The fate of tuberculous changes in the kidney largely depends on the condition of the ureter. There is no parallelism between the degree of damage to the kidney and ureter. With limited areas of destruction of the renal parenchyma, multiple specific structures of the ureter can occur, and vice versa, with polycavernous tuberculosis of the kidney, the ureter can be passable throughout. With a specific lesion of the ureter, the dynamics of urination are disturbed, which leads, on the one hand, to the progression of destructive changes in the kidney, and on the other, to the occurrence of nonspecific hydronephrotic changes. With the spread of tuberculous changes to the ureter, specific ulcers appear on its mucous membrane, which tend to quickly scarring, which leads to persistent narrowing of the lumen of the ureter. Most often, such strictures are localized in the pelvic ureter and in the area of ​​its anastomosis with the pelvis. Cicatricial narrowing of the ureter is the cause of constant dull and acute pain in the lumbar region. It leads to a sharp impairment of kidney function, impaired urinary dynamics, and expansion of the kidney cavities. With the addition of the flora of a secondary infection, chronic pyelonephritis develops against the background of kidney tuberculosis.
A specific narrowing of the ureter in its prebubble section leads to the formation of bullous edema of the mucous membrane of the bladder in the area of ​​the mouth of the ureter and the formation of further deep, sluggish granulating ulcers in this place. As a result of lympho-hematogenous introduction of a tuberculosis infection into the bladder, patches of focal hyperemia, rashes of tuberculous tubercles, ulceration appear on its mucous membrane. With the involvement of the bladder in patients, dysuric phenomena of varying intensity appear. The frequency of urination is constantly increasing, they become painful, terminal hematuria appears . Often, such patients are treated for a long time from chronic nonspecific cystitis, and only endoscopic urological examination and the presence of tuberculous mycobacteria in the urine help to establish the correct diagnosis. With the progression of changes in the bladder, its capacity is systematically reduced, the walls thicken with scar tissue. The elasticity of the walls of the bladder becomes negligible, the valve mechanism of the mouths of the ureters is disrupted. The insufficiency of the valve mechanism of the ureter is observed, as a rule, in a “healthy” kidney. A kidney affected by tuberculosis by this time is turned off, usually turning into an isolated pyonephrotic sac or calcified organ. Such patients continue to live at the expense of one kidney, the function of which is suppressed by the affected kidney and the presence of vesicoureteral reflux. Such backflow of urine into the ureter and pelvis during each urination act leads to the expansion of the kidney cavities and the formation of
hydronephrosis, hydroureter, which is a favorable soil for the development of chronic pyelonephritis.
Clinically, vesicoureteral reflux is manifested by pain in the kidney area at the height of the urge to urinate. The act of urination itself is two-stage (first, the bladder is emptied, then the sharply expanded cavity of the kidney and ureter). In such patients, paroxysmal pain in the lumbar region is often observed, accompanied by high fever and chills; chronic renal failure progresses, which is ultimately the cause of death. It is appropriate to point out the large compensatory possibilities in such patients: in some cases they are for a long time, despite chronic renal failure. continue to be operational.