Pathogenesis of acute pyelonephritis
Last reviewed: 23.04.2024
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The microorganism of E. Coli, which has the P-pili, or the type I and II-type spirits most important in the etiology, is attached to the uroepithelium receptors of the disaccharide nature.
The adhesion process can consist of two phases. In the first (reversible) type II pili (mannose-sensitive hemagglutinins) participate, in this case E. Coli will be excreted together with the tear slime.
If there are still Type I peptides (mannose-resistant hemagglutinins), then the second irreversible phase occurs, at which bacteria are tightly attached to uroepithelial receptors. In this case, more severe damage to the renal tissue, including interstitial inflammation, fibrosis, canal atrophy, is possible.
The spread of infection is facilitated by E. Coli K-antigens, which counteract phagocytosis and opsonization. In addition, the substances secreted by the microbial cell inactivate lysozyme, interferon and other factors of nonspecific resistance of the organism.
E. Coli strains bearing P-pili are able to induce ascending non-obstructive pyelonephritis with paralytic lipid A effect on peristalsis of ureters. Lipid A induces an inflammation reaction, enhances the adhesion of the microbe, and also through the prostaglandin system affects the smooth muscles of the urinary tract, causing obstruction to them, increasing pressure and developing reflux. Thus, these strains of E. Coli can cause pyelonephritis in children with an anatomically and functionally normal structure of the urinary tract. Obstruction and retention of urine predispose to the development of infection.
In the pathogenesis of pyelonephritis, a major role is played by the violation of urinary outflow, increased pressure in the pelvis and calyces, and violation of venous outflow from the kidney, which facilitates the localization of bacteria in the venous capillaries, braided tubules, and increased vascular permeability leads to the penetration of bacteria into the interstitial tissue of the kidney.
Infection can enter the kidneys with ascending urinogenous, lymphogenous and hematogenous pathways. In the pathogenesis of kidney infection and the development of pyelonephritis, the leading role is played by:
- disturbances of urodynamics - difficulty or disruption of the natural urine flow (urinary tract abnormalities, refluxes);
- damage to the interstitial tissue of the kidneys - viral and mycoplasmal infections (eg, intrauterine Coxsackie B, mycoplasma, cytomegalovirus), drug damage (eg, hypervitaminosis D), dysmetabolic nephropathy, xanthomatosis, etc .;
- bacteremia and bacteriuria with diseases of the genital organs (vulvitis, vulvovaginitis, etc.), in the presence of foci of infection (dental caries, chronic colitis, chronic tonsillitis, etc.), with violations of the gastrointestinal tract (constipation, dysbiosis);
- disturbances in the reactivity of the organism, in particular a decrease in immunological reactivity.
An undoubted role in the pathogenesis of pyelonephritis belongs to a hereditary predisposition.
Infection and interstitial inflammation primarily damage the brain layer of the kidney - the part that includes the collecting tubules and some of the distal tubules. The death of these nephron segments disrupts the functional state of the tubule sections located in the cortical layer of the kidney. Inflammatory process, moving to the cortical layer, can lead to a secondary impairment of glomerular function with the development of renal failure.
There is a violation of blood circulation in the kidneys, development of hypoxia and enzyme disorders, activation of lipid peroxidation and reduction of antioxidant protection. The liberation of lysosomal enzymes and superoxide has a damaging effect on the renal tissue and, first of all, on the cells of the renal tubules.
Polymorphonuclear cells, macrophages, lymphocytes, endothelial cells migrate to the interstitium, where they activate and release cytokines, tumor necrosis factor, IL-1, IL-2, IL-6, which enhance inflammatory processes and damage to renal tubule cells.
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