Description
Determination method See description.
Material under study Urine (average morning urine collected in a special container)
Home visit available
Study of a single morning urine sample, including determination of physical (color, transparency, specific gravity), chemical (pH, protein content, glucose, ketones, urobilinogen, bilirubin, hemoglobin, nitrites and leukocyte esterase), as well as assessment of qualitative and quantitative composition elements of urinary sediment (epithelium, leukocytes, erythrocytes, salts, mucus, etc.).
The parameters determined as part of a general urine test are listed in the table below:
| Parameter | Analyzer | Determination method | Issue form |
| Color, transparency | iChem Velocity | Method for measuring light scattering intensity, if necessary - visual inspection | Qualitatively (description of color, transparency) |
| Specific gravity | iChem Velocity | Refractive index measurement method | Quantitatively |
| Protein | iChem Velocity, Architect 8000 | "Dry chemistry", turbidimetry | Results with protein concentrations within reference values - qualitatively (NEGATIVE), above reference values - quantitatively |
| pH, Glucose, ketone bodies, urobilinogen, hemoglobin, nitrites, leukocyte esterase | iChem Velocity | "Dry chemistry" | Semi-quantitative |
| Flat epithelium, transitional epithelium, renal epithelium, leukocytes, erythrocytes, casts, salts, mucus, bacteria, fungi | Iris IQ200 | Hardware microscopy, if necessary – light microscopy |
Preparation
For the study, it is preferable to use the average portion of morning urine, which collects in the bladder during the night (unless otherwise recommended by the attending physician).
Procedure for collecting urine for research:
Carry out hygiene procedures for the external genitalia;
When urinating for the first time in the morning, release a small amount of urine (the first 1-2 seconds) into the toilet without interrupting urination, place a container and collect 50 ml in it. urine;
Close the container tightly with the screw cap;
Place the test tube downwards with the rubber stopper into the recess on the lid of the container, and the test tube will begin to fill with urine;
After urine stops flowing into the test tube, remove the test tube from the punch (Fig. 1 and 2);
Invert the tube several times to better mix the urine with the preservative (Fig. 3).
Before shipment, the biomaterial must be stored in the refrigerator at +2... +8C. The material must be delivered to the medical office on the day of collection.
Indications for use
- differential diagnosis of kidney and urinary tract diseases;
- screening and dispensary examination;
- assessment of the course of kidney and urinary tract diseases, monitoring the development of complications and the effectiveness of treatment;
- 1-2 weeks after recovery from streptococcal infection (angina, scarlet fever).
Interpretation of results
Interpretation of research 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.
When interpreting the results of a general urine test, it should be taken into account that all indicators should be analyzed in conjunction with each other, and not in isolation.
Normally, urine can be various shades of yellow (light yellow, straw yellow, yellow) and colorless (mainly in children). Discoloration can have both physiological and pathological causes.
Physiological causes of urine color change:
| Color | Cause |
| dark yellow, lemon yellow, orange | Dehydration, taking vitamins and nitrafuran drugs |
| red, light red, pink | The presence of coloring substances in food (beets, blueberries), taking medications such as antipyrine, aspirin, sulfazole. |
| dark brown | taking metronidazole, sulfonamides, bearberry-based drugs |
| blue | taking methylene blue |
| colorless (in adults) | drinking large amounts of fluid, taking diuretics |
Pathological causes of urine color change:
| Color | Cause |
| amber yellow, lemon yellow, orange | urobilinogenuria |
| amber yellow, lemon yellow, orange, light brown, green | bilirubinuria |
| red, light red, pink, brown, brown, dark brown | the presence of a large number of red blood cells or hemoglobin/myoglobin in the urine, porphyrinuria |
| dark brown | phenol poisoning |
| brown | melanuria |
| lactic | chyluria (admixture of lymphatic fluid), pyuria (large number of white blood cells) |
| Colorless (in adults) | diabetes mellitus and diabetes insipidus, nephrosclerosis |
Transparency:
Normally, urine should be clear. Turbidity of urine may be due to the presence of a large number of urinary sediment elements.
Specific gravity:
Normally, the specific gravity ranges from 1003 to 1035. An increase in values is observed with dehydration, glucosuria, and a large number of urinary sediment elements.
| Age | Values |
| up to 1 month | 5,0 - 7,0 |
| over 1 month | 5,0 – 8,0 |
Reasons for increasing values:
Urinary tract infections;
Nutritional reasons (diet errors).
Reasons for lower values:
Nutritional reasons (diet errors, starvation);
Uric acid diathesis, gout;
Normally, the protein concentration in a single portion of urine should not exceed 0.140 g/liter.
Reasons for increased protein concentration:
Normally, the glucose concentration in a single portion of urine should not exceed 2.8 mmol/l.
Reasons for increased glucose concentration:
| Physiological | Nutritional (diet errors), prolonged fasting, stress, 2-3 trimester of pregnancy, overdose or long-term use of corticosteroids |
| Pathological | febrile conditions, pancreatitis, pancreatic necrosis, diabetes mellitus; impaired reabsorption of glucose in the proximal nephron (renal diabetes), hyperthyroidism, organic kidney damage (chronic glomerulonephritis, lipoid nephrosis); pheochromocytoma, Itsenko-Cushing syndrome, meningitis, encephalitis, brain trauma and tumors, poisoning with heavy metal salts (mercury, lead, cadmium), toxic substances (ethylene glycol, carbon tetrachloride) and nephrotoxic drugs (aminoglycosides, phenacytin). |
| Substances whose presence may distort the result | Ascorbic acid, chlorine-containing oxidizers (disinfectants) |
Ketone bodies:
Normally, the concentration of ketone bodies in a single portion of urine does not exceed 1 mmol/l.
Reasons for increased concentration of ketone bodies:
Urobilinogen:
Normally, the concentration of urobilinogen in a single portion of urine does not exceed 34 mmol/l.
Reasons for increased urobilinogen concentration:
Bilirubin:
Normally, bilirubin is not detected in urine.
Reasons for increased bilirubin concentration:
Hemoglobin:
Normally, hemoglobin is not detected in urine.
Reasons for increased hemoglobin concentration::
Leukocyte esterase:
Normally, leukocyte esterase is not detected in urine.
Normally, nitrites are not detected in urine.
Squamous epithelial cells:
Normally present in urine in quantities of up to 5 per field of view. A larger number of cells indicates errors in collecting material for research.
Transitional epithelial cells:
- urolithiasis disease;
- intoxication, including those caused by drugs;
- feverish conditions;
- postoperative conditions;
Renal epithelial cells:
Normally they are not found in urinary sediment.
Appears in the following cases:
- chronic and acute renal failure;
- intoxication (taking salicylates, cortisone, phenacetin, bismuth preparations, poisoning with heavy metal salts, ethylene glycol);
- neoplasms in the kidneys.
Leukocytes:
Normally, they occur in quantities of no more than 5 cells per field of view. An increase in the number of leukocytes is observed in the following cases:
- inflammatory diseases of the kidneys and urinary tract of infectious and non-infectious origin (glomerulonephritis, pyelonephritis, nephritis, cystitis, prostatitis, urogenital tuberculosis);
- urolithiasis disease;
- feverish conditions;
- kidney transplant rejection;
- systemic inflammatory diseases of non-infectious origin (for example, lupus nephritis).
Red blood cells:
Normally, they occur in quantities of no more than 2 cells per field of view. An increase in the number of red blood cells is observed in the following cases:
- inflammatory diseases of the kidneys and urinary tract of infectious and non-infectious origin (glomerulonephritis, pyelonephritis, nephritis, cystitis, prostatitis, urogenital tuberculosis);
- urolithiasis disease;
- traumatic damage to the kidneys and urinary tract, including after instrumental studies;
- feverish conditions;
- arterial hypertension with involvement of the renal vessels;
- vitamin deficiency C;
- hemorrhagic diathesis (blood clotting disorders: hemophilia, thrombocytopenia, thrombocytopathy, etc.);
- poisoning with benzene derivatives, aniline, snake venom, poisonous mushrooms, with intolerance to anticoagulant therapy;
- neoplasms of the genitourinary system;
- systemic inflammatory diseases of non-infectious origin.
Hyaline cylinders:
Normally they are not found in urinary sediment.
Appears in the following cases:
- condition after significant physical activity;
- dehydration;
- feverish conditions;
- arterial hypertension;
- inflammatory kidney diseases;
- congestive heart failure;
- acute transplant rejection reaction.
- dehydration;
- uric acid crisis in newborns (physiological condition);
- uric acid diathesis, gout;
- strengthening the processes of protein catabolism, including in severe inflammatory-necrotic lesions, cancer, cytostatic therapy and poisoning with heavy metal salts.
Normally they can be found in urine in small quantities. An increase in the amount of urate is typical for the following conditions:
- dehydration;
- eating large amounts of animal food;
- uric acid diathesis, gout;
- strengthening the processes of protein catabolism, including in severe inflammatory-necrotic lesions, cancer, cytostatic therapy and poisoning with heavy metal salts.
Ammonium uric acid:
Normally they are not found in urinary sediment.
Appears in the following cases:
- uric acid diathesis in children;
- kidney infarction in a newborn (ammonium urate cylinders);
- in normal urine when it stands for a long time at room temperature (ammonia fermentation) in combination with tripel phosphate crystals.
Calcium oxalates:
Normally they can be found in urine in small quantities. An increase in the amount of oxalates is typical for the following conditions:
- consumption of foods high in oxalic acid (sorrel, spinach, potatoes, tomatoes, apples and other fruits and vegetables), as well as strong broths, cocoa, strong tea and excessive consumption of sugar, mineral waters with a high content of carbon dioxide and salts of organic acids;
- oxalic acid diathesis;
- diabetes;
Bacteria:
Normally they are not found in urinary sediment. The presence of bacteria can be associated both with the presence of bacteria in the kidneys and/or urinary tract, and with errors made during the collection of biomaterial for research.
Normally they are not found in urinary sediment. The presence of fungi can be associated both with a fungal infection of the urinary tract and with errors made during the collection of biomaterial for research.
Acute intermittent porphyria (AIP) is a hereditary disease belonging to the group of porphyrias, which are based on impaired heme biosynthesis, which leads to the accumulation of porphobilinogen (PBG) and δ-aminolevulinic acid (ALA) in organs and tissues, which have a toxic effect on the body and causing typical clinical symptoms. The disease usually manifests itself in young and adulthood, and of all types of porphyrias, AKI has an unfavorable prognosis. Approximately one person in 20 thousand is an asymptomatic carrier of the pathological gene, and one in 100 thousand suffers from AKI. The difficulty in diagnosing AKI is that it occurs under the guise of neurological and mental diseases.
AKI is transmitted in an autosomal dominant manner, associated with mutations in the genes of chromosome 11 and genetic defects in uroporphyrinogen synthetase, which leads to a sharp increase in PBG, ALA and dysfunction of the peripheral nervous system and gastrointestinal tract. In most carriers of the pathological gene, the disease may never manifest itself throughout life, but various unfavorable factors contribute to its manifestation. These include:
- various medications;
- pesticide;
- alcohol intoxication;
- premenstrual period;
- pregnancy;
- limiting food consumption;
- infectious diseases;
- stress.
Under the influence of these factors, the disease takes an acute course, which makes its verification possible. It should be noted that with untimely diagnosis and inadequate treatment of this disease, 60 people out of every hundred cases die. At the same time, timely diagnosis and adequate therapy can save the vast majority of patients, maintaining an acceptable quality of life.
Symptoms of acute intermittent porphyria
- prolonged, paroxysmal pain in the abdominal cavity;
- nausea;
- vomit;
- stool retention;
- increased heart rate;
- increased blood pressure;
- decreased muscle tone;
- pain in the limbs;
- decreased skin sensitivity;
- dysphagia;
- loss of voice;
- paralysis and paresis;
- respiratory paralysis;
- insomnia;
- emotional instability;
- tendency to depression;
- hysterical personality type;
- confusion;
- visual and auditory hallucinations;
- seizures;
- photosensitivity;
- skin hyperpigmentation;
- urine color in all shades of red.
SPP is especially severe during pregnancy and often ends in death.
Diagnostics
If characteristic clinical symptoms are present, the following confirmatory studies are performed:
- The reaction of urine with Ehrlich's reagent is positive.
- Determination of total porphyrins, PBG and ALA in urine: the level is increased.
- Determination of total porphyrins in feces: the level is increased.
- Molecular genetic research: identification of carriage of a mutant gene.
During the period of convalescence and remission, all indicators return to normal, which in most cases does not allow verification of the disease.
Treatment of acute intermittent porphyria
It begins with eliminating provoking factors, limiting fat in the diet and increasing the amount of carbohydrates. For outpatient treatment, patients usually take dry glucose powder. Pathogenetic drug therapy is carried out with the drug Normosang IV at a dose of 3-4 mg/kg per day for 4 to 8 days in a row, which leads to relief of an attack of AKI. In the acute phase of AKI, cimetidine is used at a dose of 800 mg per day, the duration of therapy is determined individually. Hemodialysis, plasmapheresis, and hemoperfusion are prescribed. Women stop the onset of menstruation. Symptomatic therapy is aimed at correcting neurological and psychotic symptoms, relieving pain, lowering blood pressure, and stopping tachycardia. Mandatory: personal hygiene, massage, exercise therapy. The younger the age of onset of the disease, the more serious the prognosis. All patients and their close relatives are recommended to carry with them a reminder about the presence of porphyria, in order to prevent the administration of provocative medications in the event of urgent medical care.
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 urine container in advance from any INVITRO Independent Laboratory.
Before collecting urine, it is necessary to perform a thorough hygienic toilet of the genitals. 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 (tonsillitis, 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 yellow | Swelling, burns, vomiting, diarrhea, congestive edema in heart failure | High concentration of urochromes |
| Pale, watery, colorless | Diabetes insipidus, decreased renal concentration function, taking diuretics, overhydration | Low concentration of urochromes |
| Yellow-orange | Taking vitamins, furagin | — |
| Reddish, pink | Eating brightly colored fruits and vegetables, such as beets, carrots, blueberries; medications - antipyrine, aspirin | — |
| Red | Renal colic, renal infarction | The presence of red blood cells in the urine - fresh hematuria, the presence of hemoglobin, porphyrin, myoglobin |
| Meat slop color | Acute glomerulonephritis | Hematuria (changed blood) |
| Dark brown | Hemolytic anemia | Urobilinuria |
| Red-brown | Taking metronidazole, sulfonamides, bearberry-based drugs. Phenol poisoning | — |
| Black | Marchiafava-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 |
| Whitish | Presence of phosphates or lipids in urine | — |
| Lactic | Renal lymphostasis, urinary tract infection | Hiluria, 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):
- toxicosis of pregnant women;
- oliguria.
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);
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;
- metabolic and respiratory alkalosis;
- chronic renal failure;
- renal tubular acidosis (types I and II);
- hyperkalemia;
- primary and secondary hyperfunction of the parathyroid gland;
- carbon anhydrase inhibitors;
- a diet high in fruits and vegetables;
- prolonged vomiting;
- urinary tract infections caused by microorganisms that break down urea;
- administration of certain medications (adrenaline, nicotinamide, bicarbonates);
- neoplasms of the genitourinary system.
- metabolic and respiratory acidosis;
- hypokalemia;
- dehydration;
- starvation;
- diabetes;
- tuberculosis;
- fever;
- severe diarrhea;
- taking medications: ascorbic acid, corticotropin, methionine;
- diet high in meat protein and cranberries.
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):
- nephrotic syndrome;
- diabetic nephropathy;
- glomerulonephritis;
- nephrosclerosis;
- impaired absorption in the renal tubules (Fanconi syndrome, heavy metal poisoning, sarcoidosis, sickle cell disease);
- multiple myeloma (Bence Jones protein in urine) and other paraproteinemias;
- impaired renal hemodynamics in heart failure, fever;
- malignant tumors of the urinary tract;
- cystitis, urethritis and other urinary tract infections.
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 such a result is obtained, to give 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 COMM.":
- 1.7 - 2.8 - traces;
- > 2.8 - a significant increase in the concentration of glucose in the urine.
- diabetes;
- acute pancreatitis;
- hyperthyroidism;
- renal diabetes;
- steroid diabetes (taking anabolic steroids for diabetics);
- poisoning with morphine, strychnine, phosphorus;
- dumping syndrome;
- Cushing's syndrome;
- myocardial infarction;
- pheochromocytoma;
- major injury;
- burns;
- tubulointerstitial kidney damage;
- pregnancy;
- taking large amounts of carbohydrates.
Reference values: negative.
Detection of bilirubin in urine:
- obstructive jaundice;
- viral hepatitis;
- cirrhosis of the liver;
- metastases of neoplasms to the liver.
Reference values: 0 - 17.
Increased excretion of urobilinogen in urine:
- increased hemoglobin catabolism: hemolytic anemia, intravascular hemolysis (transfusion of incompatible blood, infections, sepsis), pernicious anemia, polycythemia, resorption of massive hematomas;
- 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);
- increased urobilinogen in liver dysfunction: viral hepatitis (excluding severe forms);
- chronic hepatitis and cirrhosis of the liver;
- toxic damage: alcohol, organic compounds, toxins during infections, sepsis;
- secondary liver failure: after myocardial infarction, cardiac and circulatory failure, liver tumors;
- increased urobilinogen during liver bypass surgery: liver cirrhosis with portal hypertension, thrombosis, renal vein obstruction.
Reference values: 0 - 0,4.
"SEE COMM."
- 0.5 - 0.9 - traces;
- > 0.9 - positive.
- diabetes mellitus (decompensated - diabetic ketoacidosis);
- precomatose state, cerebral (hyperglycemic) coma;
- long-term fasting (complete refusal of food or diet aimed at reducing body weight);
- severe fever;
- alcohol intoxication;
- hyperinsulinism;
- hypercatecholaminemia;
- isopropranolol poisoning;
- eclampsia;
- glycogenosis types I, II, IV;
- lack of carbohydrates in the diet.
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:
- severe hemolytic anemia;
- severe poisoning, for example, sulfonamides, phenol, aniline. poisonous mushrooms;
- sepsis;
- burns.
- muscle damage;
- heavy physical activity, including sports training;
- myocardial infarction;
- progressive myopathies;
- Rhabdomyolysis
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:
- tumors of the genitourinary system;
- glomerulonephritis;
- pyelonephritis;
urinary tract stones;
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:
- acute and chronic pyelonephritis, glomerulonephritis;
- cystitis, urethritis, prostatitis;
- stones in the ureter;
- tubulointerstitial nephritis;
- lupus nephritis;
- 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:
- men -
- transitional epithelial cells -
- renal epithelial cells - absent.
squamous epithelial cells: women -
Detection of renal epithelial cells:
- pyelonephritis;
- intoxication (taking salicylates, cortisone, phenacetin, bismuth preparations, poisoning with heavy metal salts, ethylene glycol);
- tubular necrosis;
- kidney transplant rejection;
- 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:
- renal pathology (acute and chronic glomerulonephritis, pyelonephritis, kidney stones, renal tuberculosis, tumors);
- congestive heart failure;
- hyperthermic conditions;
- high blood pressure;
- taking diuretics.
- glomerulonephoritis, pyelonephritis;
- diabetic nephropathy;
- viral infections;
- lead poisoning;
- fever.
- chronic renal failure;
- kidney amyloidosis;
- nephrotic syndrome.
- acute glomerulonephritis;
- kidney infarction;
- renal vein thrombosis;
- malignant hypertension.
- pyelonephritis;
- Lupus nephritis in systemic lupus erythematosus.
- acute tubular necrosis;
- viral infection (for example, cytomegalovirus);
- poisoning with salts of heavy metals, ethylene glycol;
- overdose of salicylates;
- amyloidosis;
- 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):
- highly concentrated urine;
- acidic reaction of urine (after physical activity, meat diet, fever, leukemia);
- uric acid diathesis, gout;
- chronic renal failure;
- acute and chronic nephritis;
- dehydration (vomiting, diarrhea);
- in newborns.
- alkaline urine reaction in healthy people;
- vomiting, gastric lavage;
- cystitis;
- Fanconi syndrome, hyperparathyroidism.
- eating foods rich in oxalic acid (spinach, sorrel, tomatoes, asparagus, rhubarb);
- pyelonephritis;
- diabetes;
- 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 relevant 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 it. 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 (tonsillitis, 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.
Porphyria- a group of congenital disorders caused by a defect in the synthesis of heme - the iron-containing part. - acquired.
Diagnosis criteria
- characteristic symptoms and laboratory data
- identification of porphyrin and metabolites of heme synthesis in stool, plasma,
- enzyme activity measurement
- genetic testing
More than 80% of heterozygous patients with porphyria are asymptomatic.
According to the clinical course of the disease, porphyria is often divided into acute forms of porphyria and forms that occur predominantly with damage to the skin.
Acute attacks of porphyria may include abdominal pain and mental disturbances, paresthesia, fever, and less commonly, convulsions, neuromuscular weakness, etc. Acute attacks of porphyria are characteristic of acute intermittent porphyria, coproporphyria. The occurrence of an attack is provoked by medications (especially barbiturates, alcohol and sulfonamides; also diphenylhydantoin, chlordiazepoxide, ergometrine, some steroids, etc.), infection, and fasting.
The only symptom of an acute attack of porphyria may be a sharp increase in the level of porphobilinogen in the blood.
Patients with asymptomatic carriage may have only a few acute attacks of porphyria throughout their lives, and the levels of aminolevulinic acid, porphobilinogen and porphyrin in urine, feces, and blood may remain normal.
Laboratory diagnostics
To confirm the diagnosis of acute porphyria, laboratory data should include:
- daily amount of 5-aminolevulinic acid in urine,
- porphobilinogen in urine,
- uroporphyrin in urine,
- coproporphyrin in urine; urine should be frozen, since porphyrin is quickly destroyed, especially at room temperature.,
- plasma porphyrin,
- free erythrocyte protoporphyrin,
- feces for the quantitative determination of coproporphyrin and protoporphyrin,
- The Watson-Schwartz test shows the amount of porphyrin in the urine (Ehrlich's reagent or sodium acetate is added to the urine; it is considered positive if a cherry-red color occurs when adding chloroform), it is quantitative, but low-sensitivity.
Important!
- Evidence of porphyria is hemolytic anemia or liver disease; fluorescence in relevant tissues and determination of enzyme activity in erythrocytes of liver tissue and fibroblast culture. Read about diagnosing anemia in the article “”.
- Aminolevulinic acid and porphobilinogen levels are measured during acute attacks of porphyria.
- Some medications can provoke porphyria attacks (stimulate heme synthesis by affecting aminolevulinic acid), such as alcohol, antipyretics, barbiturates, estrogens, phenylhydrazine, phenytoin and sulfonamides.
- Enzyme activity measurements and DNA analysis help determine the type of porphyria.
- Tests for porphyrin in urine (fluorometric method) - some drugs also provoke fluorescence, for example, acriflavine, etoxazine, sulfamethoxazole, tetracycline, phenosopyridine.
Classification of porphyria
1. Erythropoietic forms
- Erythropoietic coproporphyria.
2. Hepatic forms
3. Hepatoerythropoietic forms
- Hepatoerythropoietic porphyria.
Comparison of types of porphyria
|
Enzyme defect |
Mutation locus | Onset of the disease |
Frequency of occurrence |
|
| Porphyria caused by aminolevulinate dehydratase deficiency |
aminolevulinic acid dehydratase, ~5% of normal |
autos. recession 9q34 7 mutations | variable |
only a few cases have been described |
| Acute intermittent porphyria |
porphobilinogen deaminase, 50% of normal |
autos. dom. 11 q23.3 more than 227 mutations | rarely until adulthood |
Lapland: 1:1000; everywhere 1.5:100000 |
| Congenital erythropoietic porphyria |
uroporphyrinogen-III-cosynthase |
autos. recession 10q25.2-26.3 | in the womb at birth |
less than 200 reported cases |
| Cutaneous porphyria | uroporphyrinogen decarboxylase | also acquired auto. dom. 1р34 | 30-40 years |
often in the USA and Europe |
| Hepatoerythropoietic porphyria |
uroporphyrinogen decarboxylase |
autos. recession | up to 2 years |
less than 20 reported cases |
| Hereditary coproporphyria |
coproporphyrin genoxidase, 50% of normal |
autos. dom. 3 ql2 36 mutations | at any time |
less than 50 reported cases |
| Mixed porphyria |
protoporphyrinogen oxidase, |
autos. dom. lq22 120 mutations | usually at 15-30 years old |
South Africa 3:1000; rare in other regions |
| Erythropoietic protoporphyria |
ferrochelatase |
autos. dom. 18q21.3 | 1-4 years |
less than 50 reported cases |
Pofiria was last modified: November 10th, 2017 by Maria Saletskaya
A comprehensive quantitative analysis that allows you to determine the level of uro- and coproporphyrins in urine: uroporphyrin, heptacarboxyporphyrin, hexacarboxyporphyrin, pentacarboxyporphyrin, coproporphyrin I, coproporphyrin III, total porphyrin. The study is intended to diagnose both congenital and acquired porphyrias. Genetically determined porphyria is based on a violation of heme biosynthesis, leading to excessive accumulation of porphyrins and their precursors in the body. Secondary porphyrias occur as a result of dysfunction of the liver or hematopoietic organs as a result of exposure to heavy metals, intoxication with lead, phosphorus, alcohol, benzene, carbon tetrachloride, with some malignant tumors and allergic conditions, cirrhosis of the liver, etc.
Research method
High performance liquid chromatography-mass spectrometry (HPLC-MS).
Units
Nmol/day (nanomole per day), µmol/day. (micromoles per day).
What biomaterial can be used for research?
Daily urine.
How to properly prepare for research?
- Eliminate alcohol from your diet for 24 hours before the test.
- Avoid (in consultation with your doctor) taking diuretics for 48 hours before collecting urine.
General information about the study
Porphyrins, cyclic compounds formed by four pyrrole rings interconnected by methenyl bridges, are synthesized from glycine and succinyl-CoA through the formation of δ-aminolevulinic acid and porphobilinogen. These are intermediate compounds in the synthesis of heme, which is part of the hemoglobin molecule that carries out oxygen transfer. 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.
It is customary to distinguish between primary and secondary porfinuria. The first, usually called porphyrias, include a group of hereditary diseases, each of which is characterized by a set of porphyrins and their precursors excreted in the urine. Secondary porfinuria occurs due to dysfunction of the liver or hematopoietic organs as a result of any primary diseases, for example severe hepatitis, intoxication with lead, phosphorus, alcohol, benzene, carbon tetrachloride, with some malignant tumors and allergic conditions, cirrhosis of the liver, etc. When In secondary porfinuria, significant amounts of coproporphyrins are found in the urine.
Seven indicators of porphyrins are measured, including total porphyrin, which allows the toxic effects of metals to be identified and what treatment is needed. Also, the indicators of specific porphyrins serve as functional markers of the toxicity of toxic metals and organic chemicals. Porphyrin tests can determine the level of biochemical damage caused by exposure to toxic substances, mercury exposure in patients, toxin levels in patients before and during chelation, drug toxicity, and differential diagnosis of heavy metal poisoning.
The effects of toxins can cause increased sensitivity to chemicals, behavioral disorders and decreased learning, immune dysfunction, chronic fatigue syndrome, neurological and mental, emotional disorders, and anemia.
It is also advisable, when determining toxicity, to study the spectrum of diseases associated with autism (ASD) and to develop therapeutic measures to eliminate insufficient detoxification and sulfation, and the accumulation of heavy metals. Sources of toxins can be fish, amalgams, polluted air and soil, fluorescent lamps, paints, ceramics, treatment using traditional medicine, groundwater, tobacco. Symptoms of intoxication: fatigue, weakness, increased chemical sensitivity, irritability, anxiety, memory loss, insomnia, numbness and tingling in the arms and legs, convulsions, gastrointestinal disorders, loss of appetite.
When is the study scheduled?
- Diagnosis of primary (hereditary) porphyrias;
- if there is suspected intoxication with lead or mercury, organic solvents, medications (anticonvulsants, analgesics, anesthetics, antipsychotics, anti-inflammatory and hormonal), as well as alcohol and its surrogates;
- diseases of the hepatobiliary system accompanied by porphyrinuria;
- hormonal changes in women during the menstrual cycle with heavy discharge;
- anorexia due to a low-calorie, low-carbohydrate diet;
- a history of acute attacks, simultaneously combining acute abdominal pain without symptoms of peritoneal irritation with the release of red or pink urine, the appearance of heart rhythm disturbances, nausea and vomiting, increased blood pressure, increased body temperature against the background of various manifestations of polyneuropathy.
What do the results mean?
Reference values
Urinary excretion of porphyrins may increase with:
- viral hepatitis;
- lymphogranulomatosis;
- damage to the central nervous system;
- liver cirrhosis;
- poisoning with salts of heavy metals, benzene and carbon tetrachloride.
Aminolevulinic acid/urinary porphobilinogen
Laboratory testing of liver function
Who orders the study?
Pediatrician, therapist, dermatologist, endocrinologist, toxicologist, cardiologist, neurologist, psychiatrist.