The development of pneumonia in patients with CLL is promoted by acute viral respiratory diseases. In the overwhelming majority of cases, pneumonia begins as focal, less frequently as lobar. However, pneumonic focus tends to spread rapidly. Often, having begun as a one-sided, pneumonia quickly spreads to another light. Pneumonia in CLL may be the first clinical symptom of the disease . Repeated pneumonia occurs in 75% of patients with CLL . The state of health of patients is sharply worsening. A patient with full somatic compensation for several hours turns into an extremely serious patient. Extrapulmonary manifestations of pneumonia predominate – fever, chills, tachycardia. . Dyspnea predominates among pulmonary manifestations. Often the disease makes its debut with a picture of endotoxic shock . Septicemia and septic shock are leading as causes of mortality among hospitalized patients with leukemia and lymphomas . The cause of septicemia can be enterococci, streptococci , or pyocyanic stick . The latent version of pneumonia in patients with chronic lymphoproliferative tumors has to be differentiated with specific tumorous lesions of the lungs .

L. Rome et. al. (2001) identified factors that contribute to the protracted course of community-acquired pneumonia . Among them, CLL patients are characterized by at least 7 factors: elderly age, the presence of a tumor neoplasm, suppression of T-cell activity, a decrease in the level of IgM, prolonged therapy with cytostatics, systemic glucocorticoids, and the presence of concomitant pathology.

Particular attention is paid to the occurrence of hospital pneumonia in patients with CLL. Nosocomial pneumonia develops in 37.1% of hospitalized hemoblastosis patients and in more than 60% of cases is fatal . Hospital pneumonia is distinguished by a large variety of etiological agents, including gram-negative flora (enterobacteria, pseudomonas bacillus, acinetobacter, etc.) and Staphylococcus aureus, which largely accounts for their severe course . Infectious complications in the hematological clinic often have the character of public- acquired infections. In specialized hematology hospitals, where patients with pronounced immunosuppression and new pathogenic pathogen pathogens appear, very often flare up “epidemics” . Therefore, it is considered necessary to hospitalize CLL patients in hospitals only for life reasons .

It should be borne in mind that in CLL, due to the lack of granulocytes in the tissues of pneumonia, a limited inflammatory focus is not always formed, giving a clear physical and X-ray picture even from 2 to 4 days after the onset of pneumonia . According to M.A. Volkova, only in 6% of patients with complicated, especially in the initial period, the course of CLL on radiographs of the lungs showed inflammatory foci. Computer tomography contributes to more accurate diagnostics . It is quite obvious that in CLL, the problem of improving the methods of early diagnosis of inflammatory and leukemic lesions of the bronchopulmonary system, contributing to the most effective treatment of complications, is relevant.

Oikonomou et al. examined radiological manifestations of influenza viral pneumonia in hematological patients. The patients underwent radiographs and high resolution computed tomography (CT). The authors developed pneumonia on the basis of the analysis of X-ray and CT images. Demonstrated new features in the diagnosis of this pathology using CT .

In 60–70 years, Gram-negative, aerobic bacteria were the main causative agents of infection in CLL patients; at present, gram-positive bacteria have become frequent pathogens, and erobic cocci and fungi . According to A. B. Bakirova (1996), among identified microorganisms in lymphoproliferative diseases of microorganisms, 51.9% were gram-negative, 48.1% gram-positive bacteria and yeast-like fungi. At that, 57.7% – streptococci, 22.8% – staphylococcus, 21.9% – Pseudomonas aeruginosa, 19.9% ​​- yeast cells, 13.6% – Klebsiella, 12.7% – Neisseries, 9.6% – Enterobacteria, 14.8% – Proteus, intestinal strand, cytobacteria and serrations. Recently serѐznoy The problems of in hematological patients and are nvazivnye mycoses . In most cases, it is candida and aspergillosis . Less commonly, invasive mycoses can be caused by other micromycetes . G.A. Klyasov et al. (2007) developed an algorithm for the treatment and prevention of candidiasis and aspergillosis in adult patients with leukemias, lymphomas and blood formation depressions .

Microbial strains isolated from patients with tumors are often characterized by multiple resistance to antibiotics . Antibiotics that are effective against gram-negative aerobic microorganisms and, above all, Escherichia coli, Klebsiella pneumonis, Ps, are used as first-line drugs of empirical antibiotic therapy. aeruginosa. This is due to the fact that infections caused by gram-negative aerobic bacteria are the most rapidly developing and dangerous bacterial shock. The mortality caused by these pathogens is 50–70%. . The most commonly used combinations are aminoglycosides II – III generation (tobramycin, sisomycin, amikacin) with cephalosporins III – IV of the generation active against the pseudomonas aeruginosa; a positive result is observed in 70–78% of patients . The combinations of III – IV generation cephalosporins with ureidopenicillin ( mezlocillin, piperacillin) have proven themselves well . Combined therapy with III-IV generation cephalosporins and imipenem is most effective against gram-negative bacteria, including Ps. aeruginoza . In a comparative study of vancomycin and a glyco- peptide antibiotic — tekop lanin, some researchers have come to the conclusion that teikoplanin ef vancomycin is more effective and less nephrotoxic [34]. Inpatients with hemoblastosis during the development of infectious complications , manifested by fever of not clear genesis, many authors of the rivers recommend to start antifungal therapy with amphotericin B, fluconazole as early as possible . In recent years, it proved high, comparable with the results of treatment with amphotericin B, Klinichev eskaya and antimycotic effectiveness ciency and trakonazola fluconazole in the treatment of fungal invariant fektsy Wu Bo lnyh hematological malignancies . G.A. Klyasov developed a protocol for empirical antibiotic therapy in patients with hemoblastosis, which consists of 4 stages, taking into account the chemotherapy and The focus of infection . This treatment protocol is currently used in most hematological clinics in Russia.

Much attention in the modern literature is given left-most cheniyu serѐznogo complications of pneumonia in patients with hemo blastosis – acute respiratory failure spine .

In addition to pneumonia in CLL, on the background of pronounced immunodeficiency, especially under the influence of active cytostatic and hormonal therapy, pulmonary tuberculosis is often diagnosed . Tuberculosis infiltration in the lungs during granulocytopenia is not always radiologically detected, not to mention the ulcer that is not detectable radiographically, ulcerous bronchoadenitis . The greatest diagnostic difficulties are posed by the differential diagnosis of pneumonia of the following forms of pulmonary tuberculosis: infiltrative pulmonary tuberculosis, limited to 1-2 segments (broncholobular infiltration); infiltrative pulmonary tuberculosis, limited to one lobe (rounded, cloud-visible infiltration, pericyssuritis and lobitis); Kaze pneumonia .

In 1991 A.G. Chuchalin described the damaging effect of cytostatic drugs on the lung tissue. According to A.N. Soko lova et al. (2007), such cytostatics used in the treatment of CLL, such as cyclophosphamide, chlorambucil, fludarabine, doxarubicin, and vincristine, have a pulmonary toxicity. V.M. Gorodetsky (1998) indicates the need for differentiation between infectious, specific lesions of the lungs in patients with hemoblastosis and pneumonitis caused by chemotherapy or radiation therapy. Since cyclophosphamide, which is often used in the treatment of CLL, reduces the level of glutathione and thereby reduces the degree of antioxidant protection, a high concentration of oxidants stimulates pulmonary damage . So far, there are no uniform criteria for predicting the pneumotoxic risk of chemotherapeutic drugs; The most informative is considered to be a rapid decrease in the diffusion capacity of the lungs at the initial stages of chemotherapy, even in the absence of significant changes in radiographs and CT scans of the lungs. . The frequency of radiation pneumonitis during irradiation of the chest is 5–15 % . Risk factors for left-of pulmonary damage during radiation exposure are involved a large amount of light (> 10%), the daily dose of radiation (> 2,67 Gy), high cumulative dose of concomitant chemotherapeutic Pius, lung collapse, young age, cancellation of glucocorticoid hormones in radiation therapy time .

One of the most severe manifestations of chronic lymphocytic leukemia is exudative pleurisy. Its nature can be different: a couple or metapneumonic pleurisy with a banal infection, tuberculosis pleurisy, lymphatic infiltration of the pleura, compression or rupture of the thoracic lymphatic duct. Infectious pleurisy is most often a complication of pneumonia . In the exudate, along with lymphocytes, there are many neutrophils . In case of compression or rupture of the thoracic lymphatic duct, the exudate will be lymphatic, but the fluid will contain large amounts of fat a (malignant fluid) .

The most frequently encountered specific lymphoproliferative pleurisy as a manifestation of lymphoid pleural infiltration . Diagnostics of lymphoproliferative pleurisy is supported by computed tomography. With CT, it is often possible to detect tumor growth in the pleura, infiltration or sarcoma nodes . The treatment of specific lymphoproliferative pleurisy is complex and long-term, its adherence is an unfavorable prognostic factor for CLL patients. Topical administration of cytostatic preparations is usually not very effective . The best results are given by the general cytostatic therapy according to the schemes COP, CHOP; sometimes it is necessary to resort to irradiation of the pleura (tangentially); with a sharply enlarged spleen, splenectomy can lead to the elimination Pleurisy for many years .

In the literature, there is a small number of works covering the course of chronic obstructive pulmonary disease (COPD) in patients with chronic lymphoproliferative diseases. V.M. Provotorov and A.Yu. Kazabtsov (1997) examined patients with COPD with concomitant lymphoproliferative diseases – CLL, lymphocytic lymphoma, and myeloma. The authors concluded that in patients with COPD on the background of chronic lymphoproliferative tumors, a violation of the tracheobronchial cleansing is more pronounced than in patients with COPD without lymphoproliferation. The course of COPD, when combined with lymphoproliferative diseases, is characterized by slow dynamics of clinical symptoms and a more severe course [204]. A.Yu. Ka- zabtsov (1998) found that in patients with COPD on the background of CLL, a violation of mucociliary transport is more pronounced than in patients with COPD without concomitant lymphoproliferation.

Much attention is paid to immunomodulatory therapy for CLL . It is necessary to conduct therapeutic and recreational activities for all related diseases in patients with CLL in an outpatient setting, as well as the appointment of prophylactic immunostimulating therapy in the autumn-spring period. Timely prevention and treatment of infectious complications in CLLs contributes to the prolongation of life of these patients .

Multiple myeloma (MM) is a lymphoproliferative disease, the morphological substrate of which is plasma cells that produce monoclonal immunoglobulin . MM is known as “elderly disease”, the average age at the time of diagnosis is 61 years . MM has a large variety of forms and options. Each of these options has its own clinical manifestations and requires special therapeutic approaches. Klee Niko-anatomical classification is based on radiological examination of the skeleton, morphological analysis of punctates and bone trepanates. Diffuse-focal (60% of observations), diffuse (24%), multiple-focal (15%), sclerosing (<1%), mostly visceral (<0.5%) forms of MM are distinguished. Immunochemical studies of monoclonal secretion of serum and urine Ig determine the immunochemical variant of MM. Myeloma G is the most common (55–65% of all cases of multiple myeloma), myeloma A is in second place (20–25%), Bens-Jones myeloma is in third place (secretion of light chains only) 12–20%), rare forms of the disease are myeloma D, E, M, non-secreting, diclonal myeloma.Depending on the size of the tumor mass at the time of the study there are three stages of MM; An additional feature of all stages, which determines substage (A or B) is the function of the kidneys . Staging MM by B.Durie and S.Salmon (1975) is generally recognized. MM remains an incurable disease . From 20 to 40% of patients are insensitive to chemotherapy treatment (primary resistance), in all patients sensitive to chemotherapy, secondary resistance to previously administered therapy develops at different times . When MM poly- primary pathological secreting IgA resistance occurs in the pa 2 for more than myeloma G . In recent years, an increase in the incidence of MM has been observed throughout the world, only partly due to the success of diagnostics and Life expectancy . With the introduction of melphalan into medical practice, the average life expectancy of a large MM has reached 36 months . Attempts to increase the life expectancy of patients with the help of various polychemotherapy schemes were not crowned with success . High-dose chemotherapy, followed by transplantation of autologous stem cells, is considered the most effective method for treating MM . The use of autologous transplantation allowed us to increase the median survival of myeloma patients to 54.4 months . However, taking into account the age structure of the patients and the complicated somatic status, this method is not applicable to all . Therefore, for a large cohort of patients with MM, even in economically developed countries, standard therapy remains the method of choice . In our country, the majority of patients receive chemotherapy without subsequent transplantation of stem cells . In addition to pathogenetic patience, the program for treating patients with MM includes: for the prevention and treatment of hypercalcemia, the improvement of the repair of bone destruction bisphosphonates ; in the presence of anemic syndrome, erythropoietin ; with a high content of protein in the serum of Crimea, plasmapheresis , etc.

According to O.A. Rukavitsin and GI Sidorovich (2006) at the time of diagnosis of MM, most often there is damage to the respiratory organs and urinary tract infections, usually they are caused by S. Pneumoniae and H. Influenzae, as a result of staphylococci and gram-negative flora begin to predominate; High-dose chemotherapy, accompanied by prolonged neutropenia, and steroid treatment promote the development of a fungal infection [211]. At different periods of MM, the risk of developing bacterial infections is not the same: in the initial phase of the disease, it is 4 times higher than in remission; and in the first two months of chemotherapy 2 times higher than during the rest of the time . Patients with MM, as well as all patients with chronic lymphoproliferative tumors, are subject to repeated respiratory infections, especially pneumonia, which are one of the main causes of mortality in this pathology . The incidence of pneumonia in patients with MM is associated with a decrease in the function of humoral and cellular immunity . In addition, susceptibility of MM patients to infections is due to activation of endogenous infection, expansion of the entrance gate for microorganisms due to damage to the skin, mucous membranes, prolonged catheterization and central veins . Especially such complications are observed during high-dose chemotherapy or after bone marrow transplantation, when the body is weakened due to both the tumor disease and the use of aggressive chemotherapy programs . In patients with chronic renal failure (CRF), the likelihood of the addition of infectious complications increases. At the same time, any infection in MM patients can lead to the development of acute renal failure .

An important factor predisposing to the lung localization of infectious processes in MM is the pathoanatomical basis of the lesion of the lungs in this disease, designated O.V. Voyno-Yasenetskaya as “pulmonary-alveoli bright paraproteinosis” . O.V. Voyno-Yasenetskaya concluded that plasma hyper-viscosity, proteinaceous intravascular stasis with an increase in the permeability of the basement membranes and increased filtration of the protein into the alveoli underlie the aerohematic barrier and lead to lysis of the elastic framework of the lung. The release of paraprotein into the septal spaces causes proliferation of septal cells and a pronounced macrophage reaction, as well as impaired lymphatic drainage, with a consequent increase in hydrostatic pressure in the capillaries. There is a deposition of three types of substances in the tissues: amyloid, amyloid-like and crystalline. The basis of pulmonary alveolar paraproteinosis in MM is the deposition of amyloid-like substance, filling of part of the alveoli with amyloid-like bodies , “hyalinosis” of membranes. Per Primary is the lesion of blood vessels (primarily capillaries) and interalveolar septa. Circulatory impairment at the level of the aerohematic barrier leads to dystrophy of the lung skeleton and emphysema, which later becomes compensatory in nature due to the shutdown of the part of the alveoli filled with the proteinaceous polysaccharide substance. The most significant changes were observed in myeloma A. Amyloid-like deposits were found in the walls of the pulmonary vessels, in capillaries, alveolar septa, septal spaces, alveolar epithelium, alveolar lumens, from vessels, walls of arterioles .

Manifestations of pulmonary alveolar paraproteinosis in MM patients were studied in the works of many authors . M.M. Ilkovich (2007) notes an important morphological difference between primary alveolar proteinosis (AP) and secondary proteinosis (found in hematological patients): during primary AP, there is a uniform staining of CHIC-positive substance in the alveoli, for secondary proteinosis it is characteristic granular staining; An additional diagnostic test is the reaction with immunoperoxidase. At present, the phenomenon described by OV Voeno-Yasenetsky as a tissue paraproteinosis is called NAMIDD syndrome (non-amyloid deposition in the tissues of monoclonal L and H chains or whole molecules of immunoglobulins) . Unlike amyloidosis, NAMIDD deposits have an amorphous non-fibrillar composition and are not detected by histological methods adopted for the diagnosis of amyloidosis .

Amyloidosis in MM is detected on average in 10–15% of patients. At the same time, according to GF. Grandma (1987), the deposition of amyloid masses in their lgk was detected in 26.3% of cases . In most patients, vessels and alveolar septa are involved in the process, which is clinically manifested by shortness of breath . X-ray examination of specific recognition can not be detected .

The susceptibility of patients with MM to bronchopulmonary infections is promoted by specific myeloma plasma cell filtration, as determined by G.A. Alekseev and N.E. Andreeva (1966) as a “myeloma light” [20]. Histological examination of the lungs shows a significant infiltration of lymphocytes and plasma cells of interstitial tissue, inter-alveolar septa, peribronchial spaces. Sometimes in bronchial cartilage and interstitial tissue there are multiple calcified foci of calcification .

Specific changes in the respiratory apparatus in MM can be divided into the following options.

1. Diffuse myelocytic cell infiltration of the lung tissue (pulmonary plasmacytosis) or the formation of individual tumor nodules in the lung tissue .

2. The lesion of the bronchi is usually combined with the lesion of the lung tissue. Lesions are revealed along the course of the large bronchi, in the peribronchial spaces ah, under the bronchial mucosa . A tumor is protruding into the lumen of the bronchus, which has grown through the wall of the bronchus, moving apart normal tissue structures and spreading further to the lung tissue along the bronchioles and between the alveolar septa .

3. Pleurisy with MM are rare . Ss Bessmaltsev and K.M. Abdulkadyrov (2004) described a case of myeloma lesion of the lung with the development of exudative pleurisy in a patient with diclonous (IgG, IgA) myeloma. Pleural sheaths in MM are rarely affected . Clinically, myeloma pleurisy is characterized by unilateral or bilateral hemorrhagic effusion. Cytological examination revealed a large number of atypical plasma cells . Biochemical and electrophoretic examination of the pleural fluid sometimes makes it possible to detect paraprotein in it .

4. Tumors of the ribot, for the second time affecting the respiratory apparatus or squeezing the corresponding zones of the lung tissue, can come from any rib, usually destroying it, while they squeeze the adjacent zones of the lung tissue and create an x-ray effect of the “ lung tumor” . Vidal et. al. (1969) described a tumor weighing 550 g emanating from the rib and accompanied by pleurisy. The destruction of the ribs in MM takes one of the first places among the tumor lesions of the chest cell .

5. plasmacytoma upper airway can was placed a throat, larynx, nasopharyngeal space, trachea, interfere with normal breathing and ventilation break lѐ soft .

6. X-ray examination of the lungs in MM patients reveals a strengthening and deformation of the pulmonary pattern according to the interstitial type, which is caused by stagnation in small vessels with the development of pneumosclerosis, as the blood flow in the pulmonary capillaries slows down due to the increased viscosity of the plasma .

Among the infectious complications of MM are acute bronchitis, pneumonia, postpneumonic abscesses . The emergence of inflammatory complications of the bronchopulmonary system in MM, in addition to the above factors, can contribute to impaired microcirculation and changes in the rheological properties of blood . Paraproteinemic hemoblastosis is characterized by increased red blood cell aggregation and impaired blood flow in the capillaries . In addition, with nitrogen-induced uremia in the respiratory tract, deep tissue changes that lead to disruption of the act of breathing due to severe intoxication are detected .

With a long course of MM, respiratory organs are damaged with the development of serosites. Radiographically, this reveals homogeneous darkening in the lung tissue, sometimes an increase in mediastinal lymph nodes, and fluid in the pleural cavity.

Data on the study of respiratory function in patients with MM in the literature are sporadic . The revealed changes indicate a decrease in the vital capacity of the light and its components, a decrease in the partial oxygen stress (pO 2 ). In the work of G.F. Babushkina (1987) revealed a violation of the function of external respiration, mainly of a restrictive type, in 76% of patients with multiple myeloma, especially in those over 50 years old, with a long duration of the disease. According to G.F. Grandmother’s morphological manifestations of a specific process in the lungs (lymphoplasmacytic infiltration, tissue paraproteinosis and paraamyloidosis), detected in 75% of cases, correlate with impaired respiratory function . E.Robin et. al. (1977) report that in patients with paraproteinemic hemoblastosis due to impaired pulmonary blood flow at the level of the microvasculature, the uptake of oxygen by the tissues is disturbed and dysoxia develops. In patients with MM “chained to the bed” due to a pronounced osteo-destructive process in the bones, energy costs are reduced, resulting in redistribution of blood and its deposit in the pulmonary circulation, thus reducing pulmonary ventilation and increasing effective pulmonary blood flow .

V.M. Provotorov and A.Yu. Kazabtsov (1997) studied the features of the course of COPD in patients with MM [204]. The authors found that patients with COPD on the background of MM have pronounced impaired phagocytic activity, impaired cellular and humoral immunity. Against the background of ongoing chemotherapy, disorders of the immune system are exacerbated. Due to the worsening of the defects of the immune system and the formation of persistent secondary immune deficiency, the course of COPD becomes heavier. In patients with COPD on the background of lymphoproliferative diseases, a violation of tracheobronchial cleansing is more pronounced. The authors concluded that it is necessary to include patients with chronic lymphoproliferative tumors with immunocorrective therapy, the use of antibacterial agents that do not have immunosuppressive de- realities, and expositors .

Kidney damage – myeloma nephropathy – the most frequent and serious manifestation of paraproteinemia . Chronic renal failure (CRF) ranks second among the causes of death in patients with MM, after infectious complications .

The study of the condition of the bronchopulmonary system in chronic renal failure is of particular importance. A.P. Zilber (1996) considers that there is no such system, to whose work the lungs would have no direct relation . There is a known relationship between the lungs and the kidneys, which is based on their participation in the regulation of many metabolic reactions . And when decompensating the functions of the kidneys, the lungs assume a significant part of the lost functions. Morphologically, lung lesions were detected at autopsies in 39-100% of patients who have depleted CRF .

There was a discrepancy between the severity of morphological changes in the lung tissue and the scarcity of clinical manifestations, often asymptomatic forms of the disease. Many authors share changes in the lungs with uraemia into three types: 1) specific for renal failure, 2) pulmonary edema due to overhydration, 3) bacterial pneumonia.

Specific lesion of the lung tissue arising from renal failure has several names: uremic pneumonia, uremic lung, uremic pneumonitis. Taking into account that peculiar changes in alveolar septa and vessels dominate, uremic pneumonitis reflects the nature of the pathological process more accurately than others and has recently been used most widely in the literature . Uncomplicated uremic pneumonitis has no clear clinical signs, and therefore the development of methods for its intravital registration is a highly relevant task. . For research purposes, Milne et al. (1995) conducted an independent study: 216 chest radiographs; 61 patients with cardiac disease, 30 with renal insufficiency and 28 with capillary edema permeability. The total diagnostic error in this study ranges from 86% to 89%. The highest accuracy was obtained in the diagnosis of capillary edema permeability (91%), and the lowest in distinguishing chronic rheumatic heart disease from uremic valve injury (81%).

Pathoanatomical studies were dominated by focal, so-called, metastatic calcifications in the soft tissues and internal organs. Much more often, calcification was determined in patients with CRF that were long treated by programmed hemodialysis, in comparison with patients who received only symptomatic therapy . The frequency of focal calcifications in the lungs is not the same in different studies. They were found in 10–70% of patients on programmed hemodialysis, and the extent of this lesion increased as the duration of dialysis treatment increased. . Calcium is deposited in the fibro-altered basement membrane of the alveolar septa, sometimes of the small bronchi in the form of linearly arranged granules and clumps inside the alveoli and bronchioles. The appearance of calcium deposits causes an inflammatory reaction with the subsequent development of fibrosis. It is important to note that metastatic pulmonary calcification may be an important etiological factor for pulmonary dysfunctions . Slightly less often, calcium in the form of individual clusters or single foci are found in soft tissues, most often in muscles.

The lifetime diagnosis of focal lung calcium is extremely difficult . When radiography of the chest, it is usually impossible to detect it because of the very small size of calcium deposits. The gentle shading arising from their combination with significant fibrosis of the alveoli and interstitium is usually mistakenly interpreted as pulmonary edema or pneumonia .

A peculiar pulmonary edema with characteristic radiological changes, rapid regression during dehydration was singled out into an independent syndrome. It is called uremic pulmonary edema . In the domestic literature, the term “nephrogenic pulmonary edema” is usually used .

Along with specific changes, many specialists have noted the accession of frequent infectious lesions of the bronchopulmonary and in patients with CRF . Fetal and interstitial forms of pneumonia are most common in hemodialysis treatment.

The most common and available methods for diagnosing pulmonary changes in chronic renal failure include radiography . Diagnosis of such clinically sluggish current lesions as uremic pneumonitis with the help of routine X-ray morphological methods of examination is very difficult. Meanwhile, while progressing, these lesions inevitably lead to impaired respiratory and non-respiratory functions of the lungs, aggravating the severity of the patients’ condition. There are extremely few works devoted to the use of such highly informative methods of radiation diagnostics as X-ray computed tomography in patients with CRF .

The morphological pulmonary changes described above in patients with chronic kidney disease, of course, lead to gross disorders of the function of external respiration. These include restrictive, obstructive disorders, deterioration of the diffusion capacity of the lungs and changes in the nature of ventilation . These disorders occur in various combinations, they may be transient, but they tend to increase and stabilize as the CRF progresses. A number of authors associate functional respiratory disorders with the development of uremic pneumonitis.

It is quite obvious that the first symptoms of pathological changes in the lungs in chronic renal failure are functional disorders, and assessment of respiratory function in the early stages of the development of a lesion is often the only way to diagnose. But the method of spirography has very limited possibilities in registering local, characteristic of the initial stages of uremic lung dysfunctions, since spirography, as is known, gives an integral (generalizing) indicator and local dysfunctions due to good compensatory lung capabilities, as a rule are not caught. Diagnostics of the earliest and, therefore, non-spread functional, yet reversible disorders is the key to adequate correction of the changes that have occurred.

AND ABOUT. Maslova (2002) conducted a comprehensive study of the bronchopulmonary system of patients with chronic kidney disease (patients with MM were not included in this study) using zonal x-ray densitometry, computed tomography and electronic x-ray tomography. The author has concluded that already in the initial period of the development of CRI, there are violations of the physiological regularity of the increase in ventilation in the apical-basal direction; as CRF progresses, zonal ventilation disorders are aggravated, mainly due to a decrease in ventilation in the middle zones (functional zones of the Vessel); when transferring patients with chronic renal failure to programmed hemodialysis with the elimination of overhydration in them, the indicators of general and regional ventilation improve; However, with an increase in the duration of dialysis treatment, a regular decrease in regional and integral lung ventilation indices was established, which is explained by the progression of lung lesions;computed tomography is essentially a verifying method of radiation examination of the chest and abdominal organs in patients with chronic renal failure, the sensitivity of CT in the detection of pulmonary changes in patients with chronic renal failure shats more than 25 times .