Kidney tuberculosis: causes and pathogenesis

The main source of infection is a patient that secretes mycobacteria into the environment. The main path of penetration of the pathogen into the kidney is hematogenous. This happens, as a rule, at the stage of formation of the pulmonary focus, when the "non-sterile" immunity to the causative agent does not function properly. However, the hematogenous distribution of mycobacterium in the body is possible already in the first hours after aerogenic or alimentary infection.

The method of invasion (penetration of the pathogen into tissues) is closely related to the peculiarities of microcirculation in the kidneys: with the vastness of the microcirculatory bed, slowed blood flow in the capillaries of the glomeruli, close contact of the vessels with the interstitial tissue. These features contribute to the formation of multiple primary foci, primarily in the cortical layer of the kidneys. Their further development can follow the path of complete reverse development with pronounced general and local resistance to tuberculosis infection, small foci size, predominantly granulomatous (without caseous necrosis), the nature of pathomorphological changes. With rather rapid activation of specific immunity, but more pronounced local changes, which cause proliferative processes, a partial reverse development with scarring can occur. And finally, with the activation of specific immunity, but with the formation of caseous-necrotic masses in the foci, their complete or partial encapsulation occurs while maintaining persistent mycobacteria. Of the common pathogenetic mechanisms underlying are the infection with tuberculosis mycobacteria or the presence of a tuberculous focus, weakening of the immunobiological forces and reactivity of the organism. Insufficiency of specific immunity is the main factor in the development of the tuberculosis process in the kidney as a result of the activation and spread of primary foci. The defeat of the capillary system, ureters and bladder appears again, it is associated with the predominant spread of tuberculosis infection through the lymphatic ways, however, direct contact of the mycobacterium with the urothelium (urinogenous pathway) is not excluded. In more than 50% of cases in men, the tubercular process affects the genitals (prostate gland, appendages, testicles). In women, this is observed much less often, no more than 5-10% of cases.

Hematogenous penetration of mycobacterium tuberculosis leads to infection of both kidneys. Any difference in the frequency of lesions of the right and left kidneys can not be established. Despite the infection of both kidneys, the subsequent development of a specific inflammatory process is usually observed on the one hand. The existence of foci of inflammation in the opposite kidney may be latent in nature; rarely they can be reversed. For the development of kidney tuberculosis, certain local conditions must arise: local circulatory disorders, which may be based on diseases, and urine passage disorders, accompanied by hypoxia of the renal cortex. It is this that can explain the predominant localization of specific changes in the cortex in the initial stages of tubercular inflammation in the kidney.

Morphological changes of kidney tuberculosis

A characteristic morphological manifestation of the tuberculosis process of any localization and kidney, in particular, is the focus of a specific inflammation (tubercle tubercle), in which the features of the infiltrative, destructive and proliferative phases of inflammation can be observed. In the center of such a focus, as a rule, there is a section of caseous necrosis, surrounded by a shaft of lymphoid, epithelioid and giant cells of Pirogov-Langgans. A characteristic trait of tuberculosis, as well as of any specific inflammation, is a pronounced productive tissue reaction, which ultimately leads to the formation of a granuloma-the separation of the focus from the surrounding healthy tissues. These foci in the process of development of inflammation can merge with each other, undergo further caseous necrosis and melt to form a cavity. One of the options for the development of the inflammatory process is scarring, often with petrification (calcification).

Classification of kidney tuberculosis

Morphological classification of renal tuberculosis includes miliary, focal, cavernous, fibrous-cavernous tuberculosis, tuberculosis pyonephrosis. There are also tubercular infarction, tuberculosis nephritis (Kohov nephrocirrhosis) and post-tuberculosis changes. Phases of development of the tuberculous focus in the kidney - acute focal and destructive, chronic focal and destructive.

[1], [2]

Clinical classification of kidney tuberculosis

From the clinician's point of view, the stages and forms of development of the tuberculosis process can be more specifically described by the clinical and radiological forms of renal tuberculosis adopted and used in phthisiourological practice. These include tuberculosis of the renal parenchyma, characterized by multiple inflammatory foci in the renal cortex and medullary zone. The next form, which characterizes more destructive tendencies, is tubercular papillitis: the process is mainly localized in the renal papilla. The cavernous zone as a result of the fusion of several foci, their destruction, caseous necrosis with delimitation by fibrous tissue can occur in the cortex, spreading to the medulla and communicating with the lumen of the calyx, where the caseous masses are gradually rejected, leading to the formation of single or multiple cavities (cavernous tuberculosis of the kidney ). Sometimes, on the background of tubercular papillitis, the cervix of one or several cups is mainly affected, they are squeezed with subsequent stenosis and obliteration. This creates a destructive purulent cavity, consisting of a zone of the destroyed papilla and a retentionally altered calyx: fibrous-cavernous tuberculosis develops, and the focus of destruction and inflammation "turns off", as the possibility of outflow of contents disappears.

One of the manifestations of the action of the body's defenses is the expressed restriction of a specific inflammatory focus with tissue proliferation and impregnation of the affected area with calcium salts. As a result, the so-called casei, or tuberculosis, are formed, and the process itself has the character of a kidney's omelocation.

[3], [4], [5]