Renal tuberculosis - Causes and pathogenesis

The main source of infection is the patient releasing mycobacteria into the environment. The main route of penetration of the pathogen into the kidney is hematogenous. This usually occurs at the stage of formation of the pulmonary focus, when the "non-sterile" immunity to the pathogen does not function properly. However, hematogenous spread of mycobacteria in the body is possible already in the first hours after airborne or alimentary infection.

The method of invasion (penetration of the pathogen into tissue) is closely related to the features of microcirculation in the kidneys: the vastness of the microcirculatory bed, slow blood flow in the glomerular capillaries, and close contact of the vessels with the interstitial tissue. These features contribute to the formation of multiple primary foci, primarily in the renal cortex. Their further development can follow the path of complete regression with pronounced general and local resistance to tuberculosis infection, small foci, and predominantly granulomatous (without caseous necrosis) nature of pathomorphological changes. With fairly rapid activation of specific immunity, but more pronounced local changes causing proliferative processes, partial regression 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 with the preservation of persistent mycobacteria. Of the general pathogenetic mechanisms, the fundamental ones are infection with tuberculosis mycobacteria or the presence of a tuberculosis focus, weakening of the immunobiological forces and reactivity of the body. Insufficiency of specific immunity is the main factor in the development of the tuberculous process in the kidney as a result of the activation and spread of primary foci. Damage to the renal pelvis, ureters and bladder appears secondarily, it is associated with the predominant spread of tuberculous infection through the lymphatic pathways, but direct contact of mycobacteria with the urothelium (urinogenic pathway) is not excluded. In more than 50% of cases in men, the tuberculosis process also affects the genitals (prostate gland, appendages, testicles). In women, this is observed much less frequently, no more than 5-10% of cases.

Hematogenous penetration of the tuberculosis mycobacterium leads to infection of both kidneys. No difference in the frequency of damage to the right and left kidneys can be established. Despite the infection of both kidneys, the subsequent development of a specific inflammatory process is usually observed on one side. The existence of foci of inflammation in the opposite kidney may be latent; rarely, they can undergo reverse development. For the development of renal tuberculosis, certain local conditions must arise: local circulatory disorders, which can be based on diseases and disturbances in the passage of urine, accompanied by hypoxia of the renal cortex. This can explain the predominant localization of specific changes in the cortex in the initial stages of tuberculous inflammation in the kidney.

Morphological changes in renal tuberculosis

A characteristic morphological manifestation of the tuberculous process of any localization and the kidney, in particular, is a focus of specific inflammation (tuberculous tubercle), in which 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 an area of caseous necrosis surrounded by a shaft of lymphoid, epithelioid and giant Pirogov-Langhans cells. A characteristic feature of tuberculous, as well as any specific inflammation, is a pronounced productive tissue reaction, ultimately leading to the formation of a granuloma - delimitation of the focus from the surrounding healthy tissues. These foci in the process of inflammation development can merge with each other, undergo further caseous necrosis and melt with the formation of a cavern. One of the options for the development of the inflammatory process is scarring, often with petrification (calcification).

Classification of renal tuberculosis

Morphological classification of renal tuberculosis includes miliary, focal, cavernous, fibro-cavernous tuberculosis, tuberculous pyonephrosis. Tuberculous infarction, tuberculous nephritis (Kochovsky nephrocirrhosis) and post-tuberculous changes are also distinguished. The phases of development of a tuberculous lesion in the kidney are acute focal and destructive, chronic focal and destructive.

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Clinical classification of renal tuberculosis

From the standpoint of a clinician, the stages and forms of development of the tuberculous process can be more specifically described by clinical and radiological forms of renal tuberculosis, accepted and applied 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, characterized to a greater extent by destructive tendencies, is tuberculous 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 arise in the cortex, spreading to the medulla and communicating with the lumen of the calyx, where caseous masses are gradually rejected, leading to the formation of a single or multiple cavities (cavernous tuberculosis of the kidney). Sometimes, against the background of tuberculous papillitis, the neck of one or several cups is predominantly affected, they are compressed with subsequent stenosis and obliteration. In this case, a destructive-purulent cavity arises, consisting of a zone of a destroyed papilla and a retentively changed cup: fibrous-cavernous tuberculosis develops, and the focus of destruction and inflammation is "switched off", since the possibility of outflow of contents disappears.

One of the manifestations of the action of the body's defenses is a pronounced limitation of a specific inflammatory focus with tissue proliferation and impregnation of the affected area with calcium salts. As a result, so-called caseomas or tuberculomas are formed, and the process itself has the character of kidney osmotication.

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