Pathogenesis of acute pyelonephritis

The most significant microorganism in etiology is E. coli, which has P-fimbriae, or pili of types I and II, and attaches to the receptors of the uroepithelium of a disaccharide nature.

The adhesion process may consist of two phases. The first (reversible) involves type II pili (mannose-sensitive hemagglutinins), in which case E. coli will be isolated along with the rejected mucus.

If type I pili (mannose-resistant hemagglutinins) are still present, the second irreversible phase occurs, in which the bacteria are tightly attached to the receptors of the uroepithelium. In this case, more severe damage to the renal tissue is possible, including interstitial inflammation, fibrosis, and tubular atrophy.

The spread of infection is also facilitated by E. coli K-antigens, which counteract phagocytosis and opsonization. In addition, substances secreted by the microbial cell inactivate lysozyme, interferon, and other factors of non-specific resistance of the organism.

E. coli strains carrying β-fimbriae are capable of causing ascending non-obstructive pyelonephritis via the paralytic effect of lipid A on ureteral peristalsis. Lipid A induces an inflammatory response, enhances microbial adhesion, and through the prostaglandin system affects the smooth muscles of the urinary tract, causing obstruction, increased pressure, and the development of reflux. Thus, these E. coli strains can cause pyelonephritis in children with anatomically and functionally normal urinary tract structure. Obstruction and urinary retention predispose to infection.

In the pathogenesis of pyelonephritis, a major role is played by impaired urine outflow, increased pressure in the pelvis and calyces, and impaired venous outflow from the kidney, which contributes to the localization of bacteria in the venous capillaries that envelop the tubules, and increased vascular permeability leads to the penetration of bacteria into the interstitial tissue of the kidney.

Infection can penetrate the kidneys by ascending urinogenous, lymphogenous and hematogenous routes. The leading role in the pathogenesis of kidney infection and the development of pyelonephritis is played by:

1. urodynamic disorders - difficulties or disturbances in the natural flow of urine (urinary tract anomalies, reflux);
2. damage to the interstitial tissue of the kidneys - viral and mycoplasma infections (for example, intrauterine Coxsackie B, mycoplasma, cytomegalovirus), drug-induced lesions (for example, hypervitaminosis D), dysmetabolic nephropathy, xanthomatosis, etc.;
3. bacteremia and bacteriuria in diseases of the genital organs (vulvitis, vulvovaginitis, etc.), in the presence of foci of infection (dental caries, chronic colitis, chronic tonsillitis, etc.), in disorders of the gastrointestinal tract (constipation, dysbacteriosis);
4. disturbances in the body's reactivity, in particular a decrease in immunological reactivity.

Hereditary predisposition undoubtedly plays a role in the pathogenesis of pyelonephritis.

Infection and interstitial inflammation primarily damage the renal medulla - the part that includes the collecting tubules and part of the distal tubules. The death of these sections of the nephron disrupts the functional state of the tubule sections located in the renal cortex. The inflammatory process, moving to the cortex, can lead to secondary dysfunction of the glomeruli with the development of renal failure.

There is a disruption of blood circulation in the kidneys, development of hypoxia and enzymatic disorders, activation of lipid peroxidation and a decrease in antioxidant protection. The release of lysosomal enzymes and superoxide has a damaging effect on renal tissue and, above all, on the cells of the renal tubules.

Polymorphonuclear cells, macrophages, lymphocytes, and endothelial cells migrate into the interstitium, where they are activated and secrete cytokines, tumor necrosis factor, IL-1, IL-2, and IL-6, which enhance inflammatory processes and damage to renal tubule cells.

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