone and other tissues).

Normally, small amounts of uro- and coproporphyrins are excreted in the urine. Increased excretion of porphyrins (porphyrinuria) is observed with liver damage. A healthy liver is capable of oxidizing and excreting metabolic products of porphyrins in the form of copro- and protoporphyrins in feces. When this pathway is turned off, the pigments return to the bloodstream, pass through the kidney filter and are excreted in increased quantities in the urine (porphyrinuria).

Alcohol intake, X-ray irradiation, physical stress, hemolysis of red blood cells, myoglobinuria lead to an increase in the level of urinary porphyrins (porphyrinuria). With renal failure, the content of porphyrins in the urine decreases.

The excretion of porphobilinogen (PBG) in the urine turns the urine red or pink and is characteristic of acute intermittent porphyria, which is accompanied by damage to the muscular, central and peripheral nervous systems. The heterozygous form has a long latent course, the homozygous form has a severe polysyndromic disease.

Test for porphyrins is a spectroscopic analysis performed to check the level of porphyrins in the patient's body. This is one of the tests used to diagnose porphyria, a genetic disease whose symptoms can be fatal. The porphyrin test checks for the presence of porphobilinogen and other porphyrins in the body. A urine test for porphyrins can usually detect this disease earlier than other tests. Research for porphyrins, unfortunately, is not carried out in the first place, since this is a rare disease, the symptoms of which are common to many other diseases.

What does an increased level of porphyrins in the body mean?

Elevated levels of porphyrins in the body mean that a person suffers from porphyria. This is a genetic disease, so all family members should also be tested. The disease can be acute, in which case the liver and nervous system are usually damaged. This may indicate that there are neurological problems such as severe and severe mood swings, which means the patient has bipolar disorder. An attack of acute porphyria may be accompanied by nausea, severe pain and shortness of breath due to muscle weakness. The cutaneous form of this disease causes the patient's teeth to turn brown.

Normal level of porphyrins in the body

Porphyria is a disease caused by the accumulation of porphyrins in the body. Porphyrins are natural chemicals that exist in the human body and are precursors to the production of heme, which subsequently forms. The problem occurs when the genes responsible for producing enzymes do not work or do not produce one or more of the eight enzymes used in heme synthesis. The only way to manage this condition is to take medications containing heme. This will reduce heme production and reduce porphyrin production.

Dangerous consequences of porphyria

Porphyria affects the skin, nervous system and liver. This is a very serious disease that causes so much pain that morphine is needed to relieve it. Certain circumstances can trigger the development of these symptoms, it is important to recognize them and seek medical help immediately. It would be a good idea to wear some kind of indicator on your clothing that would tell doctors that you are a potential patient with porphyria.

Video

Complex determination of porphyrins (7 parameters)

List of tests included in the study:

  • hexacarboxyporphyrin;
  • heptacarboxyporphyrin;
  • coproporphyrin I;
  • coproporphyrin III;
  • pentacarboxyporphyrin;
  • uroporphyrin;
  • common porphyrin.
Urine porphyrins
Urine porphyrins are intermediate compounds in the synthesis of heme, which is part of the hemoglobin molecule that transports oxygen. When heme synthesis is impaired, the concentration of porphyrins in the urine increases.

Porphyrins are orange-red fluorescent compounds consisting of 4 pyrrole rings that are formed during heme biosynthesis. They are found in all cells, take part in energy metabolism and are excreted in urine in small quantities. An increase in the level of porphyrins or porphyrinogens in the urine indicates a violation of heme biosynthesis, which can be congenital, for example, in hereditary enzymopathies, and acquired, for example, in liver diseases and hemolytic anemia.

Determination of the level of individual porphyrins or porphyrinogens in urine allows us to identify the deficiency of individual enzymes involved in heme biosynthesis. In some cases, quantitative analysis is preceded by qualitative screening tests (using a random urine sample). In case of positive results, 24-hour urine is examined.

Comparison of porphyrin levels in urine, blood plasma and feces increases the reliability of the diagnosis of porphyrias.

Porphyrin diseases
Porphyrias (porphyrin diseases) are hereditary or acquired (as a result of exposure to chemical agents) defects in enzymes involved in heme biosynthesis.

Porphyrias are classified depending on the primary location of the disorder in porphyrin synthesis:

  • erythropoietic porphyria is caused by a violation of the synthesis of porphyrins by bone marrow erythroblasts and is manifested mainly by skin photosensitivity (due to activation of ultraviolet radiation and increased deposition of porphyrins in the skin);
  • hepatic porphyria is caused by a violation of the synthesis of porphyrins in the liver and is manifested mainly by acute neurological disorders (attacks of arterial hypertension, abdominal colic, psychosis and neuropathy) without skin photosensitivity. During an attack, the concentration of porphyrin precursors - delta-aminolevulinic acid and porphobilinogen - increases in plasma and urine.
Indications:
  • anemia;
  • hepatitis;
  • lead poisoning.
Preparation
On the eve of the test, it is not recommended to eat vegetables and fruits that can change the color of urine (beets, carrots, cranberries, etc.), or take diuretics.

In the morning, empty your bladder (this portion of urine is poured into the toilet). Record the time of urination, for example: “8:00”.

Over the next 24 hours, collect all urine excreted in a dry, clean container with a capacity of 2–3 liters.

After urine collection is completed, the contents of the container must be accurately measured. The container must indicate the daily volume of urine (diuresis) in milliliters. For example: “Diuresis: 1250 ml.”

Be sure to mix the urine thoroughly and immediately pour 30–50 ml into a sterile container with a lid. There is no need to bring all the urine collected during the day.

During the entire collection period and until shipment, the biomaterial should be stored in a refrigerator at 2–8°C. The material must be delivered to the medical office on the day the collection ends.

Interpretation of results
Normal urinary excretion of uroporphyrins ranges from 27 to 52 mcg/day (SI: 32–63 nmol/day), and coproporphyrins - from 34 to 230 mcg/day (SI: 52–351 nmol/day).

An increase in the content of porphyrins and their precursors in the urine is a characteristic sign of porphyria. In addition, excretion of porphyrins may increase with viral hepatitis, lymphogranulomatosis, central nervous system damage, liver cirrhosis, as well as poisoning with heavy metal salts, benzene and carbon tetrachloride.

Factors that increase results:

  • the use of barbiturates, chloral hydrate, chlorpropamide, sulfonamides, meprobamate, chlordiazepoxide - induces porphyria or porphyrinuria; If possible, you should stop taking these medications 12 days before the study;
  • taking oral contraceptives, griseofulvin (urinary excretion of porphyrins increases);
  • pregnancy or menstruation (possible increase or decrease in the content of porphyrins in the urine);
  • the use of rifampicin increases the content of urobilinogen in the urine;
  • disruption of heme biosynthesis at different stages contributes to an increase in the content of porphyrins and their precursors in the urine and the development of porphyria.

Porphyrins (from Greek. porphires- purple, crimson) - complex organic compounds, intermediate products of heme synthesis. Porphias are hereditary and acquired disorders of heme synthesis, accompanied by an increase in the content of porphyrins, as well as their oxidation products in tissues and blood and their appearance in the urine.

Porphyrias can occur due to a genetic defect (primary) or an acquired disease (secondary). The severity of the disease can vary from asymptomatic to severe. Secondary disorders of porphyrin metabolism develop as a consequence of a number of diseases, intoxications and are associated with liver damage; disorders of porphyrin metabolism are most often the result of enzyme inhibition (drug or toxin), but not its congenital deficiency. The most common causes of this are lead poisoning, hypovitaminosis (especially PP, pantothenic and folic acids), and liver cirrhosis.

Coproporphyrins are the most frequently excreted porphyrin in secondary disorders of porphyrin metabolism. Their formation can be initiated by hexachlorobenzene, ethyl alcohol, morphine, chloral hydrate, ether, nitrous oxide, and heavy metals.

In the morning, after a thorough toilet of the genital organs, collect the first portion of urine in a container and deliver it to the laboratory for examination. The urine container should be made of dark glass or plastic and should not be exposed to light.

Biomaterial: a single portion of urine.

  • Laboratory diagnosis of porphyria;
  • Preventive examinations of persons associated with production processes where lead intoxication may occur (lead ore mining, lead smelting, battery production, cable production, printing production, painting work using lead paints, the use of lead matrices in the aviation industry).

Interpretation of the results contains analytical information for the attending physician. Laboratory data is part of a comprehensive examination of the patient performed by a doctor and cannot be used for self-diagnosis and self-medication.

The results of the study are presented in qualitative terms: if coproporphyrins are present in the sample, the answer “detected” is given; If there are no coproporphyrins in the sample, the answer “not detected” is given.

Positive result:

§ chronic ethanol intake;

§ liver disease,

§ chronic renal failure,

§ poisoning with lead, mercury, arsenic,

§ some tumors

§ protoporphyria with liver damage,

§ mixed porphyria.

§ hereditary coproporphyria

A routine research method used in the diagnosis and monitoring of a number of diseases, as well as screening examinations.

    General properties: (color, transparency, specific gravity, pH, protein, glucose, bilirubin, urobilinogen, ketone bodies, nitrites, hemoglobin);

    Microscopy of urinary sediment: (epithelium, erythrocytes, leukocytes, casts, bacteria, salts).

A general urinalysis includes assessment of the physicochemical characteristics of urine and microscopy of sediment. A general urine test for patients with diseases of the kidneys and urinary system is performed repeatedly over time to assess the condition and monitor therapy. Healthy people are recommended to perform this test 1-2 times a year.


Collection of urine for general analysis

It is necessary to purchase a container for urine in advance at any MO Independent Laboratory INVITRO.

Before collecting urine, it is necessary to perform a thorough hygienic toilet of the genital organs. Women are not recommended to take a urine test during menstruation. To properly conduct the study, during the first morning urination, release a small amount of urine (the first 1 - 2 seconds) into the toilet. Collect approximately 50ml. morning urine into a container with a blue lid. Screw the lid on tightly. Place the test tube, cap down, into the recess on the container lid. Press down on the bottom of the tube until the needle pierces the rubber stopper in the tube cap and urine begins to flow into the tube. Wait until the tube is full, then remove it from the container lid. Since the test tube contains a preservative, it is necessary to mix the contents of the test tube 8-10 times, carefully turning it 180 °.


The test tube with urine must be delivered to the medical office within a day (in accordance with the schedule for receiving the biomaterial). Please call for more details on the schedule.

    Diseases of the urinary system.

    Screening examination during medical examinations.

    Assessment of the course of the disease, monitoring the development of complications and the effectiveness of treatment.

    Persons who have had a streptococcal infection (angina, scarlet fever) are recommended to take a urine test 1 to 2 weeks after recovery.

Interpretation of study results contains information for the attending physician and is not a diagnosis. The information in this section should not be used for self-diagnosis or self-treatment. The doctor makes an accurate diagnosis using both the results of this examination and the necessary information from other sources: medical history, results of other examinations, etc.

Urine color. Normally, the urine pigment urochrome gives the urine a yellow color of various shades, depending on the degree of saturation of the urine with it. Sometimes only the color of the precipitate may change: for example, with an excess of urates, the precipitate has a brownish color, uric acid - yellow, phosphates - whitish.

An increase in color intensity is a consequence of loss of body fluids: swelling, vomiting, diarrhea.

Change in urine color may be the result of the release of coloring compounds formed during organic changes or under the influence of dietary components, medications taken, or contrast agents.


Urine color State Dyes
Straw yellow
Dark yellowSwelling, burns, vomiting, diarrhea, congestive edema in heart failureHigh concentration of urochromes
Pale, watery, colorlessDiabetes insipidus, decreased renal concentration function,
taking diuretics, overhydration
Low concentration of urochromes
Yellow-orangeTaking vitamins, furagin
Reddish, pinkEating brightly colored fruits and vegetables, such as beets, carrots, blueberries; medications - antipyrine, aspirin
RedRenal colic, renal infarctionThe presence of red blood cells in the urine - fresh hematuria, the presence of hemoglobin, porphyrin, myoglobin
Meat slop colorAcute glomerulonephritisHematuria (changed blood)
Dark brownHemolytic anemiaUrobilinuria
Red-brownTaking metronidazole, sulfonamides, bearberry-based drugs. Phenol poisoning
BlackMarchiafava-Michelli disease (paroxysmal nocturnal hemoglobinuria)
Alkaptonuria. Melanoma
Hemoglobinuria
Homogentisic acid
Melanin (melanuria)
Beer color
(yellow-brown)
Parenchymal jaundice
(viral hepatitis)
Bilirubinuria, urobilinogenuria
Greenish yellow
Mechanical (obstructive) jaundice - cholelithiasis,
pancreatic head cancer
Bilirubinuria
WhitishPresence of phosphates or lipids in urine
LacticRenal lymphostasis, urinary tract infectionHiluria, pyuria

Urine clarity
Reference values: complete.

Cloudiness of urine can be the result of the presence of red blood cells, leukocytes, epithelium, bacteria, fat droplets in the urine, precipitation of salts (urates, phosphates, oxalates) and depends on the concentration of salts, pH and storage temperature of urine (low temperature promotes precipitation of salts) . If you stand for a long time, your urine may become cloudy due to bacterial growth. Normally, slight turbidity may be due to epithelium and mucus.


Relative density (specific gravity) of urine depends on the amount of released organic compounds (urea, uric acid, salts) and electrolytes - Cl, Na and K, as well as on the amount of water released. The higher the diuresis, the lower the relative density of urine. The presence of protein and especially glucose causes an increase in the specific gravity of urine. A decrease in the concentration function of the kidneys in renal failure leads to a decrease in specific gravity ( hyposthenuria). Complete loss of concentration function leads to equalization of the osmotic pressure of plasma and urine, this condition is called isosthenuria.


Reference values(for all ages): 1003 - 1035 g/l.


Increased relative density (hypersthenuria):

    glucose in the urine in uncontrolled diabetes mellitus;

    protein in the urine (proteinuria) with glomerulonephritis, nephrotic syndrome;

    drugs and (or) their metabolites in the urine;

    intravenous infusion of mannitol, dextran or radiocontrast agents;

    low fluid intake;

    large fluid losses (vomiting, diarrhea);

  1. toxicosis of pregnant women;
  2. oliguria.

Reduced relative density:

    diabetes insipidus (nephrogenic, central or idiopathic);


    acute damage to the renal tubules;

    polyuria (as a result of taking diuretics, drinking too much).

Urine pH. Fresh urine from healthy people can have a different reaction (pH from 4.5 to 8), usually the urine reaction is slightly acidic (pH between 5 and 6). Fluctuations in the pH of urine are caused by the composition of the diet: a meat diet causes an acidic reaction in the urine; the predominance of plant and dairy foods leads to alkalization of the urine. Changes in urine pH correspond to blood pH; with acidosis, urine is acidic, with alkalosis it is alkaline. Sometimes there is a discrepancy between these indicators.


In case of chronic damage to the kidney tubules (tubulopathies), hyperchloric acidosis is observed in the blood, and the urine reaction is alkaline, which is associated with a violation of the synthesis of acid and ammonia due to damage to the tubules. Bacterial decomposition of urea in the ureters or storage of urine at room temperature leads to alkalinization of urine. The reaction of urine affects the nature of salt formation in urolithiasis: at a pH below 5.5, uric acid stones are more often formed, at a pH from 5.5 to 6.0 - oxalate stones, at a pH above 7.0 - phosphate stones.


Reference values:

    0 - 1 month — 5.0 - 7.0;

Promotion:
  1. metabolic and respiratory alkalosis;
  2. chronic renal failure;
  3. renal tubular acidosis (types I and II);
  4. hyperkalemia;
  5. primary and secondary hyperfunction of the parathyroid gland;
  6. carbon anhydrase inhibitors;
  7. a diet high in fruits and vegetables;
  8. prolonged vomiting;
  9. urinary tract infections caused by microorganisms that break down urea;
  10. administration of certain medications (adrenaline, nicotinamide, bicarbonates);
  11. neoplasms of the genitourinary system.
Demotion:
  1. metabolic and respiratory acidosis;
  2. hypokalemia;
  3. dehydration;
  4. starvation;
  5. diabetes;
  6. tuberculosis;
  7. fever;
  8. severe diarrhea;
  9. taking medications: ascorbic acid, corticotropin, methionine;
  10. diet high in meat protein and cranberries.
Protein in the urine (proteinuria). Protein in the urine is one of the most diagnostically important laboratory signs of kidney pathology. A small amount of protein in the urine (physiological proteinuria) can occur in healthy people, but the excretion of protein in the urine does not normally exceed 0.080 g/day at rest and 0.250 g/day during intense physical activity, after a long walk (marching proteinuria). Protein in the urine can also be detected in healthy people during strong emotional experiences or hypothermia. Orthostatic proteinuria (in an upright body position) occurs in adolescents.

Normally, most proteins do not pass through the membrane of the renal glomeruli, which is explained by the large size of protein molecules, as well as their charge and structure. With minimal damage in the glomeruli of the kidneys, there is primarily a loss of low molecular weight proteins (mainly albumin), therefore, with a large loss of protein, hypoalbuminemia often develops. With more pronounced pathological changes, larger protein molecules also enter the urine. The epithelium of the renal tubules physiologically secretes a certain amount of protein (Tamm-Horsfall protein). Some of the urine proteins can come from the genitourinary tract (ureter, bladder, urethra) - the content of these proteins in the urine increases sharply with infections, inflammation or tumors of the genitourinary tract. Proteinuria (the appearance of increased amounts of protein in the urine) can be prerenal (associated with increased tissue breakdown or the appearance of pathological proteins in the plasma), renal (due to kidney pathology) and postrenal (associated with urinary tract pathology). The appearance of protein in the urine is a common nonspecific symptom of kidney pathology. With renal proteinuria, protein is found in both daytime and nighttime urine. According to the mechanisms of occurrence of renal proteinuria, glomerular and tubular proteinuria are distinguished. Glomerular proteinuria is associated with pathological changes in the barrier function of the glomerular membranes. Massive urinary protein loss (> 3 g/L) is always associated with glomerular proteinuria. Tubular proteinuria is caused by impaired protein reabsorption due to pathology of the proximal tubules.


Reference values:


Presence of protein in urine (proteinuria):

  1. nephrotic syndrome;
  2. diabetic nephropathy;
  3. glomerulonephritis;
  4. nephrosclerosis;
  5. impaired absorption in the renal tubules (Fanconi syndrome, heavy metal poisoning, sarcoidosis, sickle cell disease);
  6. multiple myeloma (Bence Jones protein in urine) and other paraproteinemias;
  7. impaired renal hemodynamics in heart failure, fever;
  8. malignant tumors of the urinary tract;
  9. cystitis, urethritis and other urinary tract infections.
Glucose in urine. Glucose in urine is normally absent or found in minimal quantities, up to 0.8 mmol/l, because in healthy people, all blood glucose, after filtering through the membrane of the renal glomeruli, is completely absorbed back into the tubules. When the concentration of glucose in the blood is more than 10 mmol/l - the renal threshold is exceeded (the maximum ability of the kidneys to reabsorb glucose) or when the renal threshold is reduced (renal tubular damage), glucose appears in the urine - glucosuria is observed.

Detection of glucose in urine is important for the diagnosis of diabetes mellitus, as well as monitoring (and self-control) of antidiabetic therapy.

Note: method for studying general urine analysis in the INVITRO Independent Laboratory - Multistix diagnostic strips from Bayer (+ sediment microscopy). The result is read automatically using a Clinitek 500 analyzer from Bayer (visual determination errors are excluded). The principle of the method for determining glucose on them is glucose oxidase. The step of the test strip for analyzing urine for glucose is as follows: first there is a “negative” result, the next step is “5.5” (traces). If the true glucose value is between these values, then due to this step of the test strip, the device displays it as a minimum positive value - 5.5.

Since questions from doctors and patients about this threshold value of glucose concentration have recently become more frequent, the laboratory decided, when receiving such a result, to give out not a number, but to write “traces.” If this is the answer for glucose in the urine, we recommend additional studies, including in particular, this is a determination of fasting blood glucose, a study of daily urine excretion (hexokinase method), or, if prescribed by a doctor, a glucose tolerance test.

Reference values: 0 - 1,6.

"SEE COMMENT":

  • 1.7 - 2.8 - traces;
  • > 2.8 - a significant increase in the concentration of glucose in the urine.
Increased levels (glucosuria):
  1. diabetes;
  2. acute pancreatitis;
  3. hyperthyroidism;
  4. renal diabetes;
  5. steroid diabetes (taking anabolic steroids for diabetics);
  6. poisoning with morphine, strychnine, phosphorus;
  7. dumping syndrome;
  8. Cushing's syndrome;
  9. myocardial infarction;
  10. pheochromocytoma;
  11. major injury;
  12. burns;
  13. tubulointerstitial kidney damage;
  14. pregnancy;
  15. taking large amounts of carbohydrates.
Bilirubin in urine. Bilirubin is the main final metabolite of porphyrins excreted from the body. In the blood, free (unconjugated) bilirubin in plasma is transported by albumin; in this form, it is not filtered in the glomeruli. In the liver, bilirubin combines with glucuronic acid (a conjugated, water-soluble form of bilirubin is formed) and in this form it is released into the bile into the gastrointestinal tract. When the concentration of conjugated bilirubin in the blood increases, it begins to be excreted by the kidneys and found in the urine. The urine of healthy people contains minimal, undetectable amounts of bilirubin. Bilirubinuria is observed mainly with damage to the liver parenchyma or mechanical obstruction of the outflow of bile. With hemolytic jaundice, the urine reaction to bilirubin is negative.

Reference values: negative.

Detection of bilirubin in urine:

  1. obstructive jaundice;
  2. viral hepatitis;
  3. cirrhosis of the liver;
  4. metastases of neoplasms to the liver.
Urobilinogen in urine. Urobilinogen and stercobilinogen are formed in the intestine from bilirubin released in bile. Urobilinogen is reabsorbed in the colon and again enters the liver through the portal vein system, and then again excreted along with bile. A small part of this fraction enters the peripheral bloodstream and is excreted in the urine. Normally, in the urine of a healthy person, urobilinogen is determined in trace quantities - its excretion in urine per day does not exceed 10 µmol (6 mg). When urine stands, urobilinogen turns into urobilin.
Reference values: 0 - 17.

Increased excretion of urobilinogen in urine:

  1. increased hemoglobin catabolism: hemolytic anemia, intravascular hemolysis (transfusion of incompatible blood, infections, sepsis), pernicious anemia, polycythemia, resorption of massive hematomas;
  2. increased formation of urobilinogen in the gastrointestinal tract: enterocolitis, ileitis, intestinal obstruction, increased formation and reabsorption of urobilinogen during infection of the biliary system (cholangitis);
  3. increased urobilinogen in liver dysfunction: viral hepatitis (excluding severe forms);
  4. chronic hepatitis and cirrhosis of the liver;
  5. toxic damage: alcohol, organic compounds, toxins during infections, sepsis;
  6. secondary liver failure: after myocardial infarction, cardiac and circulatory failure, liver tumors;
  7. increased urobilinogen during liver bypass surgery: liver cirrhosis with portal hypertension, thrombosis, renal vein obstruction.
Ketone bodies in the urine (ketonuria). Ketone bodies (acetone, acetoacetic and beta-hydroxybutyric acids) are formed as a result of increased catabolism of fatty acids. Determination of ketone bodies is important in recognizing metabolic decompensation in diabetes mellitus. Insulin-dependent juvenile diabetes is often first diagnosed by the appearance of ketone bodies in the urine. With inadequate insulin therapy, ketoacidosis progresses. The resulting hyperglycemia and hyperosmolarity lead to dehydration, electrolyte imbalance, and ketoacidosis. These changes cause dysfunction of the central nervous system and lead to hyperglycemic coma.

Reference values: 0 - 0,4.

"SEE COMM."

  • 0.5 - 0.9 - traces;
  • > 0.9 - positive.
Detection of ketone bodies in urine (ketonuria):
  1. diabetes mellitus (decompensated - diabetic ketoacidosis);
  2. precomatose state, cerebral (hyperglycemic) coma;
  3. long-term fasting (complete refusal of food or diet aimed at reducing body weight);
  4. severe fever;
  5. alcohol intoxication;
  6. hyperinsulinism;
  7. hypercatecholaminemia;
  8. isopropranolol poisoning;
  9. eclampsia;
  10. glycogenosis types I, II, IV;
  11. lack of carbohydrates in the diet.
Nitrites in urine. There are no nitrites in normal urine. In urine, they are formed from nitrates of food origin under the influence of bacteria, if the urine was in the bladder for at least 4 hours. Detection of nitrites in the urine (positive test result) indicates infection of the urinary tract. However, a negative result does not always exclude bacteriuria. Urinary tract infection varies among different populations and is dependent on age and gender.

Other things being equal, the following are more susceptible to an increased risk of asymptomatic urinary tract infections and chronic pyelonephritis: girls and women; elderly people (over 70 years old); men with prostate adenoma; diabetic patients; patients with gout; patients after urological operations or instrumental procedures on the urinary tract.

Reference values: negative.

Hemoglobin in urine. There is no hemoglobin in normal urine. A positive test result reflects the presence of free hemoglobin or myoglobin in the urine. This is the result of intravascular, intrarenal, urinary hemolysis of red blood cells with the release of hemoglobin, or muscle damage and necrosis, accompanied by an increase in plasma myoglobin levels. It is quite difficult to distinguish hemoglobinuria from myoglobinuria; sometimes myoglobinuria is mistaken for hemoglobinuria.
Reference values: negative.

Presence of hemoglobin in urine:

  1. severe hemolytic anemia;
  2. severe poisoning, for example, sulfonamides, phenol, aniline. poisonous mushrooms;
  3. sepsis;
  4. burns.
Presence of myoglobin in urine:
  1. muscle damage;
  2. heavy physical activity, including sports training;
  3. myocardial infarction;
  4. progressive myopathies;
  5. Rhabdomyolysis
Microscopy of urine sediment. Microscopy of urine components is carried out in the sediment formed after centrifugation of 10 ml of urine. Sediment consists of solid particles suspended in urine: cells, protein-formed casts (with or without inclusions), crystals, or amorphous deposits of chemicals.

Red blood cells in urine. Red blood cells (blood cells) enter the urine from the blood. Physiological erythrocyturia is up to 2 red blood cells/μl of urine. It does not affect the color of urine. During the study, it is necessary to exclude contamination of urine with blood as a result of menstruation! Hematuria (the appearance of red blood cells, other formed elements, as well as hemoglobin and other blood components in the urine) can be caused by bleeding anywhere in the urinary system. The main reason for the increase in the content of red blood cells in the urine is renal or urological diseases and hemorrhagic diathesis.

Reference values:
Red blood cells in urine - exceeding reference values:

    urinary tract stones;

  1. tumors of the genitourinary system;
  2. glomerulonephritis;
  3. pyelonephritis;
  4. hemorrhagic diathesis (with intolerance to anticoagulant therapy, hemophilia, coagulation disorders, thrombocytopenia, thrombocytopathies);

    urinary tract infections (cystitis, urogenital tuberculosis);

    kidney injury;

    arterial hypertension with involvement of the renal vessels;

    systemic lupus erythematosus (lupus nephritis);

    poisoning with benzene derivatives, aniline, snake venom, poisonous mushrooms;

    inadequate anticoagulant therapy.

Leukocytes in urine. An increased number of white blood cells in the urine (leukocyturia) is a symptom of inflammation of the kidneys and/or lower urinary tract. In chronic inflammation, leukocyturia is a more reliable test than bacteriuria, which is often not detected. With a very large number of leukocytes, pus in the urine is determined macroscopically - this is the so-called pyuria. The presence of leukocytes in the urine may be due to the presence of secretions from the external genitalia in the urine due to vulvovaginitis, or insufficiently thorough toileting of the external genitalia when collecting urine for analysis.

Reference values:

  • men:
  • women, children

An increase in leukocytes in the urine is observed in almost all diseases of the kidneys and genitourinary system:

  1. acute and chronic pyelonephritis, glomerulonephritis;
  2. cystitis, urethritis, prostatitis;
  3. stones in the ureter;
  4. tubulointerstitial nephritis;
  5. lupus nephritis;
  6. kidney transplant rejection.

Epithelial cells in urine. Epithelial cells are almost always present in urine sediment. Epithelial cells originating from different parts of the genitourinary system vary (usually squamous, transitional and renal epithelium are distinguished). Squamous epithelial cells, characteristic of the lower parts of the genitourinary system, are found in the urine of healthy people and their presence usually has little diagnostic value. The amount of squamous epithelium in the urine increases with urinary tract infection. An increased number of transitional epithelial cells can be observed in cystitis, pyelonephritis, and kidney stones. The presence of renal epithelium in the urine indicates damage to the kidney parenchyma (observed in glomerulonephritis, pyelonephritis, some infectious diseases, intoxication, circulatory disorders). The presence of more than 15 renal epithelial cells in the field of view 3 days after transplantation is an early sign of the threat of allograft rejection.

Reference values:

    squamous epithelial cells: women -

  • men -
  • transitional epithelial cells -
  • renal epithelial cells - absent.
  • Detection of renal epithelial cells:

  1. pyelonephritis;
  2. intoxication (taking salicylates, cortisone, phenacetin, bismuth preparations, poisoning with heavy metal salts, ethylene glycol);
  3. tubular necrosis;
  4. kidney transplant rejection;
  5. nephrosclerosis.

Casts in urine. Cylinders are elements of cylindrical sediment (a kind of cast of renal tubules), consisting of protein or cells, and may also contain various inclusions (hemoglobin, bilirubin, pigments, sulfonamides). Based on their composition and appearance, there are several types of cylinders (hyaline, granular, erythrocyte, waxy, etc.). Normally, renal epithelial cells secrete the so-called Tamm-Horsfall protein (absent in blood plasma), which is the basis of hyaline casts. Sometimes hyaline casts can be found in healthy people.

Granular casts are formed as a result of the destruction of tubular epithelial cells. Their detection in a patient at rest and without fever indicates renal pathology. Waxy casts are formed from compacted hyaline and granular casts. Erythrocyte casts are formed when red blood cells are layered on hyaline casts, and leukocyte casts are formed by leukocytes. Epithelial casts (rarely) are derived from renal tubular cells. Their presence in a urine test a few days after surgery is a sign of rejection of the transplanted kidney. Pigment cylinders are formed when pigments are included in the composition of the cylinder and are observed with myoglobinuria and hemoglobinuria.

Reference values: are missing.

Hyaline casts in urine:

  1. renal pathology (acute and chronic glomerulonephritis, pyelonephritis, kidney stones, renal tuberculosis, tumors);
  2. congestive heart failure;
  3. hyperthermic conditions;
  4. high blood pressure;
  5. taking diuretics.
Grainy cylinders (nonspecific pathological symptom):
  1. glomerulonephoritis, pyelonephritis;
  2. diabetic nephropathy;
  3. viral infections;
  4. lead poisoning;
  5. fever.
Waxy cylinders:
  1. chronic renal failure;
  2. kidney amyloidosis;
  3. nephrotic syndrome.
Red blood cell casts (hematuria of renal origin):
  1. acute glomerulonephritis;
  2. kidney infarction;
  3. renal vein thrombosis;
  4. malignant hypertension.
Leukocyte casts (leukocyturia of renal origin):
  1. pyelonephritis;
  2. Lupus nephritis in systemic lupus erythematosus.
Epithelial casts (most rare):
  1. acute tubular necrosis;
  2. viral infection (for example, cytomegalovirus);
  3. poisoning with salts of heavy metals, ethylene glycol;
  4. overdose of salicylates;
  5. amyloidosis;
  6. kidney transplant rejection reaction.

Bacteria in urine
Isolation of bacteria in urine has significant diagnostic value. Bacteria remain in the urine for no more than 1 - 2 days after the start of antibiotic therapy. The first morning urine sample is preferable for testing. The type of bacteria can be determined and the level of bacteriuria can be assessed, as well as the sensitivity of microorganisms to antibiotics can be determined using bacteriological urine culture.

Reference values: negative.

Bacteria in urine: infections of the urinary system (pyelonephritis, urethritis, cystitis).

Yeasts . The detection of yeast of the genus Candida indicates candidiasis, which most often occurs as a result of irrational antibiotic therapy.

Inorganic urine sediment (crystals), salts in urine. Urine is a solution of various salts, which can precipitate (form crystals) when the urine stands. Low temperature promotes the formation of crystals. The presence of certain salt crystals in the urinary sediment indicates a change in the reaction towards the acidic or alkaline side. Excessive salt content in urine contributes to the formation of stones and the development of urolithiasis. At the same time, the diagnostic value of the presence of salt crystals in urine is usually small. Increased doses of ampicillin and sulfonamides lead to the formation of crystals.

Reference values are missing.

Uric acid and its salts (urates):

  1. highly concentrated urine;
  2. acidic reaction of urine (after physical activity, meat diet, fever, leukemia);
  3. uric acid diathesis, gout;
  4. chronic renal failure;
  5. acute and chronic nephritis;
  6. dehydration (vomiting, diarrhea);
  7. in newborns.
Tripelphosphates, amorphous phosphates:
  1. alkaline urine reaction in healthy people;
  2. vomiting, gastric lavage;
  3. cystitis;
  4. Fanconi syndrome, hyperparathyroidism.
Calcium oxalate (oxaluria occurs with any urine reaction):
  1. eating foods rich in oxalic acid (spinach, sorrel, tomatoes, asparagus, rhubarb);
  2. pyelonephritis;
  3. diabetes;
  4. ethylene glycol poisoning.

Mucus in urine. Mucus is secreted by the epithelium of the mucous membranes. Normally present in urine in small quantities. During inflammatory processes, the mucus content in the urine increases. An increased amount of mucus in the urine may indicate a violation of the rules of proper preparation for taking a urine sample.

Reference values: insignificant amount.

Urine analysis in the Independent Laboratory INVITRO

Analysis of urine is one of the most effective methods for diagnosing abnormalities in kidney function.

However, one should not underestimate its importance for determining other pathologies in the modern human body. These include diseases and inflammatory processes of the urinary tract (test for a weakly acidic, neutral or alkaline reaction), the genitourinary system (increased levels of leukocytes), urolithiasis (the appearance of red blood cells in the sample), diabetes mellitus (the presence of glucose in the urine), congestive processes (the presence of mucus ) and much more.

There is no doubt that such a serious type of urine analysis research must be carried out with maximum accuracy, using modern equipment and properly prepared material.

And, since the equipment used in the work of the specialists of the Independent Laboratory INVITRO is the most modern, and the level of training and, in fact, professionalism of the laboratory staff is ensured by regular trainings and confirmed by appropriate certificates, we will focus on the correct preparation of the material for urine analysis.

Let's start with the container. Mayonnaise jars for urine analysis, matchboxes for stool analysis and other “classic” containers of clinics and folklore are irrevocably a thing of the past. To collect the material, you should use special sterile containers and preservatives. An appropriate kit with detailed instructions for collecting biomaterial is provided to patients in all medical offices. Thus, the chances of foreign substances getting into the sample are minimized, and the time required to transport the sample from the patient to the diagnostic equipment, acceptable for high-quality urine analysis, is significantly increased.

Next is preparation for collecting material. The rules of personal hygiene at this moment become not just desirable, but mandatory: neither sweat nor secretions of the sebaceous glands should get into the urine. Antibacterial soap is not recommended in this case. Urine without impurities is the result of the study without errors. It is necessary to mention another type of impurities that can distort the results of a urine test: food and medications. Firstly, the night before you should not eat beets, carrots and other natural “dyes”. Remember that one of the main research parameters is the color of the material. And, if it differs from the norm, which is considered the color yellow and its shades, then let it give information not only about what you had for dinner. Both carrots and beets are certainly tasty and healthy, just take a break for one evening.

Note that a violation of the norm for the presence of pigments can make the color of urine completely unexpected - blue, brown, red, even green.

Dark color of urine may indicate problems with the liver, in particular with hepatitis. The liver stops destroying one of the enzymes, which, when reacting with air, gives such a color change.

If the urine is red, there is most likely blood in it. If it resembles milk diluted with water, there is an excess of fat in it. The grayish tint is given by the pus contained in it. Green or blue color is one of the signs of rotting processes in the intestines. Only men have foamy urine. There is nothing wrong: this happens when sperm gets into her. And, for example, no one has yet learned to control wet dreams or excess sperm.

Secondly, medications. Even harmless aspirin in large doses can turn urine pink. It is especially undesirable to take antibacterial drugs and uroseptics on the eve of a urine test. It is necessary to consult a doctor about a pause in their use. Except in cases where the main subject of the study is the concentration of drugs in the urine.

Alcohol. Probably the most effective and harmful way to waste money is to “overdo it” on the eve of the test. It turns out that in the evening the money goes to destroy the body, and in the morning - simply to pay for an ineffective urine test, and it becomes ineffective precisely because the overall picture of microelements in the urine is distorted by yesterday’s “fines” and “severances”.

On the eve of the urine test, try to drink no more and no less fluid than usual.

12 hours before the test, an intermission is required during sexual activity. The very reason “I need to get tested in the morning” is valid and, we hope, you will find understanding.

We also note that it is not advisable to take a urine test during menstruation and within a week after procedures such as cystoscopy.

The independent laboratory INVITRO offers:

  • general urine analysis (with sediment microscopy). A routine method of urine testing, used in the diagnosis and monitoring of a number of diseases, as well as screening examinations;
  • urine test according to Nechiporenko. Quantitative determination of the content of leukocytes, erythrocytes and casts in urine;
  • pH (power hydrogen). Urine acidity indicator;
  • other urine tests where urine is the test material.

What portion of morning urine is preferable to use for each specific analysis is described in detail on the pages of the corresponding analyzes on www.invitro.ru.

Remember that the main role in making a diagnosis (for example, “inflammatory process in the genitourinary system”) is played not by the presence/absence of bacteria in the urine, but by their increased number: the characteristic increase compared to the norm (2 thousand bacteria in 1 ml) is 50 times (up to 100 thousand bacteria in 1 ml of urine).

Analysis of urine prescribed for:

  • diseases of the urinary system;
  • screening examinations during medical examinations;
  • to assess the course of the disease, control the development of complications and the effectiveness of treatment.

Persons who have had a streptococcal infection (angina, scarlet fever) are recommended to take a urine test 1 to 2 weeks after recovery. We recommend that healthy people take a urine test 1-2 times a year. Remember, treatment is always more expensive than prevention.


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