MULTIPLE CHRONIC KIDNEY DISEASES

MULTIPLE CHRONIC KIDNEY DISEASES

Choriyeva Zulfiya Yusupovna

choriyevaz69@gmail.com

Toshkent tibbiyot akademiyasi Termiz filiali Anatomiya va klinik anatomiya

kafedrasi katta o'qituvchisi

Alimova Feruza Shokirovna

feruzaalimova038@gmail.com

Toshkent Tibbiyot akademiyasi Termiz filiali talabasi

Jumayeva Karomat Rustam qizi

jumayevakaromat80@gmail.com

Toshkent Tibbiyot akademiyasi Termiz filiali talabasi

Xodjamqulova Subhida Nizom qizi

subhidam112233y@gmail.com

Toshkent Tibbiyot akademiyasi Termiz filiali talabasi

Ahmedova Saltanatxon Bahromjon qizi

doctormobile551@gmail.com

Toshkent Tibbiyot akademiyasi Termiz filiali talabasi

Abstract: Kidneys perform a very important function in the body. One liter of blood passes through them in a minute, it is constantly cleaned of toxins and harmful substances. It produces biologically active substances, in particular, renin, which regulates blood pressure, and erythropoietin, which regulates the rate of formation of erythrocytes. It helps to control the water balance and the concentration of minerals such as sodium, potassium, and phosphorus in the blood. This article provides information about common kidney diseases and their treatment methods.

Key words: Kidney diseases, Bright's disease, nephrology, urology, glomerulonephritis.

Kidney diseases are different. Richard Bright began systematic study of this disease in 1872, he determined that swelling in the body, excretion of protein along with urine, is due to primary disease of the kidneys. A group of kidney diseases characterized by a number of symptoms in the form of albuminuria, hematuria and cardiac hypertrophy later became known as Bright's disease. The expansion of knowledge in the field of etiology and pathogenesis of kidney diseases, the application of methods of modern physiology, nephrology, biochemistry, immunology, urology, and pathological anatomy led to the revision of several basic rules and concepts of Bright's nephrology. Moreover, there have been changes in the structure of kidney diseases since Bright's time (nosomorphosis). Cases of acute nephritis have decreased significantly, but pyelonephritis, immune-related kidney diseases, and metabolic nephropathies have increased. Kidney diseases related to heredity, as well as due to the effects of drugs, have also increased to some extent.

Kidney diseases in men and women include various pathologies that prevent the normal functioning of these organs of the urinary system. Each of the kidney diseases has its own characteristics, different clinical manifestations and treatment methods. In fact, many kidney diseases are asymptomatic, that is, without symptoms, and patients do not know about existing problems with their health. Therefore, it is important to understand what the main diseases of the kidney are, to know their symptoms and treatment. Often, the patient accidentally finds out that he has a missed stage of kidney disease, he came to the doctor complaining of a completely different problem. Doctors even call the kidneys "dumb organs" among themselves, because the first symptoms of the disease appear only when the kidneys fail in some cases.

Of course, doctors can suspect the presence of the disease during a blood analysis, but for this, this analysis must be in the hands of a nephrologist, which happens very rarely. In most cases, patients first find out about this type of doctor when they are admitted to the hospital with a diagnosis of myocardial infarction. The kidneys perform various functions: 1) they help to remove metabolic products from the blood; 2) participates in exchange processes; 3) manages blood plasma stability and alkaline balance; 4) participates in the management of arterial pressure. Endothelial cells of the glomeruli, visceral epithelial cells with a basement membrane, Shumlyansky-Bowman capsule participate in the filtration process that takes place in the glomeruli and leads to the formation of primary urine. The total filtering surface of the ball is 1 m2. About 200 l of tissue fluid is filtered during one night. Because the pores in the membrane of the ball are very small, high-molecular substances cannot pass through the filtration site. Mesangium is also important, it traps and breaks down immune complexes.

Glomerulonephritis is the primary kidney disease that is the most important problem in nephrology because it eventually leads to chronic kidney failure. In addition, this disease is of great importance as a medical and social problem. Because people with this disease get sick more often during their prime and most of them die before reaching 40 years of age. Currently, glomerulonephritis can be considered as a disease that passes with the onset of mainly immunological damage of vascular balls and subsequent bacterial inflammation (that is, inflammation due to immunity in nature).

Nephrotic syndrome is characterized by the onset of severe proteinuria as a result of increased glomerular filtration, followed by hypoalbuminemia, hyperlipidemia, and diffuse swelling of the body. Nephrotic syndrome is caused by damage to the basement membrane of the glomeruli, which is a barrier that does not allow protein to pass from tissue fluid to urine. In most cases, the basement membrane is thickened and stained with SHIK-reactive, and remains clearly visible when viewed with a simple optical microscope (membranous glomerulonephritis). Its thickening is mainly caused by immune complexes coming to it from the visceral epithelium. At the same time, there may be no inflammatory reaction. Sometimes, when the nephrotic syndrome is significant, no structural changes can be found in the basal membranes even when examined with an electron microscope. In such cases, it is believed that the increase in permeability of the basal membrane depends on the physico-chemical alteration of this membrane. However, at the onset of nephrotic syndrome, podocyte peduncle growths are destroyed in all cases, which leads to a decrease in the number of perforations, especially in the peripheral loops of capillaries. The nephritic syndrome is characterized by the onset of hematuria, decreased glomerular filtration rate, various degrees of oliguria, azotemia, and hypertension. Nephritic syndrome begins at the site of pathological processes that occur with the beginning of a proliferative inflammatory reaction in the glomeruli. At the same time, proliferation is observed in various cell elements in balls: endothelial, mesangial and epithelial cells. Such proliferative inflammation can continue with the infiltration of capillaries, Shumlyansky-Bowman's capsule space, and sometimes perglomerular interstitium with neutrophils in some cases. Chronic glomerulonephritis is associated with uremia, which can lead to many disasters. The predominant morphological sign of such glomerulonephritis is hyalinization of the glomerulus. Such hyalinization is due to the accumulation of homogenous eosinophilic substance, which resembles the basement membrane and mesangial matrix, between the loops of the capillary and in the membrane itself. In the process of hyalinization, the path of the capillary narrows or becomes closed.

The etiology of most types of glomerulonephritis has not been determined. At the same time, a consistent theory based on the pathogenesis of glomerulonephritis, especially immune mechanisms, has been developed. Two main types of immunological damage of the balls have been identified: 1) damage of the balls as a result of accumulation of soluble antigen-antibody complexes circulating in the blood (immunocomplex disease); 2) damage to the glomerulus from antibodies (autoimmune antibody glomerulonephritis), these antibodies can affect the glomeruli in two ways: a) in situ with antigens that are insoluble, settled, including those settled on the glomerular basement membrane reacting or b) reacting with antigens circulating in the blood, in which the resulting immune complexes are then deposited on the wall of the kidney filter. Determining the nature of the antigen is difficult and a matter of great interest, but there is also the fact that the nature of the characteristic antigen for some types of glomerulonephritis is still unknown. It is now assumed that there are two main types of antigens: endogenous and exogenous antigens. The first of these include antigens found in lupus-nephritis or G immunoglobulins found in rheumatoid arthritis, renal tubule antigens, tumor antigens. Exogenous antigens are divided into viral antigens, bacterial, parasitic, fungal antigens, and iatrogenic ("drugrelated") antigens. Among them, beta-hemolytic streptococcal antigen, Coxsackie virus, hepatitis V virus, treponema, malaria plasmodium, and worm antigen are the most common. Antigens related to drugs, levamisole, rifampin, and antigens related to the effect of analgesics should be mentioned.

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