Description of urine test for microalbuminaria. Diabetic nephropathy - causes, symptoms, stages, treatment, prevention At the stage of chronic renal failure

Two interrelated processes continuously occur in the kidneys - filtration and reabsorption. From the blood passing through glomeruli of the kidney , primary urine is filtered, which receives a large amount of salts, sugar, proteins and trace elements. Then, in a healthy body, the necessary substances are reabsorbed.

With the development of pathology of the urinary system, diseases of the heart and blood vessels of the system, proteins are removed from the body. Microalbuminuria occurs.

What it is? Microalbuminuria- this is a symptom in which special proteins - albumins - are found in the urine in an amount of 30 to 300 mg / day.

The role of albumin in the human body

Proteins, in particular albumins, are the main material for all cells of the body. They maintain the balance of fluid and microelements between cellular and extracellular structures. Albumin is necessary for the functioning of all organs and systems.

Most proteins are synthesized from amino acids in liver cells. After this, they enter the systemic bloodstream and are distributed throughout the body. The synthesis of some proteins requires essential amino acids from food. The loss of such proteins in the urine is observed in serious pathologies and threatens the body with serious consequences.

24-hour urine test and albuminuria

Since at the initial stage microalbuminuria may not manifest itself in any way, it becomes of great importance 24-hour urine test.

Why should you prepare for a urine test?

To avoid false positive results, beforehow to get tested, it is necessary to prepare:

alcohol intake is excluded for two days;
Protein-rich foods (meat, legumes) are consumed in the usual amount for a particular person;
before collecting urine, toileting of the genitals without the use of disinfectants;
women need to close the vaginal opening with a sterile cotton wool or gauze swab;
collection of analysis begins with the second portion of urine, the first urination carried into the toilet;
all urine during the day going into a large sterile container with divisions indicating volume;
the urine container should be stored in the refrigerator;
after 24 hours, the urine is mixed, 100 ml of urine is taken into another sterile container and delivered to laboratory for microscopy.

It is important to collect all portions of urine in full for daily analysis, since the level of MAU in urine can change during the day.

Difference between the terms microalbuminuria and macroalbuminuria

Proteinuria divided into several types depending on the amount of protein detected. Detection in daily urine traces protein (less than 30 mg albumin) is normal and does not require treatment. When the amount of albumin ranges from 30 to 300 mg/day, a diagnosis of microalbuminuria is made. If more than 300 mg/day of albumin is found in the urine,macroalbuminuria. Microalbuminuria is often one of the first signs of the disease, while others symptoms there are no diseases.Macroalbuminuria same often appears in the advanced stage of the disease.

Indications for determining microalbuminuria in 24-hour urine

Patients for whom analysis daily allowance urine test for UIA is mandatory:

sick diabetes mellitus 1st and 2nd types;
patients with arterial hypertension;
patients with chronic kidney disease;

Norms of protein in urine for adults (men and women)

To determine the excretory function of the kidneys, it is not the total number of albumins in the urine that matters, but index ratio of albumin to creatinine. In adult men this indicator normally equal to 2.5 g/mmol, among women – 3.5 g/mmol. If thisindicator increased, this may indicate developmentrenal failure.

Need for more research

UIA is more often detected incidentally during decoding general urine analysis during medical examination. After that the doctor prescribes daily allowance urine test for microalbuminuria. For some chronic diseases daily Urinalysis should be performed regularly to monitor treatment and prevent complications. In such cases, determining the exact amount of albumin is not required, which means that as a screening method Two types of test strips can be used – quantitative and qualitative.

Quality test strips change color when immersed in urine containing albumin. If the strip does not change color, Means, protein content in urine less than 30 mg.

Quantitative test strips for UIA, when lowered into urine, change their color depending on the albumin content. The packaging shows a color scale and indicates how many albumins correspond to which color. By comparing the color of the test strip and the color of the scale, you can determine the approximate content of albumin in the urine or its absence.

What might a slight excess of protein in urine indicate?

UIA can be observed in a number of serious diseases, such as:

diabetes ;
arterial hypertension;
atherosclerosis;
chronic renal failure;
nephropathy of smokers;
tumors;
urolithiasis disease.

In rare cases, microalbuminuria develops in the absence of disease.

Non-pathological causes

If protein is detected in the urine doctor gives a direction to retake the analysis, since cause microalbuminuria may be due to protein molecules entering a container with urine during analysis collection.

In addition, a small amount of protein may appear in the urine due to the following: reasons:

If the patient's diet is rich in protein foods of plant or animal origin.
After taking certain medications, such as anti-inflammatory drugs, a short-termincrease in albuminurine. Before taking the test, you should consult with doctor regarding the withdrawal of medications taken for several days.
After intense physical activity, the body breaks down large protein molecules into smaller fragments, which can pass into the urine through the kidney filter.
During pregnancy Some protein may be detected in the urine. Normal albumin value in daily urine in pregnant women is no more than 500 mg. If quantityalbumin levels increased, this may indicate a risk of developing preeclampsia in a woman.
African Americans have severalincreased albumin content in urine can be considered the norm.
During ARVI and other acute infectious diseases, when the temperature rises to 39 degrees, permeability increasesglomerular vessels of the kidneys. Through these vessels proteins are filtered. As the febrile reaction resolves, microalbuminuria decreases.
Orthostatic microalbuminuria may occur in some children and adolescents. With this syndrome, the amount of albumin in urine collected in a standing position exceeds the norm. At the same time, in the analysis collected in the supine position,the level of albumin in urine is determined. Causes Orthostatic MAU is unknown; it is usually associated with a congenital anomaly of the renal vasculature.

In other cases, a more thorough examination of the patient using moderndiagnostic methods to identify the cause of UIA.

Diabetes

During development diabetes mellitusTypes 1 and 2 increase level blood sugar, called hyperglycemia. Long-term hyperglycemia leads to damage to large and small vessels the whole body. Microangiopathy also develops in the kidneys, causing diabetic nephropathy . With this syndrome, the wall of the renal tubules ceases to perform its function and becomes permeable to large protein molecules. UIA becomes the first sign of kidney damage.

Sick diabetes mellitus must be tested for UIA at least once every six months to promptly detect development nephropathy and provide appropriate treatment. During developmentdiabetes mellitus 1st type first microalbuminuria testsurrenders after 5 years from the onset of the disease, withdiabetes mellitusType 2 – immediately after diagnosis.

Cardiovascular diseases

In hypertension, narrowing occurs vessels organs and tissues, increased blood flow, increased blood pressure inside vessel Vascular damage kidney, called hypertensive angiopathy, leads to excessive pathological filtration of proteins through the wall glomeruli of kidneys . The presence of UIA increases stage hypertension and the risk of complications –renal failureand nephrosclerosis (wrinkling of the kidney).

With atherosclerosis, fat deposits occur in the form of atherosclerotic plaques on the walls vessels . The affected wall becomes permeable to proteins and some blood elements.

Chronic kidney infections

Chronic pyelo- and glomerulonephritis can be cause detection of protein in urine. In infectious diseases, the permeability of the glomerular apparatus increases and the process of reabsorption of urine is disrupted. Protein entering the primary urine is not reabsorbed back.

Since there may be no symptoms during treatment for chronic kidney disease, microalbuminuria may serve indicator , which evaluates the course of the disease and the effectiveness of therapy.

Urolithiasis disease

Microalbuminuria may be the first sign of the development of urolithiasis. Sand and small stones cause damage to the kidney filter, and the secretion of proteins into the urine increases. When the wall of the urinary tract is damaged, microscopic components containing protein can also penetrate into the urinary tract. urine.

Microtraumas of the genitourinary system

With microscopic injuries of the urinary tract, the processes of secretion and reabsorption in the kidneys are not impaired. Protein in urine is detected due to the components of the cell wall of the affected areas of the urinary system.

Cancer of the urinary system

Microalbuminuria may be the first sign of a malignant tumor of the urinary system in the earlystages of development. Cancer cells have invasive growth. They grow into the walls vessels and urinary tract, causing damage. Albumin penetrates into the urine through the damaged membrane.

Smoking

Heavy smokers who smoke more than one pack of cigarettes a day have dangerous concentrations of nicotine in their blood. Nicotine acts on the inner layer of the glomerular membrane, increasing its permeability to protein molecules. With constant exposure to nicotine, chronicrenal failure.

If you have a UIA, you need to find reason pathological syndrome. Development is excluded firstdiabetes mellitusand hypertension.

For diabetes mellitus characteristic:

increased glucose levels in venous blood more than 6.5 mmol/l;
level up glycated hemoglobin.

Hypertension is characterized by:

promotion blood pressureabove 140/90mm Hg. Art.;
increase in the amount of cholesterol in the blood;
increase in triglycerides.

Maintaining normal blood glucose level, blood pressure, cholesterol and fats, quitting smoking and drinking alcohol, reducing carbohydrates in the diet contribute to the prevention andtreatment of microalbuminuria.

Microalbuminuria appears at the initial stage of development of many serious diseases, so healthy people need to undergo regular medical examinations and a general urine test. In the presence of pathology fromcardiovascularand endocrine systemurine test for albuminshould be appointed doctor at least once every six months, so as not to miss the progression of the disease and to select the necessary treatment.

one of the many complications of diabetes that I listed in the article. How dangerous is diabetic nephropathy? You will find out the answers to this and other questions by reading the article to the end. Good day everyone!

As I have repeatedly said, the most dangerous thing is not the fact of diabetes itself, but its complications, because they lead to disability and early death. I also said in my previous articles, and I will not tire of repeating, that the severity and speed of development of complications completely depend on the patient himself or on the caring relative, if this is a child. Well-compensated diabetes mellitus is when the fasting blood sugar level does not exceed 6.0 mmol/l, and after 2 hours does not exceed 7.8 mmol/l, and the difference in glucose level fluctuations during the day should not exceed 5 mmol/l . In this case, the development of complications is delayed for a long time, and you enjoy life and have no problems.

But it is not always possible to compensate for the disease, and complications do not keep you waiting. One of the target organs for diabetes is the kidneys. After all, the body gets rid of excess glucose by excreting it through the kidneys in the urine. By the way, back in ancient Egypt and ancient Greece, doctors made a diagnosis by tasting the urine of a sick person; in case of diabetes, it had a sweet taste.

There is a certain limit for the increase in blood glucose levels (renal threshold) , reaching which sugar begins to be detected in the urine. This threshold is individual for each person, but on average this figure is considered to be 9 mmol/l. When it exceeds this level, the kidneys are not able to absorb glucose back, because there is too much of it and it appears in the person’s secondary urine. By the way, I will say that the kidneys first form primary urine, the amount of which is several times greater than what a person excretes per day. Through a complex system of tubules, part of this primary urine, which contains glucose (normally), is absorbed back (along with glucose), and what remains is the part that you see every day in the toilet.

When there is too much glucose, the kidneys absorb as much as needed, and the excess is excreted. At the same time, excess glucose pulls water with it, so patients with diabetes produce a lot of urine compared to a healthy person. But increased urination is typical for uncompensated diabetes. Those who keep their sugar levels normal excrete as much urine as a healthy person, unless, of course, there is some concomitant pathology.

As I already mentioned, everyone has their own renal threshold, but in general it is 9 mmol/l. If the renal threshold decreases, that is, blood sugar appears at lower values, then this means that there are serious problems with the kidneys. Typically, a decrease in the renal threshold for glucose is characteristic of renal failure.

Excess glucose in the urine has a toxic effect on the renal tubules, leading to their sclerosis. In addition, intraglomerular hypertension occurs, as well as arterial hypertension, which is often found in type 2 diabetes, also has a negative effect. Together, these factors lead to inevitable renal failure, which requires a kidney transplant.

Stages of development of diabetic nephropathy (DN)

In our country, the following classification of diabetic nephropathy has been adopted:

Diabetic nephropathy, stage of microalbuminuria.
Diabetic nephropathy, stage of proteinuria with preserved renal filtration function.
Diabetic nephropathy, stage of chronic renal failure.

But a slightly different classification has been adopted all over the world, which includes the preclinical stage, i.e., the earliest disorders in the kidneys. Here is the classification with an explanation of each stage:

Hyperfunction of the kidneys (hyperfiltration, hyperperfusion, renal hypertrophy, normoalbuminuria up to 30 mg/day).
Beginning DN (microalbuminuria 30-300 mg/day, normal or moderately increased glomerular filtration rate).
Severe DN (proteinuria, i.e. sugar is visible in a routine general urine test, arterial hypertension, decreased glomerular filtration rate, sclerosis of 50-75% of the glomeruli).
Uremia or renal failure (decrease in glomerular filtration rate less than 10 ml/min., total glomerulosclerosis).

Few people know that at the very initial stage of development the complication is still reversible, even at the stage of microalbuminuria you can turn back time, but if the stage of proteinuria is detected, then the process is irreversible. The only thing that can be done is to stop it at this stage so that the complication does not progress.

What needs to be done to reverse the changes and stop the progression? That's right, you need to normalize your sugar level first of all, and there is something else that I will talk about in the paragraph about treating DN.

Diagnosis of diabetic nephropathy

At the initial stage, this complication has no clinical manifestations and therefore is not noticed by the patient himself. When there is massive loss of protein (proteinuria), protein-free edema and increased blood pressure may occur. I think it's clear why you need to regularly monitor your kidney function.

As a screening measure, all patients are given a urine test for microalbuminuria (MAU). Do not confuse this analysis with a general urinalysis; this method is not able to detect the “small” proteins that first slip through the glomerular basement membrane. When protein appears in a general urine test, this means that there is a loss of “large” proteins (albumin) and the basement membrane already looks like a sieve with large holes.

So, the UIA test can be done at home or in the laboratory. To measure at home, you need to purchase special “Mikral-test” test strips, similar to test strips for determining the level of sugar and ketone bodies in urine. By changing the color of the test strip you will learn about the amount of microalbumin in the urine.

If you find microalbuminuria, it is recommended to retake the test in the laboratory to identify specific numbers. Usually they donate daily urine to the UIA, but some recommendations write that it is enough to donate a morning portion of urine. Microalbuminuria is considered to be the detection of protein in the range of 30-300 mg/day, if daily urine was collected, and the detection of protein in the range of 20-200 mg/l in the morning urine sample indicates MAU. But a single detection of microalbumin in the urine does not mean that DN has begun.

An increase in protein in the urine can also occur in other conditions not related to diabetes, for example:

with high protein intake
after heavy physical activity
against the background of high temperature
due to urinary infection
during pregnancy

To whom and when is testing for UIA indicated?

A urine test for microalbuminuria is carried out when protein is not yet detected in a general urine test, that is, when there is no obvious proteinuria. Analysis is prescribed in the following cases:

All patients with type 1 diabetes are over 18 years old, starting from the 5th year after the onset of the disease. Held once a year.
Children with type 1 diabetes, regardless of the duration of the disease. Held once a year.
All patients with type 2 diabetes, regardless of the duration of the disease. Conducted once every 6 months.

When detecting microalbuminuria, you should first make sure that the analysis is not influenced by the factors discussed above. When microalbuminuria is detected in patients with a duration of diabetes mellitus of more than 5-10 years, the diagnosis of diabetic nephropathy, as a rule, is not in doubt, unless, of course, there are other kidney diseases.

What's next

If microproteinuria is not detected, then you do nothing other than continue to monitor your blood glucose levels. If microalbuminuria is confirmed, then along with recommendations for compensation, it is necessary to begin certain treatment, which I will talk about a little later.

If you already have proteinuria, that is, protein appears in a general urine test, then it is recommended to repeat the test 2 more times. If proteinuria persists, further testing of renal function is necessary. To do this, blood creatinine, glomerular filtration rate, and blood pressure levels are examined. A test that determines the filtration function of the kidneys is called the Rehberg test.

How is the Rehberg test performed?

Daily urine is collected (at 6:00, night urine is poured into the toilet, throughout the day and night until 6:00 the next morning, urine is collected in a separate container; the amount of collected urine is calculated, it is mixed and about 100 ml is poured into a separate jar, which belongs to to the laboratory). In the laboratory, you donate blood from a vein and report the amount of urine per day.

A decrease in glomerular filtration rate indicates the progression of DN and the imminent development of renal failure. An increase in glomerular filtration rate indicates initial changes in the kidneys that can be reversible. After the entire examination, treatment is carried out according to indications.

But I must say that the Rehberg test is now little used, and it has been replaced by other more accurate calculation formulas, for example, the MDRD formula. For children, the Schwartz formula is used. Below I provide a picture showing the most modern formulas for calculating GFR.

The MDRD formula is considered to be more accurate than the Cockcroft-Gault formula. Normal GFR values are considered to be on average 80-120 ml/min. GFR readings below 60 ml/min indicate renal failure when creatinine and blood urea levels begin to increase. There are services on the Internet where you can calculate GFR by simply substituting your values, for example, on this service.

Is it possible to detect kidney “interest” even earlier?

Yes, you can. At the very beginning, I said that there are clear signs of the very first changes in the kidneys, which can be confirmed in the laboratory and which doctors often forget about. Hyperfiltration may indicate that a pathological process is beginning in the kidney. Hyperfiltration, i.e. glomerular filtration rate, also called creatinine clearance, is always present at the initial stage of diabetic nephropathy.

An increase in GFR of more than 120 ml/min may indicate the manifestation of this complication, but not always. It should be taken into account that the filtration rate can increase due to physical activity, excessive fluid consumption, etc. Therefore, it is better to retake the tests again after some time.

Treatment of diabetic nephropathy

Now we get to the most important thing in this article. What to do when there is nephropathy. First of all, normalize the glucose level, because if this is not done, the treatment will be in vain. The second thing to do is to keep your blood pressure under control, and if it is normal, monitor it periodically. The target pressure should be no more than 130/80 mmHg. Art.

These two postulates for the prevention and treatment of DN are recommended at any stage of the disease. Further, depending on the stage, new points will be added to the recommendations. So, for persistent microproteinuria, long-term use of ACE inhibitors (enalapril, perindopril and other drugs) is recommended. ACE inhibitors are antihypertensive drugs, but in small doses they do not have the effect of lowering blood pressure, but they retain a pronounced angioprotective effect. Drugs from this group have a positive effect on the inner wall of blood vessels, including kidney vessels, and therefore, thanks to them, pathological processes in the vascular wall reverse.

Another drug that is recommended for diabetic nephropathy is sulodexide (Wessel Du F). It also has a positive effect on the microvasculature of the kidneys. At this stage, these drugs are sufficient and there are no dietary restrictions.

At the stage of chronic renal failure, correction of phosphorus-calcium metabolism is carried out, because there is a loss of calcium with the development of osteoporosis, as well as correction of anemia with iron supplements. In the terminal stage, such patients undergo hemodialysis or kidney transplantation.

That's all for me. Take care of yourself and your kidneys. and stay informed.

Having seen the results of a laboratory test, the patient naturally wants to figure out: what is there - normal or not? But, alas, not everyone knows how to read analysis. Although there is nothing particularly complicated here. General urinalysis - OAM - is the most common, oldest and routine diagnostic tool. However, despite this, it has not lost its relevance to this day.

The general analysis of this biological fluid includes:

assessment of its physical parameters;
determination of the presence of organic substances;
microscopic examination of sediment.

Assessment of physical parameters

Color, transparency, smell of urine. In a healthy person it is yellow in color of varying intensity. Brown and even almost black urine occurs with hemolytic anemia, malignant tumors, severe alcohol and chemical poisoning. It becomes reddish in case of injury, acute inflammation, or renal infarction. Pinkish - if hemoglobin production is impaired. Colorless or pale yellow urine occurs in diabetics. Milky color indicates the presence of pus, fats, and phosphates in high concentrations.

However, urine may acquire pink, red or brown shades due to beets, carrots, iron supplements, and “5-NOK”. And the green or light brown color is due to bay leaves and rhubarb. But these are not pathological, but physiological indicators of color, that is, the norm.

Fresh urine from a healthy person is clear. Only over time does it become cloudy, as salts and other impurities dissolved in it begin to precipitate. This is also the norm. The higher the concentration of impurities, the cloudier the urine.

It always has a specific smell, not too strong. If the urine smells like ammonia, this usually indicates inflammatory processes in the kidneys or bladder. She usually gives apples to diabetics. The smell of urine becomes pungent when a person consumes foods or takes medications rich in aromatic substances. In this case, there is no pathology.

Acidity of urine. If the diet is varied and balanced, then the urine reaction is either neutral (7.0) or slightly acidic (less than 7.0). It acquires a pronounced acidic reaction during fever caused by high temperature, stones in the bladder, and kidney disease. A significant alkaline reaction appears with vomiting, diarrhea, acute inflammatory processes, urinary tract infections, and the breakdown of cancerous tumors.

Relative density. This important parameter - sg in Latin transcription - characterizes the concentration function of the kidneys. It is defined as the specific gravity of a liquid and is normally 1003-1028 units. Its fluctuations for physiological reasons are allowed within the range of 1001-1040 units. Men have a higher specific gravity of urine than women and children.

In pathologies, its stable deviations are observed. Thus, with severe edema, diarrhea, acute glomerulonephritis, and diabetes, hypersthenuria is observed when the specific gravity exceeds 1030 units.

A low relative density indicator - 1007-10015 units - indicates hyposthenuria, which can be caused by fasting, diabetes insipidus, and nephritis. And if the specific gravity is below 1010 units, then there is isosthenuria, which is characteristic of very severe kidney damage, including neurosclerosis.

You can learn more about all the main urine indicators and their interpretation in this table.

Organic substances in urine

Its Latin designation in analysis is glu (glucose). The most desired result of a test for sugar is an indicator of its absence: glu negative or glu neg. But, if it is detected, doctors note glucosuria. Most often this is the lot of diabetics.

However, it can be not only pancreatic, but also renal and hepatic, if these organs are affected. Symptomatic glucosuria is observed with injuries and diseases of the brain, stroke, adrenal tumors, hyperthyroidism, etc.

If protein is found in the urine

In the analysis, it appears under the designation pro, the decoding of which is simple: protein, that is, protein. Its concentration of more than 0.03 g is called proteinuria. If the daily loss of protein is up to 1 g, then this is moderate proteinuria, from 1 g to 3 g is moderate, and more than 3 g is severe.

A special indicator for diabetics is MAU. For them, endocrinologists and nephrologists have identified a “border zone”: microalbuminuria or MAU. Microalbumins are the smallest types of proteins that enter the urine first. Therefore, the MAU indicator is the earliest marker of renal disorders in diabetes mellitus. The daily norm of such miniproteins is up to 3.0-4.25 mmol.

MAU is a very important parameter by which one can judge the reversibility of kidney damage. After all, diabetic nephropathy is one of the main causes of disability and mortality in diabetes. The insidiousness of this serious complication is that it develops slowly, imperceptibly and does not cause painful symptoms.

Monitoring urine allows you to timely detect the level of UIA and prescribe appropriate therapy to restore the kidneys.

The method for determining MAU is the most effective, since it is very difficult to measure albumin concentration by other laboratory methods.

Bilirubin, bile acids, indican. The norm is when the analysis says: bil neg (bilirubin negative), that is, there is no bilirubin. Its presence indicates pathologies of the liver or gall bladder. If the concentration of bilirubin in the blood exceeds 17-34 mmol/l, then bile acids appear in the urine. Usually this is also a consequence of pathologies of the liver and gallbladder.

Urobilinogen, ketone bodies. A positive ubg value means the presence of urobilinogen. It can signal liver or blood diseases, myocardial infarction, infections, enterocolitis, gallstones, volvulus, and other pathologies. The daily concentration ubg is above 10 µmol.

The presence of ketone bodies - ket - containing acetone and its derivatives in the urine is a consequence of prolonged anesthesia, fasting, diabetes mellitus, thyrotoxicosis, stroke, carbon monoxide or lead poisoning, and overdose of certain drugs.

What does the asc indicator indicate? It indicates how much ascorbic acid is excreted in the urine. The norm for a healthy body is about 30 mg per day. It may be necessary to detect the level of asc in formula-fed infants, cancer patients, smokers, alcoholics, burns, depression, suspected vitamin deficiency, scurvy, kidney stones, and infectious diseases.

In addition, before testing for glucose, hemoglobin, bilirubin or nitrites, it is advisable to determine the concentration of asc. After all, if it exceeds 0.3 mmol/l, a general urine test may give unreliable results.

Microscopic analysis of urinary sediment

Leukocytes, erythrocytes. The number of leukocytes - leu - in the urinary sediment in healthy people should not exceed 0-3 for men and 0-5 for women. Deviation from the norm is a clear sign of inflammatory processes, primarily in the genitourinary system.

These inflammations, as well as malignant tumors, lead to the appearance of red blood cells in the urine - bld. Their number allows us to judge how the disease develops and how effective the treatment is. Women have a high level of red blood cells in the first time after childbirth, but this is considered normal.

Casts, epithelial cells, creatinine. The urinary sediment should always be free of all types of casts, except hyaline ones. The presence of other varieties is usually associated with kidney damage, hypertension, viral infections, thrombosis, chemical poisoning, and taking a number of antibiotics.

The presence of 3 epithelial cells - vtc - is the maximum permissible number. An increased content of squamous epithelial cells is observed with urethritis; transitional - with pyelitis, pyelonephritis, cystitis; renal - with serious kidney damage. A high vtc value most often indicates severe nephritis or nephrosis.

The norm of creatinine - cre - is 0.64-1.6 g/l for men and 0.48-1.44 g/l for women. A reduced content in the urine and at the same time a high level in the blood are characteristic of kidney pathologies. Tests for creatine are required for endocrine diseases, muscular dystrophy, and pregnancy.

Minerals, mucus, bacteria, flakes. Salts in small quantities are normal. But if these are crystals or salts of uric acid uro, then when they are detected, the development of gout, glomerulonephritis, congestive kidney or leukemia can be assumed. Oxalates are often detected in pyelonephritis, diabetes, epilepsy, phosphates - in cystitis, stones in the bladder.

There should be no mucus in the urine. It usually appears when the genitourinary organs are chronically ill. These include bladder stones, cystitis, urethritis, and prostate adenoma.

Bacteria - nit (nitrites) - are fixed in the sediment if acute infections develop in the urinary organs. In this case, flakes may also be detected. This is basically also nit - dead bacteria, as well as dead epithelial cells.

As we can see, a general urine test, deciphering the substances it contains, is very informative. Of course, only its results, even the most accurate ones, do not yet allow us to establish a specific disease. But together with data from other types of research, taking into account the patient’s clinical symptoms, a general urine test is still an important diagnostic tool today.

101analiz.ru

Diabetic nephropathy or how to preserve kidneys with diabetes

Diabetic nephropathy is one of the many complications of diabetes, which I listed in the article “Complications of diabetes do not depend on the type.” How dangerous is diabetic nephropathy? You will find out the answers to this and other questions by reading the article to the end. Good day everyone!

There is a certain limit for the increase in blood glucose levels (renal threshold), reaching which sugar begins to be detected in the urine. This threshold is individual for each person, but on average this figure is considered to be 9 mmol/l. When it exceeds this level, the kidneys are not able to absorb glucose back, because there is too much of it and it appears in the person’s secondary urine. By the way, I will say that the kidneys first form primary urine, the amount of which is several times greater than what a person excretes per day. Through a complex system of tubules, part of this primary urine, which contains glucose (normally), is absorbed back (along with glucose), and what remains is the part that you see every day in the toilet.

Stages of development of diabetic nephropathy (DN)

In our country, the following classification of diabetic nephropathy has been adopted:

Diabetic nephropathy, stage of microalbuminuria.
Diabetic nephropathy, stage of proteinuria with preserved renal filtration function.
Diabetic nephropathy, stage of chronic renal failure.

Hyperfunction of the kidneys (hyperfiltration, hyperperfusion, renal hypertrophy, normoalbuminuria up to 30 mg/day).
Beginning DN (microalbuminuria 30-300 mg/day, normal or moderately increased glomerular filtration rate).
Severe DN (proteinuria, i.e. sugar is visible in a routine general urine test, arterial hypertension, decreased glomerular filtration rate, sclerosis of 50-75% of the glomeruli).
Uremia or renal failure (decrease in glomerular filtration rate less than 10 ml/min., total glomerulosclerosis).

Diagnosis of diabetic nephropathy

An increase in protein in the urine can also occur in other conditions not related to diabetes, for example:

with high protein intake
after heavy physical activity
against the background of high temperature
due to urinary infection
during pregnancy

To whom and when is testing for UIA indicated?

All patients with type 1 diabetes are over 18 years old, starting from the 5th year after the onset of the disease. Held once a year.
Children with type 1 diabetes, regardless of the duration of the disease. Held once a year.
All patients with type 2 diabetes, regardless of the duration of the disease. Conducted once every 6 months.

What's next

How is the Rehberg test performed?

Is it possible to detect kidney “interest” even earlier?

Treatment of diabetic nephropathy

That's all for me. Take care of yourself and your kidneys. Subscribe to blog updates and stay updated.

saxarvnorme.ru

Clinical significance of microalbuminuria in medical practice. - MED-M LLC is the exclusive distributor of HemoCue in Russia.

Institution of the Russian Academy of Medical Sciences Russian Scientific Center for Surgery named after Academician B.V. Petrovsky RAMS

Morozov Yu.A., Dementyeva I.I., Charnaya M.A.

Manual for doctors

The manual discusses the pathogenesis and clinical significance of microalbuminuria. Much attention is paid to modern laboratory diagnostics of proteinuria/microalbuminuria, as well as monitoring of this condition during the course of the disease and its therapy. The important clinical significance of microalbuminuria has been shown as an indicator of the progression of pathologies such as diabetes mellitus and arterial hypertension. Methods for correcting renal disorders accompanied by microalbuminuria are presented. The manual is intended for doctors of all specialties, students, residents and graduate students of medical universities, as well as for teachers and students of the School of Diabetes and the School of Hypertension.

Morozov Yu.A., Dementyeva I.I., Charnaya M.A., 2010

A healthy adult excretes up to 150 mg of protein per day, with only 10-15 mg being albumin. The rest is represented by 30 different plasma proteins and glycoproteins - products of the activity of kidney cells. Among the proteins contained in urine, Tamm-Horsfall mucoprotein predominates. Its origin is not associated with plasma, but with cells of the ascending limb of the loop of Henle. Its excretion rate is 25 mg/day. In the absence of urinary tract infection and acute illness, increased urinary albumin excretion usually reflects pathology of the glomerular apparatus of the kidneys. The term “microalbuminuria” (MAU) refers to the excretion of albumin in the urine in amounts exceeding the physiological norm, but below the detection limits of commonly used methods (Table 1). Table 1. Definition of UIA

Rate of albumin excretion in urine 30-300 mg/24 h Rate of albumin excretion in urine 20-200 mg/min Albumin content in early morning urine 30-300 mg/l Albumin/creatinine ratio 30-300 mg/g (in the USA)

Albumin/creatinine ratio 2.5-25 mg/mmol* (in European countries

Note: In women, the lower limit of the albumin/creatinine ratio is 3.5 mg/mmol.

Normally, low molecular weight plasma proteins are easily filtered in the glomeruli. The endothelial cells of the glomerular capillaries form a barrier with pores with a diameter of about 100 nm. The basement membrane prevents the passage of molecules with a relative molecular weight of more than 100,000 D. Also, the surface of the glomerular basement membrane in contact with urine is covered with processes of visceral epithelial cells - podocytes. Their processes form numerous narrow tubules lined with negatively charged glycoproteins. Albumin in general is also negatively charged, making it difficult to filter.

Protein reabsorption occurs through pinocytosis. Pinocytotic vacuoles detach and move toward the basal part of the cell, into the perinuclear region, where the Golgi apparatus is located. They can fuse with lysosomes, where hydrolysis occurs. The resulting amino acids are released through the basal plasma membrane into the blood. The tubular cells have specific mechanisms for the separate reabsorption of various proteins - albumin, hemoglobin [Chizh A.S., 1983.].

In diseases of the glomeruli, these filtration barriers may be destroyed. The lesion, limited only to polyanionic glycoproteins, is accompanied by selective loss of negatively charged proteins (albumin) in the urine. More extensive damage, extending to the entire basement membrane, leads to the loss of large proteins along with albumin.

Various pathogenetic mechanisms underlie the disruption of the glomerular filter:

toxic or inflammatory changes in the glomerular basement membrane (deposition of immune complexes, fibrin, cellular infiltration), causing structural disorganization of the filter;
changes in glomerular blood flow (vasoactive agents - renin, angiotensin II, catecholamines), affecting glomerular transcapillary pressure, convection and diffusion processes;
lack (deficiency) of specific glomerular glycoproteins and proteoglycans, leading to the loss of a negative charge by the filter.

Tubular proteinuria is associated either with the inability of the tubules to reabsorb proteins that have passed through the unchanged glomerular filter, or due to the release of protein by the epithelium of the tubules themselves. It is observed in acute and chronic pyelonephritis, heavy metal poisoning, acute tubular necrosis, interstitial nephritis, chronic kidney transplant rejection, kalipenic nephropathy, and genetic tubulopathies.

The selectivity of proteinuria refers to the ability of the glomerular filter of the kidneys to pass plasma protein molecules depending on their molecular weight. The selectivity of proteinuria decreases as the permeability of the glomerular filter increases as a result of its damage. The appearance of large molecular proteins (α2- and γ-globulins) in the urine indicates non-selective proteinuria and deep damage to the glomerular filter of the kidneys. In contrast, urinary excretion of low molecular weight albumins indicates little damage to the basement membranes of the glomerular capillaries and a high selectivity of proteinuria. Thus, the selectivity of proteinuria can serve as an indicator of the degree of damage to the glomerular filter and, therefore, has important diagnostic and prognostic significance. It has been established, for example, that the highest selectivity of proteinuria is observed with “minimal changes” in the glomeruli, while with deeper damage to the structure of the glomerular capillaries (with membranous and especially proliferative glomerulonephritis), the selectivity of proteinuria decreases.

Depending on the severity, mild, moderate and severe proteinuria are distinguished. Mild proteinuria (from 300 mg to 1 g/day) can be observed with acute urinary tract infection, obstructive uropathy and vesicoureteral reflux, tubulopathies, urolithiasis, chronic interstitial nephritis, kidney tumors, polycystic disease. Moderate proteinuria (from 1 to 3 g/day) is observed in acute tubular necrosis, hepatorenal syndrome, primary and secondary glomerulonephritis (without nephrotic syndrome), and the proteinuric stage of amyloidosis. Severe or severe proteinuria is defined as a loss of protein in the urine exceeding 3.0 g per day or 0.1 g or more per kilogram of body weight in 24 hours. Such proteinuria is almost always associated with dysfunction of the glomerular filtration barrier in terms of protein size or charge and is observed in nephrotic syndrome.

In practically healthy people, under the influence of various factors, transient (physiological, functional) proteinuria may appear. Physiological proteinuria is usually insignificant - no more than 1.0 g/day.

Transient protein excretion in the urine in healthy people may appear after heavy physical activity (long hikes, marathon running, team sports). This is the so-called working (marching) proteinuria or tension proteinuria. The genesis of such proteinuria is explained by hemolysis with hemoglobinuria and stress secretion of catecholamines with a transient disturbance of glomerular blood flow. In this case, proteinuria is detected in the first portion of urine after physical activity.

The importance of the cooling factor in the genesis of transient proteinuria was noted in healthy people under the influence of cold baths. With a pronounced skin reaction to insolation, albuminuria solarus develops. Proteinuria has been described when the skin is irritated by certain substances, for example, iodine. The possibility of the appearance of proteinuria with an increase in the level of adrenaline and norepinephrine in the blood has been established, which explains the release of protein in the urine during pheochromocytoma and hypertensive crises. There is alimentary proteinuria, which sometimes appears after eating a large protein meal. The possibility of the appearance of centrogenic proteinuria has been proven in epilepsy and concussion. Emotional proteinuria occurs during exams [Chizh A.S., 1974].

Proteinuria of functional origin also includes the release of protein in the urine, described by some authors, during vigorous and prolonged palpation of the abdomen and kidney area (palpable proteinuria).

In newborns, physiological proteinuria is also observed in the first weeks of life.

Feverish proteinuria is observed in acute febrile conditions, more often in children and the elderly. Proteinuria persists during the period of increased body temperature and disappears when it decreases and normalizes. If proteinuria persists for many days and weeks after body temperature has normalized, then possible organic kidney disease should be excluded. In heart disease, congestive or cardiac proteinuria is often detected. As the heart failure resolves, it usually goes away.

Orthostatic (postural, lordotic) proteinuria is observed in 12–40% of children and adolescents, characterized by the detection of protein in the urine during prolonged standing or walking with a rapid disappearance (transient version of orthostatic proteinuria) or a decrease in it (persistent version) in a horizontal position. Its genesis is associated with disturbances of renal hemodynamics, developing due to lordosis, compressing the inferior vena cava in a standing position, or the release of renin (angiotensin II) in response to changes in the volume of circulating plasma during orthostasis.

Yaroshevsky A.Ya. (1971) identified three main types of pathological proteinuria. Renal proteinuria includes:

Proteinuria associated with the release of normal serum proteins through a damaged glomerular filter; - tubular proteinuria, caused by the release of protein by the tubular epithelium; - proteinuria associated with insufficient protein reabsorption due to tubular damage.

Proteinuria can be extrarenal in nature, occurs in the absence of a pathological process in the kidneys themselves and is divided into prerenal and postrenal

Prerenal proteinuria develops in the presence of an unusually high plasma concentration of low molecular weight protein, which is filtered by normal glomeruli in quantities exceeding the physiological capacity of the tubules for reabsorption. A similar type of proteinuria is observed in myeloma (low molecular weight Bence Jones protein and other paraproteins appear in the blood), with severe hemolysis (due to hemoglobin), rhabdomyolysis, myopathy (due to myoglobin), monocytic leukemia (due to lysozyme).

Postrenal proteinuria is caused by the release of mucus and protein exudate in the urine due to inflammation of the urinary tract or bleeding. Diseases that may be accompanied by extrarenal proteinuria are urolithiasis, kidney tuberculosis, kidney or urinary tract tumors, cystitis, pyelitis, prostatitis, urethritis, vulvovaginitis. Postrenal proteinuria is often very minor and practically less important.

Excretion of albumin in urine fluctuates within a wide range throughout the day. At night it is 30-50% less than during the day, which is due to the fact that at night in a horizontal position the levels of systemic blood pressure, renal plasma flow and glomerular filtration rate are lower. The level of albumin secretion increases significantly in an upright position and after physical activity, with increased dietary protein intake. High excretion of albumin in urine is more common in elderly people and people of the Negroid race. Smokers have higher urinary albumin excretion than non-smokers.

The prevalence of MAU in the general population ranges from 5 to 15%. The detection rate of MAU is practically independent of the criteria used and the gender of the individuals examined (Table 2). At the same time, there is a close relationship between the frequency of detection of UIA and smoking, body mass index, blood pressure (BP) and cholesterolemia. MAU is especially often detected in diabetes mellitus and arterial hypertension. According to various researchers, MAU occurs in 10-40% of patients with type I diabetes mellitus and 15-40% of patients with type II diabetes mellitus.

Table 2. UIA detection rate

In most laboratories, when testing urine “for protein,” they first use qualitative reactions that do not detect protein in the urine of a healthy person. If protein in the urine is detected by qualitative reactions, its quantitative (semi-quantitative) determination is carried out. In this case, the features of the methods used, covering a different spectrum of uroproteins, are important. Thus, when determining protein using 3% sulfosalicylic acid, the amount of protein up to 0.03 g/l is considered normal, but when using the pyrogallol method, the limit of normal protein values increases to 0.1 g/l. In this regard, the analysis form indicates the normal protein value for the method used by the laboratory.

To quantify the level of albumin excretion in urine, radioimmune, immunoenzyme and immunoturbidimetric methods are currently used. Usually, the albumin content is determined in urine collected over 24 hours, although it is more convenient to use for this purpose either the first morning portion of urine, or urine collected in the morning for 4 hours, or urine collected at night (8-12 hours). If the albumin content is determined in the first morning portion or in a portion of urine collected at night, then the level of albumin excretion in urine is expressed in mg per 1 liter of urine [Chizh A.S. et al., 1992]. It is often difficult to accurately measure the time during which urine is collected; in such cases, it is recommended to determine the ratio of albumin to creatinine in urine, especially in the first morning portion. Normally, the albumin/creatinine ratio is less than 30 mg/g or less than 2.5-3.5 mg/mol.

The radial immunodiffusion method is the simplest, most accessible and relatively inexpensive method. This method is not widely used, as it requires a long incubation period and highly qualified personnel.

The radioimmune method is highly sensitive. Due to the fact that the reagents have a limited shelf life due to the relatively short half-life of the iodine isotope, the method is currently used quite rarely.

When carrying out enzyme immunoassay, various variants of this method are used, differing in the material of the solid phase, methods of attaching antibodies to it, the sequence of adding reagents, options for washing the solid phase, the source of the enzyme in the conjugate, the type of substrate, and the method of expressing the results of the analysis. Instead of anti-albumin antibodies, a method has been developed using the albumin receptor obtained by genetic engineering [Gupalova T.V., Polognyuk V.V., 1997].

Immunoturbidimetry is simpler than the radioimmune method. The determination can be carried out both in kinetic and equilibrium versions.

Currently, HemoCue (Sweden) has developed and introduced into the Russian market the albumin analyzer HemoCue Albumin 201. This is a portable photometer designed to determine MAU with the ability to operate both from a battery pack and from the mains. The measuring range is 5-150 mg/l. The time to obtain the result is about 90 seconds.

The analyzer can be used for the quantitative determination of MAU for the purposes of screening, diagnosis, monitoring and treatment control. The HemoCue Albumin 201 system is based on an immunoturbidimetric reaction using antibodies to human albumin. The antigen-antibody complex changes the light transmission of the cuvette, which is measured photometrically at a wavelength of 610 nm. The albumin concentration is proportional to the turbidity and the result is shown on the display in mg/l. The system consists of a small, dedicated analyzer and individually packaged microcuvettes containing a lyophilized reagent. All that is needed to obtain a quantitative result: fill the microcuvette, place it in the analyzer and read the result.

Tests conducted on the basis of the Russian-Swiss clinical diagnostic laboratory "Unimed Laboratories" (Moscow), accredited as an expert laboratory by the Russian Ministry of Health (reg. 42-5-005-02 dated March 11, 2002) showed high reliability of the results, ease of use, which allows us to recommend portable HemoCue analyzers for use in medical institutions of various levels (laboratories in hospitals, clinics, ambulances, the Ministry of Emergency Situations and directly in departments of various profiles). Comparison of the results of MAU determination using HemoCue Albumin 201 and the Hitachi 917 analyzer showed their high correlation (r2=0.971, r=0.983)/

The analyzer differs in operation. To determine MAU, you must: Fill a microcuvette with urine, immersing its tip in the sample.
Insert the filled microcuvette into the analyzer holder.
After 90 seconds, read the result.

Chemical turbidimetric methods are based on protein precipitation with various agents, for example, sulfosalicylic acid, trichloroacetic acid, benzethonium chloride. All turbidimetric methods are based on measuring the change in light transmission of the reaction mixture due to light scattering during the formation of turbidity. The higher the concentration of protein in the urine, the greater the number of conglomerates formed. These methods are difficult to standardize and often lead to erroneous results, but despite this, they are now widely used in laboratories due to the low cost and availability of reagents. The main factors leading to incorrect results:

A large standard ratio of urine to reagent, which is, for example, 1:3 for sulfosalicylic acid, which leads to the influence of various components of urine on the test result;
Interference of many drugs, which is accompanied by “false positive” or “false negative” results.
The measured absorbance of a test sample reflects only the specific temporary state of the test sample and not the true protein concentration;
Difference in the protein composition of urine and the calibrator-albumin;
The turbidity formed from albumin is 4 times higher than the turbidity formed from globulins;
Presence of immunoglobulin light chains in urine: some samples remain completely soluble after precipitation of all other forms of proteins.

The group of colorimetric methods for determining protein includes the Lowry, biuret and methods based on the binding of protein to organic dyes. The Lowry method has high sensitivity: ~ 10 mg/l and a wide linear measurement range - up to 1 g/l. But the results of the analysis significantly depend on the amino acid composition - the intensity of staining of various proteins can vary by 300 or more times, so the method has not found wide application in practice [Chizh A.S. et al., 1992]. The biuret method is practically independent of the amino acid composition of proteins. The method is not very sensitive to various compounds present in the sample. The linear dependence is approximately 10 times wider than that of the Lowry method, and the sensitivity is ~10 times lower. Due to its low sensitivity, the method is not suitable for determining low protein concentrations. The sensitivity of the method can be increased by various modifications, one of which is to precipitate the protein and concentrate it. The biuret method with precipitation and concentration of protein is considered a reference method for determining protein in urine, but due to the high complexity of the analysis, it is practically not used for routine research in clinical laboratories [Ryabov S.I. et al., 1979].

Another group of tests for determining protein in urine are methods based on the binding of protein to organic dyes. They attract attention due to their simplicity and speed of execution, and high sensitivity. Their principle is based on the interaction of a protein with an organic dye, resulting in the formation of a colored complex, the color intensity of which is proportional to the protein concentration in the sample. Disadvantages include differences in the ability of different proteins to bind dyes. Another significant drawback is the violation of the proportional relationship between the concentration of some proteins and the optical density of the protein-dye complex [Zagrebelny S.H., Pupkova V.I., 1986, Trivedi V.D. Ital. J., 1997]. Among these tests are methods based on protein binding to Coomassie Brilliant Blue (CBG), Bromophenol Blue (BPB) and Pyrogallol Red (PHR).

Methods based on protein binding to CBG. This type of method was developed in 1976 by Bradford M.M. The protein-dye complex is formed very quickly - within 2-5 minutes with a color change from red to blue and remains stable for an hour. The complex has high absorption, which provides it with high sensitivity - 5-15 mg/l. However, the reaction does not provide a strict proportional relationship between protein concentration and solution absorption: the linear region of determination is ~ 500 mg/L. CBG has varying abilities to bind different proteins. The narrow linear measurement range and significant sorption of the dye on the walls of the cuvettes limit the use of the method in laboratory practice for routine analyzes and for adaptation to automatic analyzers; however, a number of companies produce commercial CBG reagent kits for the determination of protein in urine and cerebrospinal fluid.

Methods based on protein binding to BPS. Almost simultaneously with the use of CBG for the determination of protein in biological fluids, it was proposed to use BPS. The binding reaction of BPS with proteins occurs at pH ~ 3 for 1 min, color stability ~ 8 hours. This method is less sensitive than CBG, but there are fewer substances that interfere with its use. The sensitivity of the test is 30-70 mg/l, the linear detection range is up to 1 g/l, the coefficient of variation of measurement results does not exceed 5%. The method is accurate, sensitive, simple and accessible for laboratory practice. However, today the use of the BFS method is extremely limited: none of the well-known companies produces reagent kits using BFS and does not certify the protein in control urine solutions using the BFS method.

Methods based on protein binding to PGA. This dye for the determination of protein in urine was proposed in 1983 by Fujita Y. et al. Currently, this method has taken one of the first places among tests for determining protein in urine, gradually replacing all others. Commercial reagent kits using PGC are produced by many companies. The original method is based on the binding of protein to dye in an acidic environment (pH = 2.5). The complex is resistant to many compounds, including drugs, salts, bases, and acids. The method became widely used in laboratory practice after its modification by Watanabe N. et al. (1986). This made it possible to expand the linear measurement range to 2 g/l, which is not possible with methods using other dyes. The reproducibility of results in the range of protein concentrations from 0.09 to 4.11 g/l is 1-3%; accuracy of determination of albumin - 97-102%, globulin - 69-72%; sensitivity of the method - 30-40 mg/l; The stability of the reagent when stored in a dark place is 6 months. The PGA dye is not sorbed on the walls of cuvettes up to a protein concentration of 5 g/l, therefore the method is adapted to various types of analyzers.

Diagnostic strips provide a quick, semi-quantitative assessment of protein content in urine. The use of a device based on the principle of reflectance photometry allows the use of strips for both semi-quantitative and quantitative assessment of results [Kozlov A.V., Slepysheva V.V., 1999.]. On strips, the BFS dye in citrate buffer is most often used as an indicator. However, when testing urine with a high pH value, the buffer capacity may not be sufficient to maintain the pH in the reaction zone, resulting in a false positive result. An increase or decrease in the relative gravity of urine may also cause changes in the sensitivity of the strips. High salt content in urine reduces results. Negative results on the strips do not exclude the presence of globulin, hemoglobin, Bence Jones protein, or mucoprotein in the urine. In this regard, the strips are more suitable for detecting selective glomerular proteinuria. When assessing non-selective glomerular proteinuria (as well as tubular), the results of the study are lower than its actual level. The strips are even less suitable for detecting Bence Jones proteins. The use of diagnostic strips should be limited to screening procedures; they are convenient for rapid assessment of proteinuria directly at the patient's bedside. False-positive results on strips can also be caused by contamination of urine collection dishes with residues of detergents, chlorhexidine, amidoamines, during treatment with phenazopyridine, administration of polyvinylpyrrolidone [Pupkova V.I., Prasolova L.M., 2006.].

DIABETES

A classic description of specific kidney changes in diabetes mellitus is given in the work of P. Kimmelstiel and C. Wilson (1936), which led to the appearance of the term “diabetic glomerulosclerosis”. However, the term does not characterize the full variety of kidney damage, so the term “diabetic nephropathy” began to be used instead. In 1944, Laipply T. et al. first described the thickening of the basement membranes of the glomerular loops, indicating that similar changes are found in almost any organ that has a basement membrane in the vessels. These works identified the main component of diabetic nephropathy – damage to the microvascular bed (microangiopathy).

The results of experimental and clinical studies indicate that microangiopathy is universal in nature as a manifestation of damage to cells of loose connective tissue, considering this fact as a syndrome of deficiency of polyunsaturated fatty acids entering cells.

This concept allows us to state common pathogenetic mechanisms in atherosclerosis, hypertension, diabetes mellitus and metabolic syndrome X. (Titov V.N., 2002). A key element in the pathogenesis of these conditions is the functional blockade of apo-B-100 receptor endocytosis of low-density lipoproteins (LDL). A cell suffering from a deficiency of polyene fatty acids begins to synthesize unsaturated fatty acids, which are characterized by greater saturation of carbon bonds, which leads to a change in the structure and physicochemical properties of biological membranes, as well as synthesized prostaglandins, thromboxanes, prostacyclins, and leukotrienes. With a deficiency in the transport of ω-3-polyene fatty acids, the cell begins to synthesize mainly triene structures from ω-9 fatty acids. A decrease in the unsaturation of acyl chains leads to dense packing of annular phospholipids, which are grouped in the membrane around integral proteins: receptors, ion channels, enzymes, signaling systems. This leads to a decrease in the fluidity of the microenvironment, disruption of the function of integral proteins and membrane charge. A decrease in the number of double bonds in acyl residues of phospholipids reduces the negative charge on the surface of epithelial cells, and plasma albumin begins to be freely filtered into primary urine in increased quantities. With prolonged hyperglycemia in patients with diabetes, glucose binds to many proteins (glycosylation process), irreversibly damaging the proteins of the kidney tissue. Thus, in diabetes mellitus, nephron damage occurs due to organic damage to membranes occurring in the chain of the following processes:

Hyperfiltration leads to the deposition of proteins in the mesangium and stimulation of the synthesis of the basic substance of connective tissue by fibroblasts;
Glycosylation of basement membrane proteins reduces the negative charge and increases its permeability.
Stimulation of fibroblast proliferation and their synthetic activity: enhances lipid peroxidation, which damages the endothelium with a decrease in NO synthesis and increased endothelin synthesis, leading to vasospasm;
Increased sorbitol synthesis and decreased sialic acid synthesis aggravate tissue damage;
Stimulation of the renin-angiotensin system, especially in the presence of angiotensin-converting enzyme polymorphism (DD genotype), leads to the development of hypertension;
Hyperinsulinemia leads to proliferation and hypertrophy of vascular smooth muscle cells and mesangial cells with increased synthesis of the main substance of connective tissue;
Increased functional activity of platelets leads to the release of platelet-derived growth factors and other biologically active substances, leading to microthrombosis;
Changes in the functional activity of the endothelium, vasospasm and the development of arterial hypertension lead to irreversible changes in blood vessels and tissue sclerosis.

MAU may be the only manifestation of damage to the renal glomerulus and is an early sign of the development of nephropathy in patients with diabetes mellitus and arterial hypertension. Thus, MAU reveals dysfunction of the plasma membranes of highly differentiated cells due to changes in the structure of annular phospholipids and membrane charge.

The clinical significance of MAU is that in patients with diabetes mellitus it is the earliest and most reliable sign of the development of diabetic nephropathy. Detection of MAU in patients with insulin-dependent diabetes mellitus with an 80% probability indicates that in the next 5-7 years the patient will “get” to the clinical stage of diabetic nephropathy and the process of glomerular sclerosis begins to be irreversible [Shulutko B.I., 2002].

The frequency of detection of UIA increases with the duration of the disease in both type I and type II diabetes mellitus. For example, in a large study, the UK Prospective Diabetes Study (1998), MAU was detected in 12% of patients with newly diagnosed type II diabetes mellitus and in almost 30% of patients with a disease duration of more than 12 years. According to calculations by Parving N. et al. (1996), the frequency of new cases of UIA in patients with diabetes mellitus ranges from 1 to 3% per year. In patients with type 1 diabetes over 12 years of age, MAU is sometimes detected 1 year after the onset of the disease. In this case, MAU, as a rule, is intermittent in nature and is associated with inadequate glycemic control. Persistent MAU most often occurs 10-15 years after the development of type 1 diabetes. According to long-term observations, in 80% of patients with type 1 diabetes in whom urinary albumin excretion is 20 mcg/min (or 29 mg/day) during subsequent Diabetic nephropathy with impaired renal function develops between 10 and 14 years of age.

Kidney damage in diabetes never develops suddenly (Table 3). Usually this is a rather slow and gradual process that goes through several stages [Shestakova M.V. et al., 2003].

Table 3. Stages of renal dysfunction in diabetes mellitus

The occurrence and progression of MAU in diabetes mellitus can be influenced by various factors. With elevated blood pressure, urinary albumin excretion can increase by 60% per year. As soon as urinary albumin excretion reaches 70-100 mcg/min, the glomerular filtration rate of GFR begins to decrease (Table 4). Table 4.

Classification of stages of development of diabetic nephropathy

Stage of nephropathy	Clinical and laboratory characteristics	Development timeframe
1. Hyperfunction of the kidneys	Increase in GFR > 140 ml/min; - increased renal blood flow; - kidney hypertrophy; Normoalbuminuria (
2. Stage of initial structural changes in kidney tissue	Thickening of the basement membranes and capillaries of the glomeruli; - expansion of the mesangium; - high GFR remains; Normoalbuminuria.	In 2-5 years
3. Beginning nephropathy	MAU from 30 to 300 mg/day; - GFR is high or normal; Unstable increase in blood pressure;	In 5-15 years
4. Severe nephropathy	Proteinuria more than 500 mg/day; - GFR is normal or moderately reduced; Arterial hypertension.	In 10-25 years
	A decrease in GFR is a symptom of intoxication.	After 20 or more years or after 5-7 years from the onset of proteinuria

In type 2 diabetes mellitus, the highest correlation was found between the MAU level and the duration of the disease (r = 0.82). The highest rates of MAU were observed in patients with type 2 diabetes mellitus and arterial hypertension. At the same time, the MAU level correlated equally with the value of both systolic and diastolic blood pressure, including their daily indices [Mazur E.S., 1999]. The correlation with BP variability in type 2 diabetes mellitus was significantly lower than in hypertension without diabetes mellitus.

In a number of studies, increased urinary albumin excretion was combined with other microvascular complications of diabetes and, in particular, proliferative retinopathy. This suggests that in some patients with type 1 diabetes, MAU is an early manifestation of generalized lesions of the microvasculature. The level of MAU significantly correlates with signs of left ventricular hypertrophy (thickness of the posterior wall and interventricular septum), myocardial mass index, as well as with the manifestation of diastolic dysfunction of the left ventricle [Minakov E.V., 2008.]. This is a manifestation of the preclinical stage of diabetic cardiomyopathy. Notably, with improved glycemic control, not only does urinary albumin excretion decrease, but left ventricular diastolic function also improves.

Persistent MAU is often combined with lipid metabolism disorders. In patients with diabetes mellitus and high MAU values, plasma levels of total cholesterol, low-density lipoprotein cholesterol, triglycerides and apoprotein B are increased, and high-density lipoprotein cholesterol levels, on the contrary, are lower than in patients with normal urinary albumin excretion. In addition, close correlations were found between the MAU level and some biochemical parameters, which are a manifestation of the increased atherogenic potential of blood serum (total cholesterol, triglycerides, fibrinogen, soluble fibrin-monomer complexes) as well as with body mass index, which allows us to consider MAU as a component of the metabolic syndrome [Kobalava Zh.D., 2002].

ARTERIAL HYPERTENSION

In developed countries, primarily due to the widespread use of effective antihypertensive drugs, it has been possible to reduce the incidence of cardiovascular complications of hypertension. At the same time, in recent years there has been a steady increase in the development of end-stage renal failure in patients with hypertension and hypertension is the main or one of the main causes in 10-30% of patients on program dialysis [Preobrazhensky D.V., Sidorenko B. A., 1998].

It is known that the kidneys play an important role in the regulation of systemic circulation. The unchanged kidney responds to daily fluctuations in blood pressure adequately and stabilizingly. Protection against hyperperfusion is carried out by increasing the tone of the afferent arterioles of the glomeruli. As the duration and frequency of episodes of high blood pressure increase, structural changes in the wall of the renal vessels increase, which leads to an increase in resistance to excess blood flow [Gogin E.E., 1997.]. Morphologically, in the arterioles and interlobular arteries, moderate hypertrophy of the middle shell (media) is first determined.

As untreated hypertension continues, medial hypertrophy becomes more pronounced and leads to arteriolar stiffness. This contributes to an increase in intraglomerular pressure, which is no longer sufficiently controlled by the reaction of afferent arterioles. Increased intraglobular pressure has a damaging effect on the surface of endothelial cells due to increased mechanical stress and increased permeability of the basement membranes of glomerular capillaries for lipids and various protein components of plasma. As a result, ultrafiltration conditions are violated, the transcapillary gradient increases and MAU occurs

A group of researchers from the HOPE project (Heart Outcome Prevention Evaluation, 2008) convincingly showed that MAU is strictly associated with the risk of developing clinical manifestations of coronary artery disease, death and the development of heart failure. The risk of stroke in a patient with high blood pressure in the absence of MAU is 4.9%, while the addition of MAU increases this figure to 7.3%, the development of left ventricular hypertrophy - from 13.8 to 24%, and coronary heart disease - from 22.4 up to 31% [Kobalava Zh. D., Kotovskaya Yu. V., 2001].

Activation of the intrarenal renin-angiotensin system is believed to play an important role in the progression of kidney damage to the stage of end-stage renal failure. In the kidneys, chronic activation of the local renin-angiotensin system leads to increased formation of angiotensin II, which is accompanied by hypertrophy and proliferation of mesangial, interstitial and other cells of the renal parenchyma, increased migration of macrophages/monocytes and increased synthesis of collagen, fibronectin and other components of the extracellular matrix [Shestakova M. IN 1999.]. All this leads to sclerosis of the kidney tissue. As sclerotic changes progress, glomerular occlusion and atrophy of the renal tubules develop, and the hyperfiltration observed earlier is replaced by hypofiltration [Mareev V. Yu., 2000.]. This is accompanied by an increase in the level of creatinine and urea in the blood serum and the appearance of clinical symptoms of renal failure.

Recent studies suggest that there is a hereditary predisposition to increased urinary albumin excretion. Fauvel J.P et al. (1991) reported increased levels of albumin in urine in children with normal blood pressure, whose close relatives suffered from hypertension. Indications of hypertension in the family history were much more common in children with proteinuria/microhematuria. According to other data, the average rate of albumin excretion in urine in children with normal blood pressure, whose parents suffered from hypertension, is higher than in children with normal blood pressure, whose parents did not have arterial hypertension. Consequently, there is a family predisposition to the development of MAU, which may be combined with a predisposition to metabolic disorders [Preobrazhensky D.V. et al., 2000].

There are two indicators that indicate an increased risk of developing hypertensive angio-onephrosclerosis - glomerular hyperfiltration and MAU [Sidorenko B. A. et al., 2000.]. Today, MAU should be considered not only as a marker of kidney damage, but also as a factor determining prognosis. The appearance of proteinuria indicates a significant destructive process in the kidneys, in which about 50-75% of the glomeruli are already sclerotic, and the morphological and functional changes have become irreversible [Shestakova M. V., 1998].

According to various data, the prevalence of UIA in arterial hypertension varies widely - from 3% to 72%, depending on its severity and the presence of concomitant diseases. According to most researchers, in untreated patients with mild and moderate arterial hypertension, the prevalence of MAU ranges from 15 to 40%, averaging about 25% [Shalnova S.A. et al., 2002].

The detection rate of UIA is higher in patients with newly diagnosed hypertension and in patients not receiving antihypertensive drugs. The relationship between MAU and damage to the main target organs in hypertension has been revealed.

Slight increase in serum creatinine (115-133 µmol/l (1.3-1.5 mg/dl) in men, 107-124 µmol/l (1.2-1.4 mg/dl) in women, glomerular filtration rate 133 µmol/l (1.5 mg/dl) in men, > 124 µmol/l (1.4 mg/dl) in women, decreased glomerular filtration rate 300 mg/g) indicate a very high risk of developing cardiovascular complications.

Already elevated normal blood pressure (130-139 / 85-89 mm Hg) predisposes to the development of UIA: the likelihood of it in this category of patients increases by 2.13 times compared to strictly normotensive patients. Increase in mean blood pressure by 10 mm Hg. increases the risk of UIA by 1.41 times, systolic blood pressure by 1.27 times, and diastolic blood pressure by 1.29 times. It is the increase in blood pressure, especially systolic blood pressure, that is one of the most significant determinants of MAU in the population. In patients with arterial hypertension not combined with insulin resistance or type 2 diabetes mellitus, MAU reflects hypertensive kidney damage, the final stage of which is global diffuse nephroangiosclerosis. In patients with arterial hypertension, the dynamics of MAU should be monitored when prescribing antihypertensive therapy. MAU should be assessed once adequate BP control has been achieved.

The frequency of detection of UIA in untreated patients with hypertension depends on body weight. Mimran A. and Ribstein J. (1993) found MAU in 35% of untreated patients with arterial hypertension and obesity, but only in 26% of patients without obesity. A significantly lower incidence of MAU in patients with hypertension was reported by Pontremoli R. et al. (1997). According to their data, MAU occurred in 6.7% of 787 patients with hypertension, regardless of gender (6.4 and 7.1% in men and women, respectively). According to Ritz E. et al. (1994), increased urinary albumin excretion was found in 5.8% of patients with arterial hypertension under 60 years of age and in 12.2% of elderly patients (Table 5).

Table 5. Frequency of detection of UIA in patients with arterial hypertension depending on age and blood pressure level

Consequently, the prevalence of MAU in middle-aged outpatients with arterial hypertension receiving drug therapy is practically no different from that in the general population. Only in untreated patients and people over 60 years of age is there a higher frequency of MAU than in the general population [Preobrazhensky D.V. et al., 2000].

A significant correlation of MAU with systolic blood pressure was revealed, including depending on its level (r=0.84), variability (r=0.72), as well as with the daily index and time index of night-time systolic blood pressure. The highest level of MAU was found in hypertensive patients classified as “night-peaker” and “non-dipper”, both in terms of systolic and diastolic blood pressure. A number of literature sources note that clinically significant albuminuria is observed, as a rule, when diastolic blood pressure is more than 100 mm Hg. Art. [Litvin A.V., 2004].

The dynamics of MAU can serve as one of the criteria for the effectiveness of treatment. In arterial hypertension, a decrease in blood pressure with a simultaneous decrease in MAU is regarded as a more reliable indicator of the effectiveness of therapy than a decrease in these indicators separately. Sufficiently long-term (60 weeks) maintenance of blood pressure at the target level (

TREATMENT OF MICROALBUMINURIA

Understanding the pathogenesis of the development and progression of kidney damage in arterial hypertension and/or diabetes mellitus allows us to obtain a basis for the timing of initiation of MAU therapy and identify groups of drugs that are effective in eliminating it or slowing down the progression of MAU and its transition to proteinuria. In accordance with the mechanism of MAU formation, medications can be divided into:

affecting the process of hyperfiltration (angiotensin-converting enzyme inhibitors (ACE inhibitors), aldosterone receptor blockers, direct renin inhibitors, sympatholytics and drugs with concomitant sympatholytic effects (nebivolol, eprosartan); calcium channel blockers;
affecting the endothelium (ACE inhibitors, aldosterone receptor blockers, β-blockers, calcium channel blockers, statins).

Back in 1988, Marre M., and then Early M. (1993) and Bianchi S. (1994) tried to conduct a comparative analysis of the effectiveness of various antihypertensive drugs against MAU. They showed that the angiotensin-converting enzyme inhibitor (ACEI) enalapril was significantly more effective in reducing MAU levels than the calcium antagonist nicardipine, the β-blocker atenolol, or simply diuretics as monotherapy for arterial hypertension.

Large-scale clinical studies have found that ACE inhibitors have an advantage over other antihypertensive drugs in terms of their effect on the rate of development of nephropathy. According to double-blind comparative studies, ACE inhibitors had a greater effect on urinary protein excretion than other antihypertensive drugs, although their antihypertensive effect was the same [Moiseev V.S., 1996.], and therefore ACE inhibitors have a renoprotective effect in all patients , regardless of the antihypertensive effect.

The mechanism of the renoprotective effect of ACE inhibitors is different from the simple antihypertensive effect. The most important effect of ACE inhibitors today is considered to be the weakening of the effect of circulating angiotensin II on efferent arterioles. As the tone of the efferent arterioles decreases, the intraglomerular pressure decreases, hyperfiltration in the glomerulus weakens or disappears and, as a result, MAU and proteinuria decrease. It is important to note that the use of ACE inhibitors leads to a decrease in the synthesis of growth factors and endothelin in the interstitium, which slows down the development of nephrosclerosis. Ravid M. (1993) and Shulman N.B. (1989) showed that regular use of ACE inhibitors leads to a significant decrease in the pore diameter of the renal filter in patients with nephropathy of any origin.

The results of the CAPPP study (Captopril Prevention Project, 1998) showed that patients treated with ACE inhibitors had a significantly lower risk of developing cardiovascular complications and death than patients receiving combination therapy with a diuretic and a beta-blocker. The same study demonstrated that diabetes mellitus developed significantly more often in patients receiving a thiazide diuretic and (or) beta-blocker compared to patients treated with ACE inhibitors (by an average of 21% over 6 years of observation) [Sidorenko B.A. et al., 2000].

However, in the early stages of the development of nephropathy (both diabetic and non-diabetic) with normoalbuminuria, the advantage of ACE inhibitors in patients with hypertension has not been proven. Their effect is similar to that of other antihypertensive drugs. In all other cases, ACE inhibitors are first-line drugs when planning and conducting renoprotective therapy.

After achieving the target blood pressure in hypertension or in the case of normotension, sequential titration of the dose of ACE inhibitors or aldosterone receptor blockers to the maximum tolerated leads to a further reduction in microalbuminuria (and proteinuria) [Ivanov D.D., 2008].

Today it is becoming obvious that ACEIs with a predominantly renal route of elimination have a more pronounced (or in a shorter period of time) antihypertensive and antiproteinuric effect. Therefore, ACE inhibitors with extrarenal excretion (moexipril, monopril, quadropril) probably have advantages in the first stage of diabetic nephropathy, when the prerequisites for the appearance of MAU are just being formed. These drugs are also indispensable for reduced renal function (GFR less than 60-30 ml/min). On the contrary, perindopril and enalapril are obviously more active in stopping the progression of MAU. In the ADVANCE study (2007), the administration of noliprel forte for diabetes mellitus led to a significant reduction in the occurrence of new cases of MAU (-31%), regression of macroalbuminuria to MAU and normoalbuminuria (16%). In the ONTARGET study (2008), a direct comparison of ramipril with telmisartan showed a 12% reduction in new cases of diabetes in patients receiving ACE inhibitors.

A possible algorithm for using ACE inhibitors in diabetic kidney disease can be presented as follows (Table 7). Table 7. Algorithm for the use of ACE inhibitors for diabetic nephropathy

It is advisable to combine an ACE inhibitor with a thiazide-like diuretic (indapamide, xipamide). It is currently difficult to give preference to any of the groups of drugs (ACE inhibitors, aldosterone receptor blockers). Following published meta-analyses showing an increased incidence of ischemia with the use of aldosterone receptor blockers, their appeal over ACEIs has been questioned. An increase in the frequency of ischemic events by 9% with a more pronounced decrease in blood pressure was obtained both when prescribing aldosterone receptor blockers in comparison with ACE inhibitors, and when combining these groups of drugs, when undesirable effects, realized in a decrease in renal function, increase [ONTARGET study, 2008].

The results of numerous studies have proven the clear advantage of spirapril over other antihypertensive drugs in terms of organoprotective effects and significant improvement in the course of the disease in patients with renal dysfunction. In one of the studies [Yakusevich V.V. et al., 2000]. in the absence of changes in the levels of glucose and potassium in the blood. It was also found that spirapril in patients with arterial hypertension and concomitant diabetic nephropathy with chronic renal failure significantly reduces the fractional clearance of albumin (by an average of 25.5%) and a decrease in 24-hour MAU (by almost 29.6%).

The most important issue in practical medicine is determining the level of blood pressure below which the increase in proteinuria stops and the decrease in the level of MAU begins. According to the data presented in the Microalbuminuria Captoprili Study Group (1996), this level corresponds to 125/75 mmHg. At the same time, according to Barnas D. (1998), this is achieved when DBP is less than 90 mm Hg. In 1998, the results of the HOT (Hypertension Optimal Treatment) study were published, in which a safe blood pressure level was calculated as 138/83 mmHg. Thus, DBP is less than 90 mmHg. should be considered a goal in the treatment of patients with diabetes and hypertension.

However, as the severity of the initial condition of patients increases, the simple effect of lowering blood pressure and normalizing renal hemodynamics “slips away”. It has been established that when MAU levels are low, all drugs that normalize blood pressure and renal hemodynamics are effective. Apparently, at this stage, the degree of destruction of the renal filter is such that simple normalization of intraglomerular pressure is sufficient to level out protein loss. However, at higher levels of protein loss, success is achieved only with the use of both ACE and angiotensin II receptor blockers. The increasing nephroprotective effect of these drugs can also be observed after normalization of blood pressure.

CONCLUSION

It is a mistake to talk about UIA in a qualitative aspect – “detected” or “not detected”. The MAU level is of great importance: the higher it is, the more severe the patient’s initial condition. Therefore, gradation of MAU according to the level of severity is justified, since different tactics for choosing drug treatment are obvious for patients with different initial levels of MAU.

To diagnose chronic kidney disease in adult patients with cardiovascular disease or an increased risk of developing it, it is necessary to determine the glomerular filtration rate and the albumin/creatinine ratio in the urine (Table 8). For patients with established coronary artery disease, chronic heart failure, and risk factors (arterial hypertension, diabetes mellitus), mandatory assessment of both indicators is advisable. If a pathological value is detected in at least one of the indicators, it is necessary to repeat the study after 3 months. Chronic kidney disease is diagnosed when the pathological value of at least one of these indicators is confirmed.

Table 8. Recommendations and level of evidence for identifying renal dysfunction in adult patients with CVD or an increased risk of their development [Committee of Experts of the All-Russian Scientific Society of Cardiology and the Scientific Society of Nephrologists of Russia (2008)]

Note: MDRD formula for calculating glomerular filtration rate GFR (ml / min /) = 186 × (blood creatinine, mg / dl) - 1.154 × (age, years) - 0.203 for women the result is multiplied by 0.742, for people of the Negroid race the result is multiplied by 1.210

In the future, the doctor’s tactics are determined by the following algorithm:

Determine serum creatinine level and calculate glomerular filtration rate using the MDRD formula. If the estimated GFR
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Microalbumin in urine

A test for microalbumin in urine is prescribed by the attending physician to diagnose the urinary tract and for preventive monitoring of the patient’s health. If albumin in the urine is elevated, this may be an indicator of the onset of diabetic nephropathy and cardiovascular disease.
What it is?
Microalbumins are small-sized albumins, body proteins that dissolve in water. Normally, the kidneys excrete a certain amount of microalbumin, but they retain some due to their size (69 kDa). When the functioning of the renal glomeruli is disrupted, excess albumin is released into the urine. A urine test for microalbuminuria is prescribed if the initial stages of nephropathy and autoimmune diseases are suspected. In fact, referral for a microalbumin test is the only way to prematurely determine the primary stage of nephropathy. In rare cases, the presence of small amounts of microalbumin in the urine soon progresses to severe cases of proteinuria.

A study to determine the presence of the main blood plasma proteins - albumins - in the urine. Proteins of this particular group first begin to enter the urine in case of kidney disease. Their appearance in urine is one of the earliest laboratory indicators of nephropathy.

Synonyms Russian

Microalbumin in urine, microalbuminuria (MAU).

English synonyms

Research method

Immunoturbidimetry.

Units

mg/day (milligrams per day).

What biomaterial can be used for research?

Daily urine.

How to properly prepare for research?

Eliminate alcohol from your diet 24 hours before the test.
Avoid taking diuretics 48 hours before donating urine (in consultation with your doctor).

General information about the study

Albumins are water-soluble proteins. They are synthesized in the liver and make up the majority of serum proteins. In the body of a healthy person, only a small amount of the smallest albumin, microalbumin, is normally excreted in the urine, since the glomeruli of an unaffected kidney are impermeable to larger albumin molecules. During the initial stages of damage to the cell membranes of the renal glomerulus, more and more microalbumin are excreted in the urine; as the damage progresses, larger albumins begin to be released. This process is divided into stages according to the amount of excreted proteins (from 30 to 300 mg/day, or from 20 to 200 mg/ml in the morning urine, is considered to be microalbuminuria (MAU), and more than 300 mg/day is proteinuria). MAU always precedes proteinuria. However, as a rule, once proteinuria is detected in a patient, changes in the kidneys are already irreversible and treatment can only be aimed at stabilizing the process. At the MAU stage, changes in the renal glomeruli can still be stopped with the help of properly selected therapy. Thus, microalbuminuria is understood as the release of albumin in the urine in an amount that exceeds the physiological level of its excretion, but precedes proteinuria.

There are two periods in the development of nephropathy (both diabetic and those caused by hypertension, glomerulonephritis). The first is preclinical, during which it is almost impossible to detect any changes in the kidneys using traditional clinical and laboratory research methods. The second - clinically pronounced nephropathy - advanced nephropathy with proteinuria and chronic renal failure. During this period, renal dysfunction can already be diagnosed. It turns out that only by determining microalbumin in urine can the initial stage of nephropathy be detected. In some kidney diseases, MAU very quickly turns into protenuria, but this does not apply to dysmetabolic nephropathies (DN). MAU may precede the onset of DN for several years.

Since DN and the resulting chronic renal failure (CRF) occupy the first place in prevalence among kidney diseases (in Russia, Europe, USA), the determination of MAU in patients with diabetes mellitus (DM) type I and II is most significant.

Early detection of DN is extremely important as it has been shown to slow the progression of DN and renal failure. The only laboratory criterion that allows identifying the preclinical stage of DN with a high degree of reliability is MAU.

It is advisable to prescribe a urine microalbumin test for initial signs of nephropathy in pregnant women, but in the absence of proteinuria (for differential diagnosis).

What is the research used for?

For early diagnosis of diabetic nephropathy.
For the diagnosis of nephropathy in systemic diseases (secondary nephropathy) that occurs with prolonged hypertension, congestive heart failure.
For monitoring renal function in the treatment of various types of secondary nephropathy (primarily DN).
For the diagnosis of nephropathy during pregnancy.
To identify the early stages of nephropathy resulting from glomerulonephritis, inflammatory and cystic kidney diseases (primary nephropathy).
To identify renal dysfunction in autoimmune diseases such as systemic lupus erythematosus, amyloidosis.

When is the study scheduled?

For newly diagnosed type II diabetes mellitus (and then every 6 months).
For type I diabetes mellitus lasting more than 5 years (once every 6 months is mandatory).
For diabetes mellitus in children at an early age, with a labile course of diabetes mellitus (frequent decompensations: ketosis, diabetic ketoacidosis, hypoglycemia), after 1 year from the onset of the disease.
For long-term, especially uncompensated arterial hypertension, congestive heart failure, accompanied by specific edema.
During pregnancy with symptoms of nephropathy (if a general urine test showed the absence of proteinuria).
In the differential diagnosis of early stages of glomerulonephritis.
For systemic lupus erythematosus, amyloidosis for early diagnosis of specific kidney damage accompanying these diseases.

What do the results mean?

Reference values: 0 - 30 mg/day.

Reasons for increased microalbumin levels:

dysmetabolic nephropathy,
nephropathy caused by hypertension, heart failure,
reflux nephropathy,
radiation nephropathy,
early stage of glomerulonephritis,
pyelonephritis,
hypothermia,
renal vein thrombosis,
polycystic kidney disease,
nephropathy of pregnancy,
systemic lupus erythematosus (lupus nephritis),
kidney amyloidosis,
multiple myeloma.

Decreased microalbumin levels not diagnostically significant.

What can influence the result?

Albumin excretion in urine increases:

dehydration,
high protein diet,
diseases that occur with an increase in body temperature,
inflammatory diseases of the urinary tract (cystitis, urethritis).

Albumin excretion in urine is reduced by:

excess hydration,
low protein diet,
taking angiotensin-converting enzyme inhibitors (captopril, enalapril, etc.),
taking non-steroidal anti-inflammatory drugs.

Total protein in urine
Creatinine in daily urine
Urea in daily urine
Rehberg test (endogenous creatinine clearance)

Who orders the study?

Nephrologist, therapist, endocrinologist, urologist, general practitioner, gynecologist.

Literature

Keane W. F. Proteinuria, albuminuria, risk, assessment, detection, elimination (PARADE): a position paper of the National Kidney Foundation / W. F. Keane, G. Eknoyan // Amer. J. Kidney Dis. – 2000. – Vol. 33. – P. 1004-1010.
Mogensen C. E. Prevention of diabetic renal disease with special reference to microalbuminuria / C. E. Mogensen, W. F. Keane, P. H. Bennett // Lancet. – 2005. – Vol. 346. – R. 1080-1084.
Saudi J Kidney Dis Transpl. 2012 Mar;23(2):311-5. Ambulatory blood pressure monitoring in children and adolescents with type-1 diabetes mellitus and its relation to diabetic control and microalbuminuria. Basiratnia M, Abadi SF, Amirhakimi GH, Karamizadeh Z, Karamifar H.

This is a disease of the endocrine system in which the production of insulin or the sensitivity of body tissues to it is disrupted. The popular name for diabetes mellitus (DM) is “sweet disease”, since it is believed that sweets can lead to this pathology. In reality, obesity is a risk factor for developing diabetes. The disease itself is divided into two main types:

Type 1 diabetes (insulin dependent). This is a disease in which there is insufficient insulin synthesis. The pathology is typical for young people under 30 years of age.
Type 2 diabetes (non-insulin dependent). Caused by the development of resistance of body tissues to insulin, although its level in the blood remains normal. Insulin resistance is diagnosed in 85% of all cases of diabetes. It is caused by obesity, in which fat blocks tissue sensitivity to insulin. Older people are more susceptible to type 2 diabetes because glucose tolerance gradually decreases as people get older.

If microalbuminuria or proteinuria is detected repeatedly, you need to look for a pathological cause of this condition.

Since the onset of nephropathy is often gradual, without clinical manifestations, such an asymptomatic stage is rarely diagnosed. There are only minor changes in laboratory parameters, and the patient has no subjective complaints.

The only way seems to be to detect slightly elevated albumin in the urine. Therefore, laboratory tests of this kind are extremely important for diagnosing nephropathies at an early stage.

Classification of stages of nephropathy progression

In our country, the following classification of diabetic nephropathy has been adopted:

Diabetic nephropathy, stage of microalbuminuria.
Diabetic nephropathy, stage of proteinuria with preserved renal filtration function.
Diabetic nephropathy, stage of chronic renal failure.

Hyperfunction of the kidneys (hyperfiltration, hyperperfusion, renal hypertrophy, normoalbuminuria up to 30 mg/day).
Beginning DN (microalbuminuria 30-300 mg/day, normal or moderately increased glomerular filtration rate).
Severe DN (proteinuria, i.e. sugar is visible in a routine general urine test, arterial hypertension, decreased glomerular filtration rate, sclerosis of 50-75% of the glomeruli).
Uremia or renal failure (decrease in glomerular filtration rate less than 10 ml/min., total glomerulosclerosis).

Few people know that at the very initial stage of development the complication is still reversible, even at the stage of microalbuminuria you can turn back time, but if the stage of proteinuria is detected, then the process is irreversible. The only thing that can be done is to stop it at this stage so that the complication does not progress.

Can a child get diabetes?

Unfortunately, diabetes is also found in children. Most often this happens by accident during a urine or blood test to detect a disease.

Type 1 disease is congenital, but there is a risk of developing it in childhood or adolescence.

Insulin-dependent diabetes (type 2) can develop not only in adults, but also in children. If the sugar concentration is not at the critical level that defines diabetes, the further development of the disease can be influenced. In this case, the sugar level is stabilized through a special diet selected by the doctor.

Laboratory diagnostics: urine for MAU

eating foods high in protein;

race;

place of residence;

the presence of other pathological processes in the body.

Due to these circumstances, it is not always possible to obtain a 100% analysis result after the first examination of a biological fluid. Based on this, doctors recommend doing a series of studies over 3 months. The total number of procedures can reach 6 times.

In order for the urinary test for UIA to be as reliable as possible, before taking it, you need to exclude all possible factors that could distort the laboratory test.

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An effective way to cleanse your kidneys at home

According to statistics, 10-15% of all patients who have undergone this medical test receive a positive result.

People at risk are:

overweight;
suffering from insulin resistance;
having bad habits;
with dysfunction of the left ventricle of the heart;
aged people.

Unlike women, men are more prone to this pathology.

There are a number of symptoms or diseases on the basis of which a doctor may recommend a urine test for UIA. If there is a need for such a study, then you should not refuse the proposed diagnosis.

Indications for analysis may include:

initial diagnosis of type 2 diabetes mellitus;
type 1 diabetes mellitus, which has lasted for more than 5 years;
the child has diabetes;
heart failure accompanied by edema;
lupus erythematosus;
kidney pathology;
amyloidosis.

In addition to kidney dysfunction, increased levels of this protein in the urine may indicate other pathological processes in the body. Therefore, if the MAU indicator exceeds the norm for the entire group of tests performed, then additional types of examination of other systems and organs may be required, for example, in case of hypertension or heavy metal poisoning.

What will the analysis tell you?

The main goal is an accurate diagnosis. If you suspect diabetes, you should contact a therapist or endocrinologist - a specialist and prescribe the necessary instrumental or laboratory tests. The list of diagnostic tasks also includes the following:

correct selection of insulin dosage;
monitoring the dynamics of prescribed treatment, including diet and compliance;
determination of changes at the stage of compensation and decompensation of diabetes mellitus;
self-monitoring of sugar levels;
monitoring the functional state of the kidneys and pancreas;
control of treatment during pregnancy for gestational diabetes;
identifying existing complications and the degree of deterioration of the patient’s condition.

Basic tests to determine diabetes involve donating blood and urine to patients. These are the main biological fluids of the human body, in which various changes are observed during diabetes - tests are performed to identify them. Blood is taken to determine glucose levels. The following tests help with this:

general;
biochemical;
glycated hemoglobin test;
C-peptide test;
serum ferritin test;
glucose tolerance test.

In addition to blood tests, the patient is also prescribed urine tests. With it, all toxic compounds, cellular elements, salts and complex organic structures are removed from the body. By studying urine parameters, changes in the condition of internal organs can be identified. The main urine tests for suspected diabetes are:

general clinical;
daily;
determination of the presence of ketone bodies;
determination of microalbumin.

There are also specific tests to detect diabetes - they are carried out in addition to donating blood and urine. Such studies are carried out when the doctor has doubts about the diagnosis or wants to study the disease in more detail. These include the following:

For the presence of antibodies to beta cells. Normally, they should not be present in the patient's blood. If antibodies to beta cells are detected, diabetes or a predisposition to it is confirmed.
Antibodies to insulin. They are autoantibodies that the body produces against its own glucose and specific markers of insulin-dependent diabetes.
On insulin concentration. For a healthy person, the norm is a glucose level of 15–180 mmol/l. Values below the lower limit indicate type 1 diabetes, above the upper limit indicate type 2 diabetes.
To determine antibodies to GAD (glutamate decarboxylase). This is an enzyme that is an inhibitory transmitter of the nervous system. It is present in its cells and the beta cells of the pancreas. Testing for type 1 diabetes requires the determination of antibodies to GAD, since most patients with this disease have them. Their presence reflects the process of destruction of pancreatic beta cells. Anti-GAD are specific markers that confirm the autoimmune origin of type 1 diabetes.

Blood tests

Initially, a general blood test is performed for diabetes mellitus, for which it is taken from a finger. The study reflects the level of quality indicators of this biological fluid and the amount of glucose.

In addition to general and biochemical studies, blood is taken for some other tests. They are more often taken in the morning and on an empty stomach, since this way the diagnostic accuracy will be higher.

Microalbuminuria is a serious disorder that poses a fatal threat to humans in the later stages of progression. Such a disorder can only be determined by laboratory testing of urine for albumin. This substance is present in human blood, so its appearance in biological fluid does not bode well.

What is microalbuminuria, how can it be dangerous for the patient’s health, and how to collect urine to test for the presence of albumin? Let's take it in order.

This procedure is appropriate in the following cases:

if there are symptoms indicating diabetes;
if necessary, control the course of the disease;
to determine the effectiveness of the treatment complex;
to assess kidney function.

Two days before the proposed test, you should avoid taking medications that have a diuretic effect. It is recommended to discuss the discontinuation of diuretics with your doctor. The consumption of alcoholic beverages should be avoided the day before the test. The half hour preceding the test should be spent in peace, excluding physical activity.

A glucose test involves submitting a single sample of urine. You can conduct your own research using special disposable test strips.

With their help, you can determine how urine parameters change. Indicator strips help identify the presence of metabolic failures, as well as learn about existing kidney pathology.

This analysis takes no more than 5 minutes and does not require special skills. The result is determined visually.

It is enough to compare the color of the indicator part of the strip with the scale applied to the packaging.

The test allows you to determine the presence of sugar in the urine. Its presence indicates hyperglycemia in the body (high concentration of glucose in the blood) - a symptom of diabetes mellitus.

In the urine of a healthy person, the glucose content is insignificant and is approximately 0.06 - 0.083 mmol/l. When conducting an independent analysis using an indicator strip, it is necessary to take into account that coloring occurs if the amount of sugar is at least 0.1 mmol/l.

The absence of staining indicates that the concentration of glucose in the urine is insignificant.

Renal diabetes is a disease characterized by an imbalance in the transport of glucose through the renal tubules. Urinalysis reveals the presence of glycosuria, which is the main symptom accompanying the course of the disease.

Treatment of diabetic nephropathy

These two postulates for the prevention and treatment of DN are recommended at any stage of the disease. Further, depending on the stage, new points will be added to the recommendations.

So, for persistent microproteinuria, long-term use of ACE inhibitors (enalapril, perindopril and other drugs) is recommended. ACE inhibitors are antihypertensive drugs, but in small doses they do not have the effect of lowering blood pressure, but they retain a pronounced angioprotective effect.

Drugs from this group have a positive effect on the inner wall of blood vessels, including kidney vessels, and therefore, thanks to them, pathological processes in the vascular wall reverse.

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