Proteinuria types of laboratory assessment methods. Proteinuria. What is daily proteinuria

Proteinuria is the excretion of protein in the urine in quantities exceeding normal values. This is the most common sign of kidney damage. Normally, no more than 50 mg of protein, consisting of filtered plasma low-molecular proteins, is excreted into the urine per day.

Defeat renal tubules(interstitial nephritis, tubulopathies) leads to impaired reabsorption of filtered protein and its appearance in the urine.
Hemodynamic factors - the speed and volume of capillary blood flow, the balance of hydrostatic and oncotic pressure are also important for the appearance of proteinuria. The permeability of the capillary wall increases, contributing to proteinuria, both with a decrease in the speed of blood flow in the capillaries, and with glomerular hyperperfusion and intraglomerular hypertension. The possible role of hemodynamic changes should be taken into account when assessing proteinuria, especially transient proteinuria, and in patients with circulatory failure.

Symptoms and diagnosis of proteinuria

Types of proteinuria
in connection with diseases	by source	by composition	by size or severity
1. Functional. 2. Pathological.	1. Prerenal (“overflow”). 2. Renal: glomerular and tubular. 3. Postrenal.	1. Selective. 2. Non-selective.	1. Microalbuminuria. 2. Low. 3. Moderate. 4. High (nephrotic).

In connection with diseases Proteinuria is divided into functional and pathological.

Functional proteinuria observed in patients with healthy kidneys. Functional proteinuria is low (up to 1 g/day), usually transient, isolated (there are no other signs of kidney damage), rarely combined with erythrocyturia, leukocyturia, cylindruria. There are several types of functional proteinuria:

Orthostatic. Occurs in young people 13-20 years old, does not exceed 1 g/day, disappears in the supine position. This type proteinuria is diagnosed using an orthostatic test - the patient collects the first morning portion of urine without getting out of bed, then performs a small physical activity (walking up the stairs), after which the second portion of urine is collected for analysis. The absence of protein in the first portion and the presence of urine in the second portion indicate orthostatic proteinuria.
Feverish (up to 1-2 g/day). It is observed during febrile conditions, more often in children and the elderly, disappears when body temperature normalizes, it is based on an increase glomerular filtration.
Tension proteinuria (marching). It occurs after severe physical stress, is detected in the first portion of urine, and disappears with normal physical activity. It is based on the redistribution of blood flow with relative ischemia of the proximal tubules.
Proteinuria in obesity. Associated with the development of intraglomerular hypertension and hyperfiltration against the background increased concentration renin and angiotensin. For weight loss and treatment ACE inhibitors may decrease and even disappear.
Physiological proteinuria. Pregnancy can lead to its appearance, since it is accompanied by an increase in glomerular filtration without an increase in tubular reabsorption. The level should not exceed 0.3 g/day.
Idiopathic transient. Detected in healthy individuals when medical examination and is absent on subsequent urine tests.

Pathological proteinuria detected in kidney diseases, urinary tract, as well as when exposed to extrarenal factors.

By source Proteinuria can be prerenal, renal and postrenal.

Prerenal, or proteinuria "overflow", observed in multiple myeloma (Bence Jones proteinuria), rhabdomyolysis, Waldenström macroglobulinemia, massive intravascular hemolysis. Overflow proteinuria can range from 0.1 to 20 g/day. High proteinuria (more than 3.5 g/day) in this case is not a sign of nephrotic syndrome, since it is not accompanied by hypoalbuminemia and its other signs. To identify myeloma nephropathy, the patient needs to have his urine tested for Bence-Jones protein.

Renal proteinuria According to the mechanism of occurrence, it can be glomerular and tubular.

Glomerular proteinuria is observed in most kidney diseases - glomerulonephritis (primary and with systemic diseases), renal amyloidosis, diabetic glomerulosclerosis, as well as hypertension, “stagnant” kidney.

Tubular proteinuria is observed with interstitial nephritis, pyelonephritis, congenital tubulopathies (Fanconi syndrome) and other kidney diseases with predominant defeat tubules.

Glomerular and tubular proteinuria are differentiated by the presence of α1-microglobulin and a quantitative comparison of the levels of albumin and β2-microglobulin in the urine, which normally range from 50:1 to 200:1. An albumin to β2-microglobulin ratio of 10:1 and α1-microglobulin indicate tubular proteinuria. With glomerular proteinuria, this ratio will exceed 1000:1.

Postrenal proteinuria has extrarenal origin, develops in the presence of bacterial inflammatory process in the urinary system (pyelonephritis) due to increased exudation of plasma proteins into the urine.

By composition There are selective and non-selective proteinuria.

Selective proteinuria characterized by the release of protein with low molecular weight, mainly albumin. Prognostically, it is considered more favorable than non-selective.

At non-selective proteinuria protein is released with medium and high molecular weight (α2-macroglobulins, β-lipoproteins, γ-globulins). A wide protein spectrum of non-selective proteinuria indicates severe kidney damage and is characteristic of postrenal proteinuria.

By severity (magnitude) They distinguish microalbuminuria, low, moderate, high (nephrotic) proteinuria.

Microalbuminuria- excretion in urine of minimal albumin, only slightly exceeding the physiological norm (from 30 to 300-500 mg/day). Microalbuminuria is the first early symptom diabetic nephropathy, kidney damage due to arterial hypertension, kidney transplant rejection. Therefore, categories of patients with such indicators should be prescribed a 24-hour urine test for microalbuminuria in the absence of changes in general analysis urine.

Low(up to 1 g/day) and moderate(from 1 to 3 g/day) are observed when various diseases kidneys and urinary tract (glomerulonephritis, pyelonephritis, nephrolithiasis, kidney tumors, tuberculosis, etc.). The amount of proteinuria depends on the degree of kidney damage and the severity of the inflammatory process in the urinary tract.

At high (nephrotic) proteinuria protein loss is more than 3.5 g/day. The presence of high proteinuria combined with hypoalbuminemia is a sign of nephrotic syndrome.

It should be remembered that the protein concentration in single portions of urine varies throughout the day. For a more accurate idea of the severity of proteinuria, daily urine is examined (daily proteinuria).

Normal in urine healthy people protein present in minimal quantities - in the form of traces (no more than 0.033 g/l), which cannot be detected using qualitative methods. Higher levels of protein in the urine are classified as proteinuria.

Proteinuria is the appearance of protein in the urine in quantities at which qualitative reactions to protein become positive.

Depending on the protein content in the urine, there are:

mild proteinuria - up to 1 g/l;
moderate proteinuria - 2-4 g/l;
significant proteinuria - more than 4 g/l.

Proteinuria occurs when protein filters from the blood into the kidneys or protein attaches to urine in the urinary tract. Depending on the reason there are the following types proteinuria:

Renal (renal):

functional;
organic.

Extrarenal (extrarenal).

Renal (renal) proteinuria occurs as a result of increased permeability of the renal filter due to damage (organic) and without damage (functional) to the kidneys.

Functional proteinuria occurs due to an increase in the permeability of the renal filter in response to strong external irritation or a slowdown in the passage of blood in the glomeruli.

Among them are:

Physiological proteinuria in newborns happens quite often in the first 4-10 days after birth and is caused by the presence of a functionally fragile renal filter in the newborn, as well as, probably, by birth trauma;
Alimentary proteinuria - occurs after eating protein foods (egg whites);
Orthostatic proteinuria - more often observed in adolescents, emaciated people, asthenics with lordosis of the lower thoracic spine. Protein in the urine can appear in significant quantities during prolonged standing, severe curvature of the spine (lordosis), and also in the case of sudden change body position from lying to standing;
Feverish proteinuria - occurs when elevated temperature body up to 39-40 °C at infectious diseases. The causative agent of the infection and the increased temperature irritate the kidney filter, leading to an increase in its permeability;
Proteinuria caused by nervous (emotional) and physical (marching) overloads of the body;
Proteinuria in pregnant women;
Congestive proteinuria - observed in patients with cardiac vascular diseases, with ascites, abdominal tumors (up to 10 g/l). When blood movement slows down in the vascular glomeruli of the nephron, glomerular hypoxia develops, which leads to an increase in the permeability of the renal filter. Prolonged stagnation of blood can cause organic kidney damage and lead to organic proteinuria.

So, the cause of functional renal proteinuria is an increase in the permeability of the renal filter (in particular the wall of the glomerular vessels); damage to the renal filter does not occur. Therefore, functional proteinuria is usually: mild (up to 1 g/l); are represented by low molecular weight proteins (albumin), short-term (disappear after the end of the stimulus on the renal filter).

Organic proteinuria occurs due to increased permeability of the renal filter as a result of damage to the renal parenchyma. This type of renal proteinuria is observed in acute and chronic nephritis, nephrosis, nephrosclerosis, infectious and toxic kidney damage, as well as in persons with congenital anatomical abnormalities of the kidneys, for example, in the case of polycystic disease, when anatomical changes cause significant organic damage kidney tissue.

The severity of proteinuria does not always indicate the severity of damage to the renal parenchyma. Sometimes acute glomerulonephritis with high proteinuria can quickly end in recovery, and chronic glomerulonephritis with low protein content in the urine can last a long time and even cause death. Reduction of proteinuria in case of acute glomerulonephritis basically is good sign, and when chronic forms such a decrease is very often accompanied by a deterioration in the patient’s condition, as it may be due to functional failure of the kidneys with a decrease in their filtration capacity due to the death of a large number of renal glomeruli. Moderate proteinuria is recorded in acute and chronic glomerulonephritis, systemic lupus erythematosus, and renal amyloidosis. Significant proteinuria is characteristic of nephrotic syndrome.

Acute and chronic glomerulonephritis. Proteinuria occurs as a result of damage to the renal filter. In glomerulonephritis, antibodies attack the renal filter, which leads to an increase in its filtration capacity, but since tubular reabsorption is not impaired, most of filtered protein is reabsorbed into the blood as urine passes through the tubular system. Thus, with glomerulonephritis, proteinuria is a constant phenomenon, its level is moderate (up to 5 g/l).

Nephrotic syndrome. Proteinuria occurs due to impaired tubular reabsorption of filtered protein as a result of damage to the renal tubules. Therefore, in nephrotic syndrome, proteinuria is a constant phenomenon, the level of proteinuria is significant (10-30 g/l). It is represented by albumins and globulins.

So, the pathogenesis of organic renal proteinuria is based on an increase in the permeability of the renal filter due to organic damage kidney parenchyma. Therefore, organic proteinuria is usually moderate or pronounced; long-term; combine with others pathological changes in the urine (hematuria, cylindruria, disfoliation of the renal tubular epithelium).

Extrarenal (extrarenal) proteinuria is caused by protein impurities (inflammatory exudate, destroyed cells), which is released through the urinary tract and genitals. Occurs in cystitis, urethritis, prostatitis, vulvovaginitis, urolithiasis and tumors urinary tract. The amount of protein in extrarenal proteinuria is insignificant (up to 1 g/l).

Extrarenal proteinuria is usually combined with other pathological changes in the urine (leukocyturia or pyuria and bacteriuria).

Differentiation various types proteinuria is produced by microscopy of urinary sediments and quantification shaped elements urinary sediment according to Nechiporenko. Thus, renal organic proteinuria is determined by the presence of renal epithelium, erythrocytes and different types cylinders And extrarenal proteinuria is combined with the presence of a large number of leukocytes and bacteria in the urine.

Caused by the breakdown of cellular elements during prolonged standing of urine; in this situation, proteinuria exceeding 0.3 g/day is considered pathological.

Sedimentary protein samples give false positives if there are iodine-containing substances in the urine contrast agents, a large number of antibiotics (penicillins or cephalosporins), metabolites of sulfonamides.

IN early stages During the development of most nephropathies, predominantly low molecular weight plasma proteins (albumin, ceruloplasmin, transferrin, etc.) penetrate into the urine. However, it is also possible to detect high-molecular proteins (alpha2-macroglobulin, γ-globulin), which are more typical for severe kidney damage with “large” proteinuria.

Selective proteinuria includes proteins with a low molecular weight of no more than 65,000 kDa, mainly albumin. Nonselective proteinuria is characterized by increased clearance of medium- and high-molecular-weight proteins: the composition of urine proteins is dominated by α2-macroglobulin, beta-lipoproteins, and γ-globulin. In addition to plasma proteins, proteins of renal origin are determined in the urine - Tamm-Horsfall uroprotein, secreted by the convoluted tubule epithelium.

Glomerular (glomerular) proteinuria is caused by increased filtration of plasma proteins through the glomerular capillaries. It depends on the structural and functional state the walls of glomerular capillaries, the properties of protein molecules, pressure and blood flow velocity, which determine GFR. Glomerular proteinuria is a mandatory feature of most kidney diseases.

The wall of the glomerular capillaries consists of endothelial cells (with rounded holes between them), a three-layer basement membrane - a hydrated gel, as well as epithelial cells (podocytes) with a plexus of pedunculate processes. Thanks to complex structure The glomerular capillary wall can “sift” plasma molecules from the capillaries into the space of the glomerular capsule, and this “molecular sieve” function is largely dependent on the pressure and speed of blood flow in the capillaries.

Under pathological conditions, the size of the “pores” increases, deposits of immune complexes cause local changes in the capillary wall, increasing its permeability to macromolecules. In addition to the size of the glomerular “pores,” electrostatic factors are also important. The glomerular basement membrane is negatively charged; The foot processes of podocytes also carry a negative charge. IN normal conditions the negative charge of the glomerular filter repels anions - negatively charged molecules (including albumin molecules). The change in charge promotes the filtration of albumin. It is assumed that the fusion of the stalked processes is the morphological equivalent of a change in charge.

Tubular proteinuria is caused by the inability of the proximal tubules to reabsorb plasma low molecular weight proteins filtered in normal glomeruli. Proteinuria rarely exceeds 2 g/day, excreted proteins are represented by albumin, as well as fractions with even lower molecular weight (lysozyme, beta 2-microglobulin, ribonuclease, free light chains of immunoglobulins), which are absent in healthy individuals and in glomerular proteinuria due to 100 % reabsorption by convoluted tubule epithelium. Characteristic sign tubular proteinuria - the predominance of beta 2-microglobulin over albumin, as well as the absence of high molecular weight proteins. Tubular proteinuria is observed with damage to the renal tubules and interstitium: with tubulointerstitial nephritis, pyelonephritis, kalipenic kidney, acute tubular necrosis, chronic kidney transplant rejection. Tubular proteinuria is also characteristic of many congenital and acquired tubulopathies, in particular Fanconi syndrome.

Proteinuria “overflow” develops with an increase in the concentration of low molecular weight proteins (immunoglobulin light chains, hemoglobin, myoglobin) in the blood plasma. In this case, these proteins are filtered by unchanged glomeruli in quantities exceeding the reabsorption capacity of the tubules. This is the mechanism of proteinuria in multiple myeloma (Bence Jones proteinuria) and other plasma cell dyscrasias, as well as myoglobinuria.

The so-called functional proteinuria is distinguished. Development mechanisms and clinical significance most of its variants are unknown.

Orthostatic proteinuria occurs with prolonged standing or walking (“proteinuria en marche”) with rapid disappearance in a horizontal position. In this case, the amount of protein excretion in urine does not exceed 1 g/day. Orthostatic proteinuria is glomerular and nonselective and, according to long-term prospective studies, is always benign. When its nature is isolated, there are no other signs of kidney damage (changes in urinary sediment, increased blood pressure). More often observed in adolescence(13-20 years), in half of people it disappears after 5-10 years from the moment of occurrence. Characteristic is the absence of protein in urine tests taken immediately after the patient is in a horizontal position (including in the morning before getting out of bed).
Proteinuria of tension, found after intense physical activity in at least 20% of healthy individuals, including athletes, is also apparently benign. According to the mechanism of its occurrence, it is considered tubular, caused by the redistribution of intrarenal blood flow and relative ischemia of the proximal tubules.
For fever with a body temperature of 39-41 ° C, especially in children and the elderly and old age, detect so-called febrile proteinuria. It is glomerular, the mechanisms of its development are unknown. The occurrence of proteinuria in a patient with fever sometimes indicates the addition of kidney damage; This is supported by simultaneous changes in urinary sediment (leukocyturia, hematuria), large, especially nephrotic levels of protein excretion in the urine, as well as arterial hypertension.

Proteinuria exceeding 3 g/day - key feature nephrotic syndrome.

Proteinuria and progression of chronic nephropathies

The significance of proteinuria as a marker of the progression of kidney damage is largely due to the mechanisms of the toxic effect of individual components of the protein ultrafiltrate on the epithelial cells of the proximal tubules and other structures of the renal tubulointerstitium.

Components of protein ultrafiltrate that have a nephrotoxic effect

Protein	Mechanism of action
Albumen	Increased expression of pro-inflammatory chemokines (monocyte chemoattractant protein type 1, RANTES*) Toxic effect on epithelial cells of the proximal tubules (overload and rupture of lysosomes with the release of cytotoxic enzymes) Induction of the synthesis of vasoconstriction molecules, aggravating hypoxia of tubulointerstitial structures Activation of apoptosis of epithelial cells of proximal tubules
Transferrin	Induction of synthesis of complement components by epithelial cells of proximal tubules Increased expression of pro-inflammatory chemokines Formation of reactive oxygen radicals
Complement components	Formation of cytotoxic MAC** (C5b-C9)

* RANTES (Regulated upon activation, normal T-lymphocyte expressed and secreted) - activated substance expressed and secreted by normal T-lymphocytes.
** MAK - membrane attack complex.

Many mesangiocytes and vascular smooth muscle cells undergo similar changes, meaning they acquire the basic properties of a macrophage. Monocytes from the blood actively migrate into the renal tubulointerstitium and also transform into macrophages. Plasma proteins induce processes of tubulointerstitial inflammation and fibrosis called proteinuric tubulointerstitial remodeling.

IN healthy condition a small amount of protein is released into the primary urine. After this, it undergoes reabsorption, which occurs in the renal tubules. A normal protein level is below 0.033 g/l, that is, an excretion of 30 to 60 mg per day.

If 60 to 300 mg of protein molecules are released per day, then they speak of microalbuminuria. Albumin easily passes into urine due to its small molecular size. A loss of 300 mg to 1 g of protein per day is considered minimal proteinuria.. Moderate proteinuria is recorded when the excretion ranges from 1 g to 3.5 g of protein per day. Massive proteinuria occurs with a loss of more than 3.5 g of protein per day. It provokes the development of nephrotic syndrome.

Classification

There are pathological and physiological proteinuria. Physiological proteinuria is classified according to the etiological factor:

proteinuria due to hypothermia;
nutritional - due to eating foods rich in proteins;
central origin - after concussions and seizures;
emotional;
labor, which occurs during intense physical activity;
orthostatic - when standing in an upright position for a long time;
febrile.

Pathological proteinuria is sign of defeat excretory system . There are renal (renal) and non-renal proteinuria. Non-renal pathology is also divided into prerenal and postrenal. Prerenal pathology is provoked systemic reasons, postrenal manifests itself as damage to the urinary tract.

Causes

Proteinuria is provoked by a combination of physiological and pathological causes.

Physiological etiological factors include:

exceeding permissible physical activity;
eating foods with high content squirrel;
impaired blood flow caused by prolonged stay in an upright position;
bearing a child;
exceeding the permissible time spent in the sun;
hypothermia;
psycho-emotional stress.

Pathological causes of proteinuria include:

stagnation in the organs of the excretory system;
increased blood pressure;
nephropathy;
inflammatory diseases of the excretory system;
hereditary disorders;
tubular necrosis;
kidney transplantation;
hemolysis;
oncological pathologies - myeloma;
myopathies;
kidney;

The variety of etiological factors determines the nonspecific nature of the symptom of proteinuria. The excretion of protein in the urine does not always indicate a pathology of the urinary system. It may be caused by extrarenal causes and signal systemic problems.

Symptoms

The clinical manifestations of proteinuria depend on protein, which is excreted in the urine in greater quantities than required.

Albumin. Its deficiency provokes a decrease in oncotic pressure. The clinic is characterized by swelling, hypovolemia, hypotension, hyperlipidemia.

Antitrobin III. When this protein is deficient, thrombin inactivation is impaired, resulting in hypercoagulation and thrombotic conditions.

Complement system proteins. Their deficiency causes opsonization pathology, which impairs resistance to infection.

Lipoproteins high density . Due to their deficiency, cholesterol transport is disrupted, which provokes accelerated atherogenesis.

Immunoglobulins. Increasing their elimination reduces the body's resistance to various types of infections.

Metalloproteins(transferrin, ceruloplasmin). Iron, zinc and copper ions are excreted in the urine. This can provoke anemic conditions, dysgeusia, and impaired wound healing.

Orosomucoid. The lack of this protein contributes to damage to the lipoprotein lipase enzyme. Because of this, hypertriglyceridemia develops.

Procoagulants. Their deficiency increases the tendency to bleeding.

Thyroxine binding protein. Under conditions of its deficiency, the concentration of thyroxine increases, which causes functional.

Transcortin. Due to its removal, the concentration of free cortisol increases. This increases the likelihood of developing exogenous Cushing's syndrome.

Vitamin D binding protein. Its deficiency provokes hypocalcemia, osteitis, osteomalacia and muscle weakness.

Loss of protein in the urine causes swelling and increases the body's susceptibility to infections. Muscle tone decreases and weakness appears.

Diagnostics

Determining protein in urine is the only way to diagnose the condition. There are several approved methods and a large number of test systems that are capable of high accuracy detect the level of protein in the urine.

It should be noted that proteinuria is often accompanied by cylindruria.

The cylinders are formed on the basis of aggregated serum proteins and Tamm-Horsfall protein. Most often, the casts are characterized by renal origin.

Also, the appearance of protein in the urine is combined with bacteriuria, leukocyturia and hematuria. In isolated form, proteinuria occurs rarely in a number of diseases, such as nephroptosis and.

The doctor prescribes a test to detect protein in the urine for the following pathologies:

of various etiologies;
sclerosis of the renal glomeruli;
nephrosis;
other primary glomerulopathies;
connective tissue pathologies;
diabetes;
anemia;
oncological pathologies.

Test for detecting protein in urine allows you to evaluate its level in both morning and daily urine. The measurement is carried out using the colorimetric method. Before collecting urine, you should avoid alcohol and diuretics to avoid false results. A single detection of protein does not prove proteinuria; several sequential diagnostic procedures are necessary.

Treatment

Therapy should be comprehensive, but its main direction is elimination etiological factor . Measures should also be taken symptomatic treatment. A correct diagnosis will allow you to get rid of proteinuria with high efficiency.

With moderate and severe proteinuria, nephrotic syndromes of various etiologies are detected. In this case, it is necessary to hospitalize the patient, provide him bed rest, limit salt and liquid intake.

Drug therapy may include:

corticosteroids;
immunosuppressants;
cytostatic drugs;
anti-inflammatory drugs;
antihypertensive drugs;
ACE inhibitors.

Also, in some cases, plasmapheresis and hemosorption are required. Only a highly qualified specialist can choose the right treatment regimen.

Prevention

Includes normalization of circadian rhythms, correct mode food, refusal bad habits . You should limit your intake of liquid and salt. It is also necessary to promptly treat diseases that provoke the development of proteinuria.

Forecast

The prognosis for treatment of proteinuria is usually favorable subject to the obligatory condition of strict and responsible compliance with all therapeutic measures.

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IN Lately In the domestic literature, the question is often discussed: what is considered proteinuria? If earlier proteinuria was simply called the detection of protein in urine using conventional qualitative or quantitative methods, the sensitivity and specificity of which were not very high, now, given the increasing introduction into practice of more sensitive and specific methods, proteinuria is said to be when the level of protein in the urine exceeds the norm . The concept of normal protein in urine also varies - which is due to the use of both old and new methods for determining protein in urine, which differ in sensitivity and specificity. Some authors, taking into account the presence of protein in the urine of a healthy person, understand the term proteinuria as generally the excretion of protein in the urine and, for simplicity, divide proteinuria into physiological and pathological, which is now also being debated. Usually under the term proteinuria refers to an increase in protein content in the urine.

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 (or 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, it is necessary to indicate in the analysis form normal value protein for the method the laboratory uses.

When determining the minimum amounts of protein, it is recommended to repeat the analysis; in doubtful cases, the daily loss of protein in urine should be determined. Normally, daily urine contains protein in small quantities. Under physiological conditions, the filtered protein is almost completely reabsorbed by the epithelium of the proximal tubules and its content in the daily amount of urine varies, according to different authors, from traces to 20 - 50, 80 - 100 mg and even up to 150 - 200 mg. Some authors believe that daily protein excretion in the amount of 30–50 mg/day is physiological norm for an adult. Others believe that urinary protein excretion should not exceed 60 mg/m2 of body surface per day, excluding the first month of life, when the amount of physiological proteinuria can be four times higher than the indicated values.

The general condition for the appearance of proteins in the urine of a healthy person is their sufficiently high concentration in the blood and a molecular weight of no more than 100 - 200 kDa.

In practically healthy people under the influence various factors may appear transient proteinuria. This proteinuria is also called physiological, functional or benign, since it, unlike pathological, does not require treatment.

Physiological proteinuria

March proteinuria

Transient protein excretion in the urine in healthy people may appear after severe physical activity(long hikes, marathon running, team sports). This is the so-called working (marching) proteinuria or tension proteinuria, observed and described by many researchers. The works of these authors, illustrating the possibility of the development of proteinuria under the influence of physical activity, indicate high degree its severity, as well as its reversibility. 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.

Albuminuria solaris

Known albuminuria solaris, which occurs when there is a pronounced reaction of the skin to insolation, as well as when the skin is irritated by certain substances, for example, when it is lubricated with iodine.

Proteinuria with increased levels of adrenaline and norepinephrine in the blood

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.

Nutritional proteinuria

Highlight nutritional proteinuria, sometimes appearing after eating a large protein meal.

Centrogenic proteinuria

The possibility of occurrence has been proven centrogenic proteinuria– for epilepsy, concussion.

Emotional proteinuria

Described emotional proteinuria during exams.

Palpable proteinuria

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).

Feverish proteinuria

Feverish proteinuria observed in acute febrile conditions, more often in children and the elderly. Its mechanism is poorly understood. This type of 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 returned to normal, then possible organic kidney disease, either new or existing, should be excluded.

Congestive (cardiac) proteinuria

In heart disease, it is often detected stagnant, or cardiac proteinuria. As the heart failure resolves, it usually goes away.

Proteinuria of newborns

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

Orthostatic (postural, lordotic) proteinuria

Orthostatic (postural, lordotic) proteinuria observed in 12–40% of children and adolescents, characterized by the detection of protein in the urine during prolonged standing or walking with rapid disappearance (transient variant of orthostatic proteinuria) or its decrease (persistent variant) 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.

Physiological proteinuria is usually insignificant - no more than 1.0 g/day.

Modern methods studies reveal a number of changes in the microstructure of the kidneys, the consequence of which is the so-called physiological proteinuria. Based on such considerations, many authors doubt the validity of identifying “functional” proteinuria.

Pathological proteinuria

Pathological proteinuria can be of renal or extrarenal origin.

Renal proteinuria

Renal proteinuria is one of the most important and permanent signs kidney disease and maybe glomerular, or glomerular, And tubular, or canalicular. When these two types are combined, it develops mixed type proteinuria.

Glomerular proteinuria

Glomerular proteinuria caused by damage to the glomerular filter, occurs with glomerulonephritis and nephropathies associated with metabolic or vascular diseases. At the same time, from blood to urine large quantities plasma proteins are filtered.

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.

Glomerular proteinuria is observed in acute and chronic glomerulonephritis, amyloidosis, diabetic glomerulosclerosis, renal vein thrombosis, congestive kidney, hypertension, nephrosclerosis.

Glomerular proteinuria can be selective or non-selective depending on the severity of damage to the glomerular filter.

Selective proteinuria

Selective proteinuria occurs with minimal (often reversible) damage to the glomerular filter ( nephrotic syndrome with minimal changes), is represented by proteins with a molecular weight of no higher than 68,000 - albumin and transferrin.

Non-selective proteinuria

Non-selective proteinuria more common with more severe damage to the filter, characterized by increased clearance of medium- and high-molecular plasma proteins (urine proteins also contain alpha2-globulins and gamma globulins). Nonselective proteinuria is observed in nephrotic and mixed forms glomerulonephritis, secondary glomerulonephritis.

Tubular proteinuria (tubular proteinuria)

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.

Tubular proteinuria is observed in acute and chronic pyelonephritis, heavy metal poisoning, acute tubular necrosis, interstitial nephritis, chronic kidney transplant rejection, kalipenic nephropathy, genetic tubulopathies.

Extrarenal proteinuria

Extrarenal proteinuria occurs in the absence pathological process in the kidneys themselves and is divided into prerenal and postrenal.

Prerenal proteinuria

Prerenal proteinuria develops in the presence of an unusually high plasma concentration of a low molecular weight protein, which is filtered by normal glomeruli in an amount 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

Postrenal proteinuria 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.

Proteinuria severity

Depending on the severity, mild, moderate and severe proteinuria are distinguished.

Mild proteinuria

Mild proteinuria(from 300 mg to 1 g/day) can be observed with acute infection urinary tract, obstructive uropathy and vesicoureteral reflux, tubulopathies, urolithiasis, chronic interstitial nephritis, kidney tumors, polycystic disease.

Moderate proteinuria

Moderate proteinuria(from 1 to 3 g/day) is observed in acute tubular necrosis, hepatorenal syndrome, primary and secondary glomerulonephritis (without nephrotic syndrome), proteinuric stage of amyloidosis.

Severe (pronounced) proteinuria

Under severe, or severe proteinuria define a loss of protein in the urine that exceeds 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.

Identification and quantification proteinuria is important both for diagnosis and for assessing the course of the pathological process and the effectiveness of treatment. In conclusion, it should be noted that the diagnostic significance of proteinuria is assessed in conjunction with other changes in the urine.

Literature:

L. V. Kozlovskaya, A. Yu. Nikolaev. Tutorial according to clinical laboratory methods research. Moscow, Medicine, 1985
A. V. Papayan, N. D. Savenkova "Clinical nephrology childhood", St. Petersburg, SOTIS, 1997
Kurilyak O.A. "Protein in urine - methods of determination and normal limits ( current state Problems)"
A. V. Kozlov, “Proteinuria: methods for its detection,” lecture, St. Petersburg, SPbMAPO, 2000.
V. L. Emanuel, “ Laboratory diagnostics kidney diseases. Urinary syndrome,” - Directory of the head of the clinical laboratory, No. 12, December 2006.
O. V. Novoselova, M. B. Pyatigorskaya, Yu. E. Mikhailov, “ Clinical aspects detection and assessment of proteinuria,” Directory of the Head of the Clinical Clinical Laboratory, No. 1, January 2007.