Authors' team

A. K. Veshkin, I. B. Getman, V. F. Gladenin, M. G. Drangoy, E. S. Dyuzhakova, M. V. Kabkov, N. R. Kazaryan, E. I. Kobozeva, E. A. Kozlova, N. D. Levanova, A. Yu. Neganova, O. V. Osipova, S. E. Osmanov, E. Yu. Polyakova, S. S. Firsova, L. V. Shilnikov

Decoration Elena Demchenko

Introduction

Currently, the interest of most people (including doctors of various specialties and areas) in reference literature has greatly increased, since it is from it that one can borrow the necessary minimum of knowledge that would help study any area of ​​interest in more detail. The primary condition for effective treatment of a sick person is correct and timely recognition of his illness. It should be borne in mind that each person will have a different course of the same disease. This is determined by the individual characteristics of the body, therefore, each medical worker, when solving problems of practical medicine, must proceed from a scientific understanding of the essence of the disease. These facts, which characterize deviations from the normal functioning of various organs and systems, are determined by the doctor during a systematic and holistic examination of the patient.

Disease by its nature represents the body's response to a changing environment. The disease is caused by a disorder of vital functions that appears under the influence of various factors. The disease is provoked not only by harmful environmental influences (physical, chemical, microbial, viral), but also by ordinary physiological irritants (with bronchial asthma, allergies, etc.). When thinking about the treatment of any disease, one should keep in mind the nature of the interaction between the environment and the body with its changing reaction.

Important signs of the disease are its pathological consequences, protective-adapted phenomena, realized mainly by reflex devices.

You should be aware that as a result of environmental influences, under certain conditions, the genetic properties of the organism can also change in a pathological direction, even despite the significant constancy of heredity. Heredity, as a result, is a product of environmental influences in previous generations. The environment influences the occurrence of diseases and the life activity of higher organisms, acting through the central nervous system.

The development of medicine as a science has come a long and difficult way. Translated from Latin, the word “medicine” means “to prescribe a remedy.” However, medicine not only provides treatment for any disease, but also takes care of the prevention and prevention of the occurrence of diseases. The origins of healing appeared in the initial stages of human life. According to the famous physiologist I.P. Pavlov, “medical science is the same age as the first man.” The results of our knowledge about diseases and methods of treating them in those ancient times were the excavations of settlements and burials of primitive man, the study of some groups of peoples who are now at the initial stage of evolution.

The medicine of Ancient Greece and Ancient Rome borrowed from its ancestors some magical types and methods of treatment (spells, various rituals), expedient techniques, and various healing remedies of traditional medicine (mainly herbal medicine).

The medical art of the era of the slave system reached its apogee in the activities of the famous and great ancient Greek physician Hippocrates, who is rightly called the father of medicine and who turned observation of the patient into a method of study, made a description of the external features of most diseases, and his concept of the main varieties of physique and character (temperament) ) in people has proven an individual approach to diagnosing and treating a patient.

The initial desire to identify the dependence and connection between the structure and functions of the human body dates back to the famous Alexandrian doctors Herophilus and Erasistratus, who made their discoveries and observations by dissecting animal corpses. But the greatest influence on the formation of medicine was exerted by the Roman physician Galen, who systematized data on anatomy, pathology, physiology, hygiene, obstetrics, toxicology, etc.

As for the history of medicine in the Middle Ages, Ibn Sina had a great influence on its development, whose book (pentalogy “The Canon of Medicine”) was a kind of encyclopedic set containing information about almost all knowledge in the field of medicine.

Medicine has since undergone a number of changes: in many European countries in past centuries, the method of experimenting on animals in order to observe the pathology caused by a particular disease became popular; Along with curative medicine, preventive medicine began to develop, the main task of which is to prevent the occurrence of disease; an etiological direction was born, with the help of which doctors began to look for the cause of diseases and study most pathologies at the microbial level (R. Kokh, D. I. Ivanovsky, D. K. Zabolotny, N. F. Gamaleya, L. A. Tarasovich, G. N. Gabrichevsky, A. M. Bezredka, etc.). In Russia, the main contribution to the development of both medicine itself and experimental pharmacology was made by the research of N. P. Kravkov, works on physiology by I. P. Pavlov, etc.

The founder of medicine in Russia is the first professor of medicine at Moscow University - S. G. Zybelin. He defended the importance of maintaining a hygienic regime from the first years of a person’s life, work processes and positive emotions as the best preventive measure.

The founder of Russian clinical science in the first third of the 19th century. there was a representative of the Moscow school M. Ya. Mudrov. In his scientific, practical and social activities, he showed the way to other figures in Russian medicine. He argued that “knowing the disease is half the cure,” that is, the basic principles of clinical medicine constitute scientific data about the essence of the disease. M. I. Mudrov formed his own thinking, based on an individual approach to the diagnosis, prognosis, treatment of the patient and under no circumstances analyzed the disease as an abstract category. And at present, his words contain a deep meaning: “You should not treat a disease by its name alone, but you should treat the patient himself, his composition, his organs, his strength.” He carried out appropriate active therapy, in which a general regimen and special medications played an important role. He gave first place to preventive medicine and developed special anti-epidemic measures. Getting to know medicine is unimaginable without knowledge of a number of disciplines. First of all, you need to be familiar with anatomy (the structure of the human body); one part of it studies the corresponding arrangement of parts and organs - the so-called topographic anatomy; study of the smallest tissue structure - histology; Embryology is the science of the formation of tissues and the entire body. Physiology deals with the study of functions in a healthy state, and general pathology deals with the study of their disorders, and bacteriology studies their disorders depending on the smallest fungi, etc.

The theoretical basis of modern medicine and its preventive purposes is not only the natural sciences, but also the doctrine of the relationship between social, physiological, psychological and biological factors that influence the physical and mental health of a person. The diagnosis is based not only on the patient’s main complaints and the disease itself, but also on other anomalies found in the patient along with an indication of functional disorders, the degree of compensation of the process, etc. Such an accurate diagnosis is the basis for the prognosis and treatment of each patient . Regular treatment of the patient is preceded by questioning about the complaints and course of the disease, as well as about all previous diseases and living conditions of the patient. This analysis is a significant factor from the point of view of modern medicine, since any influence on the body in the past does not pass without leaving a mark on the nervous system, higher nervous activity and, therefore, can determine the course of further diseases that arise without a clear connection with diseases in the past. When making a diagnosis, data from special studies (chemical, microbiological, radiological, psychological, electrocardiographic, etc.) have only auxiliary value, subordinate to the general clinical examination of the patient.

When treating a patient with a combination of medicinal and other methods, it is necessary to take into account the characteristics of the patient’s higher nervous activity, although science does not yet have simple and accurate methods for individual typological characteristics.

Prevention should be based on knowledge of the nature of the disease and the likelihood of targeted changes in both environmental circumstances and the individual characteristics of the organism.

When writing sections of this encyclopedia, the authors tried to describe everything new that modern medicine and pharmacology have achieved, as well as knowledge about what a doctor might need in his work. The peculiarity of this book is that, firstly, it is called homemade (that is, it is intended, on the one hand, for medical workers, and on the other, for people who do not have a medical education); secondly, the diseases are systematized into specialized chapters.

The encyclopedia is written according to the following structure: definition of the concept, term of the disease; necessary anatomical and physiological information about the pathologically altered organ; modern research methods; clinical picture, which examines the main signs of the disease and how it progresses; diagnostics; types of treatment in certain situations and management of patients.

The book provides important information at a modern scientific level about diagnostics, differential diagnosis, prevention and treatment of emergency conditions in gynecology, diseases of the genitourinary system, children's, nervous, dental, internal, ENT diseases, endocrinology, toxicology, therapy, etc. It also contains information about diseases of various organs and systems of the human body.

1. Obstetrics and gynecology

A

ABORTION

Definition

The term “abortion” should be understood as termination of pregnancy, which can be spontaneous (due to a certain number of reasons) and artificial (under the influence of surgical manipulations). An artificial abortion can be performed at the request of a woman up to 12 weeks of pregnancy; at a later stage, it is more difficult to perform an artificial termination of pregnancy, and it is performed if there are medical indications. Moreover, such manipulation must be carried out in a specialized clinic after a series of specific examinations. Depending on the duration of pregnancy, the general condition of the woman, and the presence or absence of chronic diseases, there are different ways to terminate a pregnancy.

1. Medical abortion (up to 6 weeks of pregnancy) - this type of abortion is the safest and most gentle modern method of terminating a pregnancy. This method is preferable for young girls who have not given birth, since an important advantage of medical abortion is the absence of the need for surgical intervention. The only thing that needs to be taken into account is the period of possible use of the method - up to 6 weeks of pregnancy (up to 63 days of amenorrhea). The most common drugs for performing medical abortion include Mifegin (the active ingredient is mifepristone) or the Russian analogue, Pencrofton. As already noted, the main advantage is the ability to avoid the risks associated with anesthesia and surgery, and also eliminates the risk of infection, as well as the development of adhesions and damage to the inner wall of the uterine cavity and cervix. But this method adversely affects the subsequent reproductive function of a woman. Another important advantage of the method is the ability to terminate pregnancy at the earliest stages, which reduces the risk of developing all kinds of complications. It must be said that the high effectiveness of the drug is possible only with strict adherence to the regimens and doses of natural medications, as well as the correct use of support drugs (prostaglandins).

2. Mini-abortion. This manipulation can be performed from the moment the fertilized egg is detected (according to ultrasound) until 4–5 weeks of pregnancy. The technical implementation of the manipulation requires the use of a vacuum suction. This method of termination of pregnancy is characterized by minimal trauma to the uterus and also reduces the time of the operation.

3. Surgical abortion - this method of termination of pregnancy is also called the classical method (instrumental) and involves mechanical curettage of the uterine cavity (curettage), can be performed during pregnancy from 6 to 12 weeks of pregnancy. Surgical abortion should be performed exclusively by highly qualified specialists using modern effective anesthetics.

ADIPOSOGENITAL DYSTROPHY (PECHKRANZ-BABINSKI-FERLICH SYNDROME)

Definition

Adiposogenital dystrophy, or Pechkranz-Babinski-Fröhlich syndrome, is a neuroendocrine disease characterized by the presence of obesity of hypothalamic-pituitary origin and dysfunction of the gonads (hypogonadism).

The development of adiposogenital dystrophy is caused by damage to the nuclei of the hypothalamus, which are responsible for the regulation of appetite and in which the synthesis of gonadoliberin hormones occurs, stimulating the production of the hormones lutropin and follitropin in the pituitary gland. However, in the absence or reduced amount of lutropin and follitropin, stimulation of the production of gonadal hormones does not occur, which ultimately leads to insufficiency of the direct function of the gonads.

Etiology and pathogenesis

The causes of adiposogenital dystrophy are diverse:

– previous infectious lesions of the brain;

– viral and bacterial meningitis, encephalitis;

– meningoencephalitis;

– arachnoiditis;

– toxoplasmosis.

A number of influences can lead to the destruction of the nuclei of the hypothalamus, such as intrauterine infections and intoxications, birth injuries to the head, and toxoplasmosis suffered by the mother during pregnancy. Also, sometimes brain tumors localized in this area lead to damage to the hypothalamus.

Clinical picture

Adiposogenital dystrophy occurs in childhood, but most often manifests itself during puberty (puberty), as serious changes occur in the body. It should be noted that boys and girls get sick equally often. In this case, the earliest sign of the disease is intense weight gain. Typical for boys is enlargement of the mammary glands (gynecomastia), a decrease in the size of the testicles and penis. Cryptorchidism (undescended testicle into the scrotum) occurs quite often in boys. During adolescence, puberty is delayed. Secondary female and male sexual characteristics in such adolescents are poorly formed. Boys are characterized by sparse hair growth on the pubis and armpits, and the growth of a beard and mustache is absent for a long time. It should be noted that scanty hair persists into adulthood, as do underdeveloped genitals.

Girls are also characterized by underdevelopment of the external genitalia. In addition, menstruation is delayed (later than the usual period of menarche) and may not even appear at all. At the same time, both sexes are characterized by a disorder of skeletal development (eunuchoidism): tall stature, long limbs, the span of which exceeds height by several centimeters. In addition, inferiority of the ligamentous-articular apparatus occurs: the joints are pathologically mobile, hyperextended, and flat feet are formed. Patients are severely obese. The accumulation of subcutaneous fat occurs mainly in the abdomen, thighs, chest and face. Patients' skin is usually thin and dry.

There may also be changes in the internal organs: disturbances occur in the gastrointestinal tract, the outflow of bile is often disrupted, and constipation occurs. The cardiovascular system also suffers, dystrophic changes in the heart muscle and myocardial dystrophy are noted. As for intellectual development, it is usually normal and corresponds to age and education.

Diagnostics

It is possible to suspect the diagnosis of adiposogenital dystorphia on the basis of characteristic complaints and the appearance of patients; a decrease in the blood concentration of follitropin, lutropin, testosterone and estrogens helps to confirm it.

Treatment

For effective treatment it is necessary to establish the etiology of the disease. Therefore, first of all, if possible, treatment of the underlying disease is prescribed, which led to damage to the hypothalamus with the development of symptoms of diposogenital dystrophy. In particular, if the tumor is of a tumor nature, radiation therapy or surgical treatment is prescribed. It is necessary to carry out adequate and comprehensive treatment of inflammatory diseases, after which pathology may develop: broad-spectrum antibiotics and antiviral drugs are used. Drugs that improve the condition of brain tissue are mandatory: Actovegin, Nootropil, Diavitol, Cerebrolysin, Cavinton. In order to regulate metabolism and normalize weight, it is recommended to follow a diet with a reduced calorie content, limiting fats and easily digestible carbohydrates. In complex treatment, physical therapy with sufficient physical activity must be prescribed. In cases of severe clinical picture of adiposogenital dystrophy, boys are prescribed hormone replacement therapy with human chorionic gonadotropin, which is used from the age of 12. Such therapy helps to achieve puberty, and already at the age of 15–16 years, male sex hormones are prescribed: testosterone, methyltestosterone, sustanon. In turn, teenage girls are recommended, on the contrary, female sex hormones - estrogens, and then treated with complex estrogen-progestin drugs. It should be noted that with timely treatment of this condition and a constant diet, you can maintain good health throughout your life.

ADNEXIT

See "Oophoritis".

ADRENOGENITAL SYNDROME

Definition

Adrenogenital syndrome is a neuroendocrine pathology associated with a monogenic mutation.

Etiology and pathogenesis

Adrenogenital syndrome is characterized by mild signs of virilization. Currently, it is customary to distinguish pubertal and postpubertal forms of adrenogenital syndrome. The pubertal form is characterized by the presence of excessive synthesis of androgens immediately with the onset of puberty, and there is a coincidence with the physiological activation of the hormonal function of the adrenal glands.

Clinical picture

Girls are characterized by rapid growth that exceeds the usual growth spurt, and a physique - broad shoulders, a narrowed pelvis, less fat deposits on the hips and buttocks, and somewhat hypoplastic mammary glands, which gives them a certain athletic type. In this regard, such girls play sports willingly, and good muscle development allows them to achieve success in sports that require endurance. In this case, there is hypertrichosis, which is usually mildly expressed - single shaft hairs above the upper lip, cheeks (“sideburns”), on the paranasal areas, hair growth on the white line of the abdomen, perineum, thighs, and legs. Hyperandrogenism is manifested by multiple acne, porous, oily skin of the face and back.

Often there is moderate hypoplasia of the labia minora and majora, a slightly increased distance from the base of the clitoris to the external opening of the urethra, and moderate hypoplasia of the uterus. In this case, menarche occurs at 14–16 years of age, menstruation after this is irregular and tends to be delayed. The postpubertal form develops in women who are sexually active and experience irregular, scanty menstruation, absence of pregnancies, and hypertrichosis. Quite often, such women experience spontaneous abortions in the early stages (up to 7-10 weeks). A survey of the patient reveals that immediately after menarche the woman began to notice delayed menstruation and excess hair growth. Such signs indicate the onset of hyperandrogenism at puberty. The main pathogenetic link of this pathology is the excessive release of androgens (a genetically determined increase in the synthesis of androgens by the adrenal cortex), as a result of which the release of gonadotropins is inhibited and cyclic processes in the ovaries are disrupted. The disorders that develop in the ovaries can be different:

– with suppression of the growth and maturation of follicles in the early stages of folliculogenesis and the development of amenorrhea;

– with inhibition of growth, maturation of follicles and eggs unable to ovulate, development as a result of anovulation and oligomenorrhea. There may be the presence of ovulation with the subsequent development of an inferior corpus luteum. Despite regular menstruation, there is insufficiency of the luteal phase of the cycle. The main thing in this syndrome is the development of infertility in all types of ovarian disorders. In this case, pregnancy can occur, but usually ends spontaneously in the early stages, before the formation of the placenta.

Diagnostics

In addition to the symptoms described above, hormonal studies help in establishing a diagnosis, especially with mild adrenogenital syndrome. In clinical practice, the determination of 17-CS - androgen metabolites in urine before and after taking glucocorticoid drugs (test with dexamethasone) is used. It is known that today the more common and accurate method for determining DHEA, testosterone and 17-OHP before and after the specified test. A decrease in the content of 17-CS in the urine and testosterone, 17-OHP and DHEA in the blood after the use of drugs that inhibit the release of ACTH indicates the adrenal origin of androgens. It is important to note that difficulties in diagnosis arise when a woman with adrenogenital syndrome develops polycystic ovaries, which themselves are a source of increased androgen production.

Treatment

In order to correct disorders of the hormonal function of the adrenal cortex, glucocorticoid drugs are used in treatment. Cortisol has been used in treatment for a very long time, although today dexamethasone is more widely used. The dosage of the drug is determined by monitoring the content of 17-KS in the urine, testosterone, DHEA and 17-OHP in the blood, the level of which, while taking dexamethasone, should not exceed the upper limit of normal. The effectiveness of the treatment can be judged by changes in basal temperature and the nature of the menstrual cycle. Shortening the intervals between menstruation and the appearance of biphasic temperature are reliable signs of a positive effect of treatment. In turn, the lack of effect of therapy indicates the presence of polycystic ovaries, which often develop, in particular, against the background of chronic anovulation with adrenogenital syndrome. Clomiphene is added to hormonal therapy in cases where there is no full second phase of the menstrual cycle. Against the background of complex therapy, pregnancy occurs quite often, which necessitates the further use of glucocorticoid drugs in order to avoid miscarriage or stop the development of the fertilized egg. In order to reduce hypertrichosis, the antiandrogen cyproterone acetate is used; it reduces the level of testosterone both in the blood and in the urine, without suppressing the adenocorticotropic and gonadotropic functions of the pituitary gland. Veroshpiron (spironolactone) also has antiandrogenic properties. A similar effect has been noted from the use of synthetic progestins (oral contraceptives containing estrogens and gestagens). It should be noted that the use of synthetic progestins in women with adrenogenital syndrome should not be long-term.

It is typically characterized by the appearance of protein in the urine during prolonged standing or walking, with rapid disappearance in a horizontal position.

Characteristics of proteinuria: usually does not exceed 1 g/day, glomerular, non-selective, the mechanism of its occurrence is not clear. It is more often observed in adolescence; in half of the patients it disappears after 5-10 years.

The diagnosis of orthostatic proteinuria is made if the following criteria are present:

The patient's age is between 13-20 years;

The isolated nature of proteinuria is the absence of other signs of kidney damage (other changes in urine, increased blood pressure, changes in the vessels of the fundus);

The exclusively orthostatic nature of proteinuria - in urine tests taken immediately after the patient is in a horizontal position (including in the morning before getting out of bed), protein is absent.

To confirm the diagnosis, it is necessary to perform an orthostatic test. Urine is collected in the morning before getting out of bed, then after 1-2 hours of staying in an upright position (walking, preferably with hyperlordosis, with a stick behind the back to straighten the spine). The test gives even more accurate results if the morning (night) portion of urine is poured out (since there may be residual urine in the bladder), and the first portion is collected after the subject has been in a horizontal position for 1-2 hours.

Idiopathic transient proteinuria.

In adolescence, idiopathic transient proteinuria can also be observed, which is detected in otherwise healthy individuals during medical examination and is absent in subsequent urine tests.

Tension proteinuria.

Proteinuria of tension, detected in 20% of healthy individuals (including athletes) after sharp physical stress with the detection of protein in the first collected portion of urine, has a tubular (tubular) character. It is assumed that the mechanism of this proteinuria is associated with the redistribution of blood flow and relative ischemia of the proximal and distal tubules.

Feverish proteinuria.

Feverish proteinuria is observed in acute febrile conditions, especially in children and the elderly; it is predominantly glomerular in nature. The mechanisms of these types of proteinuria are poorly understood. A possible role of increased glomerular filtration is suggested along with transient damage to the glomerular filter by immune complexes.

It is important to establish the fact of proteinuria and the degree of its severity, since in the vast majority of cases proteinuria is one of the main signs of kidney damage.

High (“large”, “massive”) proteinuria

High proteinuria is the excretion of protein in the urine in amounts of more than 3 g/day, which often leads to the development of nephrotic syndrome. This type of proteinuria is observed in acute and chronic glomerulonephritis, kidney damage due to systemic diseases (SLE, hemorrhagic vasculitis, etc.), renal amyloidosis, subacute infective endocarditis. Severe proteinuria can also be observed in myeloma and renal vein thrombosis, as well as diabetic nephropathy.

Moderate proteinuria.

Moderate proteinuria - protein excretion in the urine in an amount of 0.5 to 3 g/day; it is observed in all of the diseases listed above, as well as in malignant arterial hypertension, periarteritis nodosa, hypertension, atherosclerosis of the renal vessels (ischemic kidney disease) and other diseases.

Hematuria.

Hematuria (blood in the urine) is a common, often the first sign of kidney and urinary tract diseases, as well as diseases and conditions not associated with kidney damage (acute leukemia, thrombocytopenia, overdose of anticoagulants, heavy physical activity, etc.).

Types of hematuria:

Macro- and microhematuria are distinguished by intensity. To cause gross hematuria, 1 ml of blood per 1 liter of urine is sufficient. Microhematuria is diagnosed when there are more than 1000 red blood cells in 1 ml of urine or more than 5 red blood cells in the field of view (under a microscope at high magnification).

If there is heavy bleeding, the urine may be the color of scarlet or dark blood. Urine takes on the appearance of “meat slop” when it contains a large number of red blood cells, leukocytes, and mucus (for example, with AGN). To assess the degree of hematuria, it is necessary to use quantitative methods (analysis according to Nechiporenko, Amburge, Kakovsky-Addis).

By nature, there are initial (at the beginning of the act of urination), terminal (at the end of the act of urination) and total hematuria.

The nature of hematuria can be clarified using a three-glass or two-glass test. Total hematuria can be caused by unilateral or bilateral lesions, which can only be determined by cystoscopy or special radiological examination.

According to clinical features, hematuria is distinguished recurrent and persistent, painful and painless.

Hematuria in nephropathies (renal hematuria), as a rule, is persistent, bilateral, painless, and is often combined with proteinuria, cylindruria, and leukocyturia. Nevertheless, forms of glomerulonephritis have been described that occur with recurrent isolated painful macrohematuria.

The pathogenesis of renal hematuria is not completely clear. It is believed that the involvement of the mesangium is of great importance, as well as damage to the interstitial tissue and convoluted tubule epithelium, since significant hematuria is most often observed with mesangial nephritis and interstitial nephritis. Hematuria can be caused by necrotizing inflammation of the renal arterioles, renal intravascular coagulation, or renal infarction.

Japanese authors have recently proven in a series of electron diffraction patterns that red blood cells can penetrate even the smallest ruptures of the BMK, changing their shape. True gross hematuria should be distinguished from false. Unlike true hematuria, false hematuria is caused by urine turning red not from red blood cells, but from other substances.

Hemoglobinuria occurs in cases of massive hemolysis (hemolytic anemia, transfusion of incompatible blood, malaria, poisoning with hemolytic poisons - phenol, Bertholet's salt, poisonous mushrooms), paroxysmal nocturnal hemoglobinuria, etc.

Myoglobin appears in the urine during the breakdown of muscle tissue (long-term crush syndrome, muscle infarctions due to occlusion of a large artery, alcoholic polymyopathy, etc.); prolonged hyperthermia, especially in combination with convulsions; familial myoglobinuria.

Uroporphyrinuria is observed in hemochromatosis, porphyria; melaninuria - with melanosarcoma.

Urine may become red when consuming certain foods (beets, red berries), red food dyes (confectionery, ketchups, tomato paste, etc.), certain drugs, such as phenolphthalein (for alkaline urine), phenazopyridine.

Renal hematuria is observed with AGN, CGN, as well as with many nephropathies that occur against the background of systemic diseases.

Acute nephritis syndrome is manifested by hematuria, proteinuria (usually moderate), edema, arterial hypertension... However, at present, most acute nephritis occurs atypically, and a number of symptoms, including massive hematuria, may be absent. Recurrent acute nephritis syndrome often manifests itself as a mesangioproliferative variant of CGN, which differs from acute nephritis in its morphological picture.

One of the most common causes of isolated hematuria is IgA nephropathy, or Berger's disease (focal mesangial nephritis). IgA nephropathy is detected, as a rule, in children and adults under 30 years of age, more often in men; manifests itself as attacks of macrohematuria (less commonly, persistent microhematuria) with dull pain in the lower back, recurrent against the background of pharyngitis. Proteinuria is usually minimal. The course of the disease in children is usually benign; in adults the prognosis is worse.

Similar hematuric IgA nephritis with an increase in the concentration of IgA in the blood serum is also characteristic of patients with chronic alcoholism. It is detected mainly in people over 40 years of age against the background of alcoholic liver damage in combination with other systemic manifestations of alcoholism (damage to the pancreas, heart, polyneuropathy). Unlike Berger's disease, “alcoholic” glomerulonephritis is manifested by persistent painless microhematuria and is more severe - arterial hypertension is often associated, and renal failure develops faster.

Hematuria is a characteristic sign of interstitial nephritis, including acute drug-induced nephritis. The cause of hematuria can be a wide variety of drugs, most often sulfonamides, streptomycin, kanamycin, gentamicin, analgesics (phenacetin, analgin), pyrazolidone derivatives (butadione), as well as heavy metal salts.

A special painful variant of hematuric nephropathy has been described - lumbalgic-hematuric syndrome, observed mainly in young women using oral estrogen-containing contraceptives, but isolated cases of the disease have also been described in men. Clinically, this syndrome is manifested by attacks of intense pain in the lumbar region in combination with hematuria (usually gross hematuria) and often intermittent fever. Attacks are triggered by colds and heavy physical activity. During the interictal period, no pathological changes are noted in urine analysis. There are also no signs of immunological activity. Angiographic examination may reveal changes in the intrarenal arteries in the form of their partial or complete occlusion, tortuosity, and fibroelastosis.

Hereditary nephritis with hearing loss and decreased vision (Alport syndrome) is predominantly manifested by hematuria; the disease has an unfavorable prognosis.

Benign familial recurrent hematuria has a much better prognosis; biopsy often reveals unchanged renal tissue, sometimes focal glomerulonephritis.

In recent years, special forms of chronic interstitial nephritis, manifested by hematuria, have been described in children - with hyperoxalaturia.

Bilateral renal hematuria is characteristic of secondary glomerulonephritis in a number of systemic diseases.

Nephritis in hemorrhagic vasculitis can develop from the very beginning of the disease or occur several years after the onset of skin, articular and abdominal syndromes. Kidney damage in most cases occurs as hematuric glomerulonephritis (gross hematuria is observed in 40% of cases) with an increase in serum IgA levels and is characterized by a persistent or slowly progressive course. With the development of nephrotic syndrome, the prognosis is much worse.

Glomerulonephritis in infective endocarditis, which can occur against the background of a full-blown clinical picture of the disease (fever, damage to the heart valves, splenomegaly, anemia), but can also be the first manifestation of the disease, usually occurs with hematuria, sometimes with gross hematuria, moderate proteinuria; The nephrotic variant of nephritis is less common. In 40-60% of cases of infective endocarditis, kidney infarctions with gross hematuria occur.

Nephropathy in classic periarteritis nodosa (Kussmaul-Mayer disease) manifests itself several months after general symptoms - fever, weight loss, muscle-joint pain, asymmetric polyneuritis, and is characterized by microhematuria (in more than half of the cases), moderate proteinuria and malignant arterial hypertension. Gross hematuria with severe lower back pain may manifest itself in a rarer form of nephropathy with periarteritis nodosa - more often it is a rupture of an intrarenal artery aneurysm.

Microscopic polyangiitis is a form of necrotizing vasculitis with damage to small vessels (capillaries, venules, arterioles). In the blood, antibodies to the cytoplasm of neutrophils are detected (antineutrophil cytoplasmic antibodies - ANCA), which react with the myeloperoxidase of their granules and give a perinuclear type of luminescence in the immunofluorescence test. Most often the skin (purpura), lungs (hemorrhagic alveolitis with hemoptysis up to pulmonary hemorrhage), and kidneys are affected. Gastrointestinal vasculitis, myalgia, and peripheral neuritis are also possible. The kidneys are affected in 90-100% of cases (urinary and nephrotic syndromes, arterial hypertension are observed; in more than 50% of cases, nephritis becomes rapidly progressive). A renal biopsy reveals proliferative glomerulonephritis with foci of necrosis; immunofluorescence studies reveal the absence or a small amount of immune deposits (pauci-immune - “low-immune” glomerulonephritis).

Kidney damage in Wegener's granulomatosis develops against the background of granulomatous-necrotic lesions of the upper respiratory tract and lungs and is manifested by hematuria (gross hematuria in 25% of cases) in combination with moderate proteinuria. Arterial hypertension and nephrotic syndrome develop rarely, but already in the first years of the disease, most patients show signs of renal failure.

Goodpasture's syndrome is characterized by damage to the lungs (hemorrhagic alveolitis with repeated pulmonary hemorrhages) and the addition, usually after a few months, of RPGN with massive micro- or macrohematuria.

Thrombotic microangiopathies are characterized by widespread damage to small vessels, occurring with Coombs-negative hemolytic anemia, intravascular coagulation, thrombocytopenia, hematuria, often with the development of acute renal failure. This group includes largely similar diseases - thrombotic thrombocytopenic purpura - TTP and hemolytic-uremic syndrome - HUS.

Despite the fact that the list of nephropathies that lead to the appearance of blood in the urine is very large, when hematuria is detected, urological diseases (urolithiasis, tumors and kidney tuberculosis) should first be excluded. It should be remembered that even minimal hematuria (less than 10 red blood cells in the field of view of the microscope) may be the first sign of a tumor of the genitourinary system.

To exclude urological diseases, it is of great importance to familiarize yourself with the patient’s complaints, medical history, as well as physical and laboratory examination.

Hematuria, observed only at the beginning or at the end of the act of urination, is characteristic almost exclusively of urological diseases; These same diseases are more characterized by hematuria, accompanied by severe pain in the lower back, especially paroxysmal pain.

Initial and terminal hematuria can be easily detected using a three-glass test. Detection of blood only in the first portion of urine is typical for diseases of the urethra, only in the last portion - for diseases of the bladder, prostate gland, and seminal tubercles. In the presence of total hematuria (in all three portions of urine), the source of bleeding can be either the renal parenchyma, the pyelocaliceal system or the ureter. It is often useful to carry out an orthostatic test (physical stress test), which consists of obtaining two portions of urine: the first - morning, taken immediately after waking up, preferably lying down, before moving to an upright position, and the second - taken 1-2 hours after the transition in a vertical position and light physical activity (walking, climbing stairs). The number of red blood cells in both portions is counted. A significant increase in hematuria is characteristic of nephroptosis and urolithiasis. Renal hematuria is characterized by the presence of red blood cell casts in the sediment. It is assumed that the cylinders can be destroyed during centrifugation, therefore it is proposed to isolate the urinary sediment not by centrifugation, but by filtration through fine-pored filters.

The issue of the significance of unchanged and altered red blood cells in urinary sediment has been discussed for a long time. In recent decades, the predominance of certain red blood cells has not been given diagnostic significance. Since the late 70s, phase-contrast microscopy has been used to study erythrocytes in urinary sediment. It has been shown that red blood cells in kidney diseases differ significantly from red blood cells in urological diseases. Red blood cells of glomerular origin appear noticeably deformed as a result of their passage through the BMC and further through liquid media with sharp changes in pH, osmolarity and electrolyte composition of urine in various parts of the renal tubules. The presence of more than 70% of “dysmorphic” erythrocytes in urine sediment indicates their glomerular origin. When bleeding from damaged vessels in patients with urological diseases, red blood cells entering the urine retain the size and shape inherent in normal red blood cells (“unchanged” red blood cells). This method can be the primary test of differential diagnosis, determining the direction of further thorough urological examination.

Instrumental and X-ray radiological examination is especially important for excluding urological pathology: cystoscopy with catheterization of the ureters and separate urine collection, ultrasound of the kidneys, excretory urography (preferably lying and standing to exclude pathological mobility of the kidney), if necessary, retrograde pyelography, CT, selective angiography. Recently, radioisotope angiography and renoscintigraphy with radioactive Tc99 have been used. These methods are simpler and safer, they can identify local hemo- and urodynamic disorders characteristic of unilateral hematuria with renal venous hypertension, renal vein thrombosis, and fornical bleeding.

Approximately 15% of hematuria are caused by tumors of the genitourinary tract. In 60% of cases these are bladder tumors, which can only be accompanied by painless hematuria; The diagnosis is confirmed by cystoscopy. Approximately 20% of urinary tract tumors are renal parenchymal cancer (dull lower back pain, fever, anemia or erythrocytosis, hypercalcemia), sometimes occurring with paraneoplastic reactions, including membranous nephropathy; To confirm the diagnosis, it is necessary to perform intravenous urography and angiography.

One of the most common causes of hematuria is urolithiasis. The typical clinical picture includes sharp paroxysmal pain in the lower back, radiating to the groin area, followed by gross hematuria. About 90% of kidney stones contain calcium and can be detected by plain imaging of the kidney area.

Hematuria in combination with leukocyturia and moderate proteinuria (usually up to 1 g/l) is often found in nonspecific inflammatory diseases of the urinary system. Microhematuria in chronic pyelonephritis is caused by damage to the interstitial tissue of the kidney. In acute pyelonephritis and exacerbation of chronic pyelonephritis, episodes of gross hematuria may develop, usually caused by necrosis of the renal papillae, the pathogenesis of which is ischemia of the papillae (vascular embolization) or compression by inflammatory infiltrates. Lower urinary tract infection (the number of microbial bodies in 1 ml of urine is at least 105) can sometimes cause hematuria; A fungal infection may occur with hematuria. Women may experience episodes of gross hematuria with cystitis and urethritis.

With tuberculosis of the urinary system, hematuria is usually combined with pyuria and slight proteinuria, but sometimes it is isolated. Diagnosis is complex and requires careful bacteriological (repeated urine cultures, sediment microscopy), X-ray and ultrasound examinations.

Hematuria is often detected with congestive venous hypertension in the kidney, the cause of which may be nephroptosis, cicatricial stenosis of the renal vein, thrombosis of the renal vein, anomalies of the renal veins, etc. Renal venous hypertension can manifest itself as microhematuria, which significantly increases with physical activity, in combination with slight proteinuria. Gross hematuria in these conditions is in most cases caused by an increase in venous pressure and a breakthrough of the thin septum between the veins and the renal calyx (fornical bleeding).

Hematuria (usually unilateral) is observed with renal infarction, as well as with thrombosis of the renal veins. Kidney infarction develops with embolism of the renal artery or its thrombosis, and can be observed with infective endocarditis and polyarteritis nodosa. Characterized by low back pain, transient hematuria and proteinuria, and sometimes arterial hypertension. Renal vein thrombosis is characterized by pain, massive proteinuria and hematuria with the rapid onset of nephrotic syndrome. In acute complete thrombosis, gross hematuria is possible; nephrotic syndrome is often combined with transient renal failure. Chronic thrombosis usually occurs with little or no pain and is manifested by microhematuria and nephrotic syndrome. For precise localization of thrombosis, lower venocavagraphy is used in combination with renal venography and arteriography. Recently, in all these situations, Doppler ultrasound, including color scanning, has been increasingly used for diagnostic purposes.

Nephrotic syndrome

One of the most characteristic and serious manifestations of acute and especially chronic kidney diseases is nephrotic syndrome. This is one of the “big” nephrological syndromes, which represents a prognostically very serious clinical and laboratory symptom complex, including massive proteinuria (above 3.0-3.5 g/day, in children above 50 mg/kg day), hypoproteinemia (hypoalbuminemia - albumin blood less than 30 g/l) and edema. A common symptom of nephrotic syndrome is hypercholesterolemia (more precisely, hyperlipidemia).

A wide range of changes in the body systems responsible for maintaining homeostasis during nephrotic syndrome leads to its identification as extremely important not only due to the occurrence of significant widespread edema, but also due to the possibility of developing serious complications (primarily infections, vascular thrombosis), complex therapy, severity of prognosis.

Nephrotic syndrome develops most often in children aged 2 to 5 years and in adults from 17 to 35 years. Along with this, cases of nephrotic syndrome have been described in earlier stages of life - in newborns, as well as in old age (85-95 years).

Spontaneous remissions in adults are rare, and although usually, even with extremely pronounced signs of nephrotic syndrome, a satisfactory GFR remains for a long time, there is no arterial hypertension or hematuria, yet in most cases the disease continuously progresses with the development of chronic renal failure.

In this regard, timely detection of nephrotic syndrome, correct interpretation of its origin and attempts at active treatment are very important.

Nephrotic syndrome is usually based on damage to the glomeruli of the kidneys: various types of glomerular lesions (from minimal, detected only by electron microscopic examination, to severe variants of glomerulo-nephritis, including fibroplastic and focal segmental glomerulosclerosis), as well as amyloidosis, diabetic glomerulo-sclerosis .

Nephrotic syndrome may be caused by drug exposure. Medicines that can cause kidney damage with the development of nephrotic syndrome include antiepileptic drugs, bismuth, gold, mercury, D-penicillamine, antibiotics, vitamins, etc. In this case, along with isolated kidney damage, the development of a severe drug-induced disease involving almost all systems and organs (including the kidneys) is possible.

It is necessary to note the possibility of paraneoplastic nephrotic syndrome, which occurs most often with bronchogenic cancer, cancer of the kidney parenchyma, stomach and colon.

Finally, there are rare congenital and genetically determined diseases in which the main clinical manifestation is nephrotic syndrome. Such diseases include congenital nephrotic syndrome of the Finnish type, nephrotic syndrome that occurs with damage to the nail plates and kneecaps, etc.

In all of these diseases, nephrotic syndrome is realized through the above-mentioned two variants of kidney damage - changes in the type of glomerulonephritis and amyloidosis, with one or another frequency of each of these variants characteristic of a particular disease. Thus, in periodic disease, nephrotic syndrome is caused by amyloidosis in almost 100% of cases; in SLE, the basis of nephrotic syndrome is always glomerulonephritis; in rheumatoid arthritis, amyloidosis with nephrotic syndrome often develops; glomerulonephritis, including medicinal ones, is less common; in subacute infective endocarditis, glomerulonephritis and amyloidosis occur at approximately the same frequency.

Causes of nephrotic syndrome

Primary kidney diseases

Minimal changes

Focal segmental glomerulosclerosis

Membranous glomerulonephritis

Mesangioproliferative glomerulonephritis

Mesangiocapillary glomerulonephritis (types I, II, III)

Secondary nephrotic syndrome (with other diseases)

Infectious diseases: infective endocarditis, “shunt” nephritis, hepatitis B and C, mononucleosis, malaria

Medicines: gold preparations, mercury, D-penicillamine, antibiotics, captopril

Systemic diseases: SLE, hemorrhagic vasculitis, necrotizing vasculitis, rheumatoid arthritis, cryoglobulinemia, amyloidosis

Tumors: lymphoma, lymphogranulomatosis, carcinoma, melanoma

Hereditary diseases: Alport syndrome, Fabry disease

Thus, the etiology of nephrotic syndrome is different, and its numerous manifestations are nonspecific, which is to a certain extent due to the commonality of pathogenetic mechanisms.

Damage to the glomeruli of the kidneys and massive proteinuria lead to other “major” symptoms of nephrotic syndrome, which together form the clinical picture of this condition.

Hypoalbuminemia developing after massive proteinuria is a mandatory sign of nephrotic syndrome. Most often, the decrease in the level of albumin and total protein in the blood is quite significant, which leads to a drop in plasma oncotic pressure. Hypoalbuminemia is said to occur when the serum albumin level is less than 35 g/l; in severe nephrotic syndrome, the albumin content can decrease to 15-20 and even 8-10 g/l. Hypoalbuminemia determines a decrease in the amount of total protein in the serum, a decrease in serum oncotic pressure, and a decrease in the transport function of albumin as a carrier of a number of substances, including many drugs.

Hypoproteinemia is a constant symptom of nephrotic syndrome. The content of total protein in the blood serum decreases to 30-40 and even 25 g/l. Hypoproteinemia is often aggravated by loss of protein in the intestines, increased catabolism of body proteins, including immunoglobulins, decreased reabsorption of protein by the tubules due to protein blockade of the lymphatic system of the kidney and edema of the renal interstitium.

In addition to hypoalbuminemia, nephrotic syndrome also reveals other signs of dysproteinemia - there is almost always severe hyper-α2-globulinemia and often hypogammaglobulinemia.

Important signs of nephrotic syndrome include hyperlipidemia - increased blood levels of triglycerides, total cholesterol, low-density lipoproteins (LDL), apoprotein B, and non-esterified fatty acids. Nephrotic hyperlipidemia is aggravated by the persistent course of nephrotic syndrome and GC therapy. The mechanism of development of hyperlipidemia in nephrotic syndrome is explained by a decrease in oncotic pressure and plasma viscosity, as well as loss of liporegulatory substances in the urine.

In parallel with disturbances in protein and lipid metabolism in nephrotic syndrome, changes in the coagulation and anticoagulation systems often develop, resulting in the formation of a symptom of blood hypercoagulation.

Nephrotic syndrome is characterized by severe disturbances in water and electrolyte balance, leading to the development of edema. As the edema progresses, it reaches the level of anasarca with edema of the cavities (ascites, hydrothorax, hydropericardium), which usually determines the main complaints of patients. The immediate cause of edema is sodium and water retention, which occurs through various mechanisms explained by two widely accepted theories.

The first, most well-known (“classical”) theory places the main emphasis on hypoproteinemia with a decrease in plasma oncotic pressure and the release of water and electrolytes into the interstitial tissue, which leads to hypovolemia. Hypovolemia causes compensatory activation of mechanisms that regulate blood volume, primarily the renin-angiotensin-aldosterone system and ADH. As a result, the reabsorption of sodium and water by the kidneys increases. This theory is called the hypovolemic, or (which is the same thing) the “incomplete channel” theory and quite convincingly explains the retention of sodium and water in those 30-40% of patients with a truly detectable decrease in blood volume.

In patients with normo- or hypervolemia (60-70% of patients with nephrotic syndrome) and lack of activation of the renin-angiotensin-aldosterone system, the development of edema is explained primarily by renal sodium retention due to a decrease in its filtration or an increase in tubular reabsorption (the “crowded bed” theory) ). The idea of ​​the volume of blood volume in nephrotic syndrome is of great practical importance, justifying the indications for the prescription of diuretics and ultrafiltration.

Typically, nephrotic edema, like other signs of nephrotic syndrome, develops gradually as proteinuria increases, while nephrotic syndrome can occur at the onset of the disease, without recurring or rarely relapsing in the future, which is considered the most favorable option for the course of the disease. An unfavorable variant includes the continuously relapsing course of nephrotic syndrome, especially the constantly existing severe variant, when arterial hypertension is often present simultaneously. In all cases, the prognosis is largely determined by the duration of remission of nephrotic syndrome, spontaneous or drug-induced, and the frequency and duration of relapses.

The severity of the condition with nephrotic syndrome can be aggravated by a number of complications, among which the most serious are the following:

Infections (bacterial, viral, fungal);

Hypovolemic nephrotic crisis (shock);

Edema of the brain, retina;

Vascular complications, hypercoagulation and thrombosis.

Infections (pneumonia, pneumococcal peritonitis, sepsis) most often determined the prognosis of patients with nephrotic syndrome in the pre-antibacterial era; they are explained primarily by a decrease in immunity and are aggravated by the active immunosuppressive therapy of nephrotic syndrome used in our time.

The development of infection, including the clinical picture of erysipelas, can be facilitated by a violation of the integrity of the skin (cracks in the area of ​​​​edematous skin, injuries during subcutaneous injections). The inflammation that occurs in these cases is usually caused by β-hemolytic streptococcus (erysipelas), as well as staphylococcus or other gram-positive bacteria and requires treatment with antibiotics.

Erysipelas should be differentiated from erythema migrans during nephrotic crisis. If painful migrating erysipelas-like erythema of various locations (usually in the abdomen, lower extremities) are accompanied by severe abdominal pain, often with peritoneal symptoms and decreased diuresis, then one can think about the development of the so-called nephrotic crisis - one of the initial manifestations of hypovolemic shock.

Nephrotic crisis is an abacterial complication of nephrotic syndrome, characterized by anorexia, vomiting and abdominal pain in the presence of anasarca and severe hypo-albuminemia, vascular collapse (hypovolemic shock). It is hypovolemia that is the main pathophysiological element of the nephrotic crisis. Nephrotic crisis should be differentiated from vascular thrombosis, which is characterized by severe pain, hemorrhagic rashes, thrombocytopenia, and corresponding changes in the coagulogram (a dynamic study of the coagulogram is mandatory for a patient with nephrotic syndrome).

AKI is an important, although rare, complication of nephrotic syndrome. It develops as a result of thrombosis of the renal veins, an acute crisis of local (renal) hypercoagulation, hypovolemic shock, in sepsis, during therapy with diuretics and NSAIDs, and the administration of large quantities of X-ray contrast agents. In children, the most common causes of acute renal failure are sepsis and thrombosis.

Cerebral edema in nephrotic syndrome occurs very rarely, usually at the height of the development of massive edema. It manifests itself as lethargy, lethargy of the patient, and can sometimes develop into a coma. The prognosis is serious. The condition requires immediate resuscitation measures. Retinal edema often develops in edematous patients. As general edema decreases and albumin levels increase, retinal edema decreases.

Vascular complications of nephrotic syndrome include peripheral phlebothrombosis, pulmonary embolism, thrombosis of the renal artery with the development of infarctions of its parenchyma. Finally, with nephrotic syndrome, taking into account the hyperlipidemia characteristic of these patients, atherosclerosis may accelerate with the development of coronary heart disease (CHD), myocardial infarction and strokes.

Long-term nephrotic syndrome, regardless of its cause, leads to the development of chronic renal failure. Persistent “large” proteinuria itself damages the renal structures - tubules and interstitium, causing interstitial inflammation and tubulointerstitial fibrosis. Moreover, the degree of damage and the risk of progression of renal failure clearly correlate with the amount of proteinuria. Once again, it should be emphasized that persistent “large” non-selective proteinuria is one of the main factors in the progression of chronic kidney diseases.

The first term is due to Teisser (1892), and the second is due to Stirling (1887). Robinson and Glenu (1964) showed that albumin release occurs in the supine position at a rate of 1.1 ± 1.0 mg/min and in the standing position at 12.0 ± 11 mg/min. This may be due to the fact that vasoconstrictor amines (L-norepinephrine and L-epinephrine) increase the protein concentration in the glomerular filtrate. In an upright position, due to slower blood circulation, more protein diffuses into the glomerulus, while at the same time, diuresis in an upright position decreases.

The importance of posture and excessive lordosis was demonstrated by Rowe and Soothill (1961), who found that a strictly upright posture released more albumin than a relaxed posture. Regarding the type of proteins released, Hartmann et al. (1959) showed that with mild proteinuria, albumin, transferrin and some γ-globulins were released; When concentrating urine, one can note the appearance in it of haptoglobin, ceruloplasmin, seromucoid and other larger molecular fractions. Greiner and Henry (1955), who did a lot to elucidate the pathogenesis of orthostatic proteinuria, showed that simultaneously caused skin hyperemia and bandaging of the extremities, worsening blood flow in the kidneys, lead to reversible oliguria and proteinuria. The pronounced position of lordosis by itself did not cause proteinuria, but in combination with peripheral hyperemia led to it. This proteinuria disappeared if blood flow to the heart was increased through massage. However, in 1955, Lowgren discovered another mechanism of orthostatic proteinuria - the admixture of protein-rich lymph into the urine as a result of pyelolymphatic reflux in the fornix area.

It is extremely important to determine the clinical significance of orthostatic proteinuria. In this regard, the progress of our knowledge came when it became possible to study the morphological changes occurring in this type of proteinuria using puncture biopsy. It is characteristic that in his 1951 review, Parkin comes to the conclusion that “postural proteinuria is not associated with any kind of kidney damage,” but already in 1959, King indicated that the nature of orthostatic proteinuria is organic in nature, and the latter is observed in persons recovering from glomerulonephritis, in patients with early stages of pyelonephritis, as well as in cases of renal vascular damage. He also presented the results of observations of 250 individuals with orthostatic proteinuria for 6 years. It turned out that in 90% of those examined it remained, and in 30% it became permanent. Undisputed kidney diseases were found in 1/3 of those examined. In a carefully conducted study, Robinson et al. (1961), based on 56 biopsies, came to the conclusion that with constant orthostatic proteinuria (15% of all subjects), it is based on anatomical changes in the glomeruli. In the transient form, 47% of the glomeruli were normal. Three years later (1964), the same author, having examined 5 biopsy specimens using electron microscopy, showed that protein loss in orthostatic proteinuria is the result of a focal defect in the basement membrane, which has not yet been identified anatomically. These abnormalities allow protein to pass through the wall of the glomerular capillaries under conditions of changes in renal hemodynamics when moving to an upright position, although the hemodynamic changes themselves do not differ from those in healthy people when changing position. Therefore, the issue is not in hemodynamics, but in the permeability of the renal filter to protein. This is also evidenced by the data that albuminuria in healthy people in a lying position was equal to 1.1±1.0 ү/min and in a standing position - 12-4-±11.9 ү/min, and for orthostatic proteinuria, respectively, 18 .0±8.0 and 160±820 u/min. In 1965, Mith found normal renal tissue during biopsy in only 31% of cases. Lecoeq et al (1966), observing 5 years of young men with orthostatic proteinuria, showed that it persisted in 70% of individuals, and 10% of them had diabetes, hypercalciuria or hyperuricemia.

In their monograph “Molecular Biology of Human Proteins”, Schultze and Heremans (1966) provide data on the presence of glomerular changes found on biopsy in 55% of cases of orthostatic proteinuria. Moreover, Herdman et al. (1966) suggested that orthostatic proteinuria may reflect nephrotic syndrome with minimal histological changes, and in these cases respond to steroid therapy, in contrast to orthostatic proteinuria after glomerulonephritis. In 1967, Morel-Maroger, Leroux-Robert, Amiel and Richet performed kidney biopsies in 33 patients with isolated proteinuria, including those with orthostatic proteinuria. In 12 of them, arterial damage was detected (fibroplastic endarteritis of the interlobular arteries, deposition of hyaline and fibrinoid in the juxta- and preglomerular arteries in combination with hyalinosis of the loops).

(slope test) is a method for studying and diagnosing the state of the cardiovascular and nervous systems. This simple test can detect problems in the regulation of the heart. The essence of the test is to transfer the body from a horizontal to a vertical position.

Indications for orthostatic test

It is prescribed to patients suffering from sudden changes in body position, dizziness, low blood pressure and even fainting. The orthostatic test is designed to record these sensations based on physiological characteristics.

Methods of conducting

Patient on a special inclined table

The test should be performed before meals, preferably in the morning. Perhaps the doctor will prescribe you to carry out tests over several days, then you need to carry them out at the same time.

The person being diagnosed lies down for at least 5 minutes, and then slowly rises to his feet. This method is called active orthostatic breakdown.

In addition, there is another option for conducting an orthostatic test, which is called an inclined test - this is passive orthostatic test. In this case, the person being diagnosed is placed on a special rotating table. The technique itself is the same: 5 minutes in a horizontal position, then quickly move the table to a vertical position.

During the study, the pulse is measured three times:

• (1) in a horizontal body position,
• (2) when rising to your feet or moving the table to a vertical position,
• (3) three minutes after transition to a vertical position.

Evaluation of results

Based on the heart rate values ​​and their difference, conclusions are drawn about the functional state of the cardiovascular system.

The norm is an increase in heart rate of no more than 20 beats per minute. It is permissible to reduce the upper pressure (systolic), as well as a slight increase in the lower (diastolic) pressure - up to 10 mm Hg. Art.

1. If after rising to a vertical position your heart rate increases at 13-16 beats per minute or even less, and then after three minutes of standing it has stabilized to +0-10 beats from the initial (measured lying down), then your orthostatic test readings are normal. In addition, this indicates good training.
2. Greater change in heart rate (up to +25 beats per minute) indicates that the body is poorly trained - you should devote more time to physical exercise and a healthy diet.
3. Increase in heart rate by more than 25 beats per minute indicates the presence of diseases of the cardiovascular and/or nervous systems.

« Healthy heart» / Published: 02.21.2015

If you are involved in medicine or sports, then you already know that this procedure is associated with changes in pulse and pressure in the circulatory system under the influence of changes in the position of the body in space. But how and why does our heart rate change, and how can athletes benefit from an orthostatic test?

This question remains open for many. So let's figure out what is really happening to our body, causing such a sharp change in heart rate, and how, by making daily observations, any athlete can determine even hidden indicators of overtraining and overload of the autonomic nervous system.

When our body is in a horizontal position, the forces of gravity act approximately equally on all its parts, and with a sharp change in position to a vertical one, blood outflows from the upper parts of the body and deposits (stagnation) of that same blood in its lower parts. The degree of severity of the body's reaction, expressed in changes in heart rate and pressure, indicates its current condition.

Reasons for measuring heart rate

If the blood stagnates in the veins of the legs that are large enough in volume, it returns to the heart far from being in its full composition. And our main circulatory organ needs to compensate for the lack of blood return in order not to disrupt the normal trophism (nutrition) of various tissues and organs of our body.

Since the flow of venous blood is not enough, an increase in heart rate becomes a compensatory mechanism, that is, the heart begins to work faster, hence the increase in pulse.

In sports, the orthostatic test is an extremely important indicator of the stability of the cardiovascular system under load, and if minor instability is acceptable for young athletes, then in the case of adult athletes there are no such concessions.

A sharp rise is stressful for our body, so the centers of the sympathetic department of the autonomic nervous system are overexcited. This is the department that monitors the state of our internal organs in stressful situations. Due to its excitement, the neurotransmitter norepinephrine is released into the blood, which also helps to increase heart rate.

Depending on the fitness of the athlete’s body and general condition autonomic nervous system, orthotest indicators will deviate significantly or within normal limits. Thus, with minimal time and effort, it is possible to quickly diagnose the condition of athletes by analyzing pulse rate and pressure. More accurate data on sympathetic arousal is shown by studying heart rate variability (HRV or HRV) using specialized applications.

Test methods

There are the following methods for conducting an orthostatic test:

Active orthostatic test

The first, and most common among athletes, is an active orthostatic test. The idea is that they first take measurements in the person’s normal state, then measure the indicators while the person is in a horizontal position, after which the subject changes the position to a vertical one and the pulse is measured in a vertical position of the body over the next 3-5 minutes. Usually, the test is carried out in the morning, immediately after waking up.

Controlled test

The second, and most common among medical workers. It is used if there is a risk of fainting due to a sudden change in position.

This type of orthostatic test is also carried out first in a standard position, then in a horizontal position, but measurements of the vertical position are carried out much more interesting than in the first method. If, as mentioned above, a person has a risk of fainting, then the risks should be minimized, so the subject is tightly attached to the bed and, instead of actively rising, the position of the bed is changed, measuring the pulse immediately and 3 to 5 minutes after rising. The violation of the accuracy and meaning of the study is minimal, because the change in gravitational forces remains the same, only the action of the muscles changes. An example in the picture for clarity.

Modified orthostatic test

And the third, modified orthostatic test, is suitable for weakened people. The technique is almost identical to the active orthostatic test, but the distinguishing factor is that the subject stands at a distance of one foot from the wall on which he rests his back. With this research method, in order for the patient to achieve a state of significant relaxation, a roller with a diameter of 12-14 cm is placed under the sacrum, due to this the angle of inclination becomes approximately 75-80 degrees, as a result of which the required body position is achieved

Taking measurements

Measurements in the orthostatic test can be carried out either by classical heart rate measurement (on the wrist, on the carotid or femoral arteries), or using heart rate monitors, the functions of which, today, are found in smart watches, smart bracelets and applications.

In practice, working with an orthostatic test does not end with getting your heart rate (HR) three to four times in a week; you must be able to correctly evaluate the results obtained. To do this, you need to rely on normal pulse and blood pressure values.

Norm and results of pulse measurement

Normal heart rate is 60-80 beats/min. Changes in heart rate when changing position can be assessed at the following levels:

• from 0 to +10 can be considered an excellent result
• from +11 to +16 – good
• from +17 to +22 – normal
• more than +22 – already unsatisfactory

Deviations in the negative direction (i.e., slowing of the pulse during an orthostatic test) are also considered an unsatisfactory result.

Norm and results of pressure changes

The normal deviation of systolic pressure (first indicator) is a deviation from 0 to +20

The normal deviation of diastolic pressure (the second indicator) is also a deviation from 0 to +20

For clarity, let's look at an example:

During the active test, the heart rate increased by 19 beats per minute, which corresponds to normal values

In addition to measuring heart rate, the minimum and maximum blood pressure was measured in both tests. Deviations above the norm are not observed; the subject has close to normal fitness of the cardiovascular system.

To save time, it is recommended to take blood pressure measurements once a week. Orthotest measurements of heart rate - at least 3-4 times a week in the active phase of the training cycle.

The study of orthostatic stability is quite simple and requires minimal costs, both energy and material.

• An orthostatic test is strongly recommended for athletes, especially for those whose sport is associated with changes in body position in space (artistic gymnastics, rhythmic gymnastics, acrobatics, trampolining, diving, high jumping, pole vaulting, etc.)
• Also, an orthostatic test is often performed by those people who are trying to maintain the condition of varicose veins in good shape, thereby monitoring the effectiveness of training and other procedures.
• Everyone else who cares about their own health is recommended to regularly carry out an orthostatic test, and the mechanism of its implementation is so simple that everyone has the opportunity to conduct an orthostatic test at home,

If we take into account the number of devices that facilitate an already fairly easy study, take for example various kinds of “smart” watches like the Polar smart watch, then this study becomes tantamount to prevention.

How to take measurements

When starting data collection, six baseline measurements must be completed over a period of no more than two weeks. Take the average. This is your baseline. It should be understood that basic orthostatic tests should be performed during normal training weeks. It is advisable to avoid ultra-intense workouts to which your body is not yet accustomed.

Once baseline data has been obtained and a baseline has been established, it is recommended to continue testing at least two to three times per week. This way, if there is a sudden change in training volume or intensity, you can compare the new orthotest values ​​with the normal level and determine the level of your overtraining. A heart rate deviation of more than +25 points (while maintaining all initial conditions) is a clear signal of under-recovery of the body.

An orthostatic test is performed in the morning, on an empty stomach, immediately after waking up. It is advisable to take key measurements after a recovery day (deviation should be minimal) and after a training day (higher deviation is expected). You can also do research before and after your workout. Tests in the absence of training or with irregular training may not be reliable enough. After a break of two or more weeks, it is recommended to re-establish the initial (basic) indicators

During the test itself, you must lie or sit quietly. Remember, for subsequent trials, you should have the same starting position as the previous times.

The advantage of such watches is that they allow you to test them at home, in the gym, at work and in other places convenient for you. The only important thing is that nothing should disturb you at the time of the study; you should exclude any distracting factors, such as sounds, smells, flashes of light and even people.

2-3 hours before the procedure, stop smoking, food and alcohol. It is recommended to carry out the test regularly and at the same time, then you can achieve more accurate results.

Methods of taking measurements using modern means

In modern conditions, an orthostatic test can be carried out using a watch with a built-in heart rate monitor, specialized applications on a smartphone, and other available cardio sensors.

Using a smart watch

Let's look at the step-by-step instructions using a Polar watch as an example. Sample collection is similar in other models.

Select Tests > Orthostatic test > Relax and start measuring

The display shows the following message: Heart rate determination. After determining your heart rate, a message will appear on the display: Take a lying position and relax.

• As your heart rate begins to graph on the screen, relax and try to remain still for three minutes.
• Then, 3 minutes after the start of the orthostatic test, the watch will emit a sound signal and the message “Stand up” will appear on the display.
• You must remain upright for the next three minutes.
• After the end of the second stage, the watch will again signal with a sound signal that the orthostatic test has been completed.

If the test has to be interrupted, you can take the test again. Click the “back” button to cancel this procedure.

How to choose a watch

• Choose a watch with a heart rate monitor.
• Assess the requirements you place on the device. If you are new to sports, do not overpay for the brand and extra functionality, take the basic model.
• Please note additional features. Such as GPS, altimeter or maps. For some this will be a necessity, but for others it will be a pleasant addition at the right time. Consider the brands Garmin, Polar, Suunto, Sigma.

Smart watch Polar V800 H1

This model is perfect for serious sports. A nice addition will be to protect the watch from impacts, scratches, water, snow and other damage. They hold a charge for up to 30 days. Suitable for both cyclic and strength training and endurance training.

As for the medical stuff, Polar V800 allows you to take orthostatic tests, determine the maximum oxygen capacity (VO2max), calculate the R-R intervals of the cardiac cycle (HRV) and much more.

Polar 430 sports watch

The device uses the most accurate optical heart rate monitor in its class, which allows continuous heart rate monitoring. The watch weighs only 51 grams and holds a charge for up to 10 days. The Polar Flow system contains training programs for races of 5, 10 km, half marathon or marathon, which are scheduled for every day for 2-3 months. The system also makes it possible to create a personal training plan with the ability to further track progress.

Just like the previous model, it allows you to track aerobic running efficiency and maximum oxygen consumption (VO2max). Analytics of sleep duration and quality is also available. A nice addition is the built-in GPS system.

Using mobile applications

If you still haven’t decided on the need to buy a sports watch, but want to control your health indicators now, you can use alternative methods. Namely, applications that will always be at your fingertips.

Today, there are already many applications that can quite accurately read a person’s pulse using a camera directly from the tip of the finger. Here are some of them:

Runtastic Heart Rate Pulse and Heart Rate

This application will allow you to find out your heart rate in any place convenient for you. The application also has a statistics function, thanks to which you can track your data

Unique Heart Rate Monitor

The application allows you to read your pulse and immediately enters the result into statistics, asking you what state you were in, taking measurements, be it rest, training or time after training. A nice addition will be the ability to leave a comment for each result.

Azumio Heart Rate Monitor

The application is entirely in English. Compared to the previous ones, it takes a little longer to read the pulse. It also allows you to leave notes for each result.

Blood Pressure History

There are applications that have the function of reading pulse and pressure at the same time, for example Blood Pressure History

Like the previous one, this application is entirely in English, but the functionality can be understood even with complete ignorance of the language. Calculates systolic, diastolic pressure and heart rate by touching the phone screen with your finger. Keeps a history log of your past measurements.

Well, the last application that we would recommend to those who want to get more serious sports indicators on the screen of their smartphone

HRV4Training

The application is paid, but by downloading it, you will receive not only more accurate indicators, but also the possibility of both classical and orthostatic
data collection. Plus, the program has the ability to synchronize with the training log in other applications. But you must understand that you can only get the full range of functions if you have an HR heart rate monitor

With this set of knowledge about the orthostatic test and how to take its measurements, you are fully prepared for self-diagnosis and better training.