What causes pyelonephritis?

Causes and pathogenesis of pyelonephritis

The most common causes of pyelonephritis are representatives of the Entembacteriaceae family (Gram-negative rods), of which Escherichia coli accounts for about 80% (in acute uncomplicated flow), less often as a causative agent are Proteus spp., Klebsiella spp., Enterobacter spp., Citrobacter spp. With complicated pyelonephritis, the frequency of Escherichia coli release sharply decreases, the value of Proteus spp., Pseudomonas spp., Other gram-negative bacteria, and Gram-positive cocci increases: Staphylococcus saprophytics, Staphylococcus epidermidis, Enterococcus faecalis; mushrooms. Approximately 20% of patients (especially those who are in the hospital and with the urinary catheter installed) have microbial associations of two or three kinds of bacteria, often a combination of Escherichia coli and Enterococcus faecalis. For the development of the inflammatory process, factors such as:

• type of pathogen;
• virulence;
• presence of pili;
• ability to adhesion;
• the ability to produce factors that damage the epithelium of the urinary tract.

The ability of microorganisms to adhesion is due to the presence of specialized organelles - pimples (pili), which allow bacteria to attach to the cells of the urinary tract and move against the urine flow. Capsular antigens (K-Ar) contribute to suppression of opsonization, phagocytosis and complement-dependent bactericidal activity of the blood. Endoplasmic antigens (O-Ag) cause an endotoxic effect that reduces the peristaltic activity of the smooth muscles of the urinary tract until it is completely blocked. Among the uropathogenic strains of Escherichia coli, possessing antigens 02, 06, 075, 04, 01 are included. Serogroups 02 and 06 are considered the most frequent causative agents of chronic recurrent pyelonephritis.

Persistence of the infection is facilitated by the existence of non-envelope forms of pathogens (L-forms and protoplasts), which are not detected in the usual urine culture, but pathogenic properties and drug resistance are preserved. Under favorable conditions, they can pass into active forms. Factors supporting the vital activity of bacteria include high osmolarity and the concentration of urea and ammonium salts in the medulla of the kidney, low resistance of the kidney parenchyma to infection.

The main routes of infection to the kidneys include urogenital (ascending) and hematogenous (in the presence of acute and chronic infection in the body: appendicitis, osteomyelitis, postpartum infection, etc.). Lymphogenous way is possible to infect the kidney against a background of acute and chronic intestinal infections.

Violation of urodynamics due to organic or functional changes that interfere with the outflow of urine, creates favorable conditions for the introduction and reproduction of microorganisms, increases the likelihood of an inflammatory process. Increase of intra-laconic and intracapital pressure leads to compression and rupture of thin-walled veins of the fornate zone of calyx with direct infection from the pelvis into the venous bed of the kidney.

[1], [2], [3], [4], [5], [6], [7]

Risk factors for pyelonephritis

Among the risk factors the most significant for the development of pyelonephritis are:

• refluxes at various levels (vesicoureteral, ureteral-pelvic);
• dysfunction of the bladder ("neurogenic bladder");
• nephrolithiasis;
• urinary tract tumors;
• prostate adenoma;
• nephroptosis, dystopia and kidney hyperplasia;
• malformations of the kidneys and urinary tract (doubling, etc.);
• pregnancy;
• diabetes mellitus;
• polycystic kidney disease.

Important factors are also risk factors for pyelonephritis, such as:

• metabolic disturbances (oxalate-calcium, urate, phosphate crystalluria);
• instrumental research of urinary tract;
• the use of drugs (sulfonamides, cytostatics, etc.);
• exposure to radiation, toxic, chemical, physical (cooling, trauma) factors.

In young women, especially important is the inflammatory diseases of the genital organs, defloration cyst and gestational pyelonephritis.

Pyelonephritis, caused by reflux of urine, leads to a rapid and significant replacement of the kidney tissue with connective tissue, which contributes to the loss of kidney function.

Pathomorphology of pyelonephritis

Renal damage in acute pyelonephritis is characterized by focal signs of inflammation of the interstitial tissue with destruction of tubules:

• interstitial edema of the stroma;
• neutrophil infiltration of the medulla of the kidney;
• perivascular lymphohistiocytic infiltration.

The most characteristic signs of chronic pyelonephritis are:

• connective tissue growths (scars);
• Lymphoid and histiocytic infiltrates in interstitium;
• sections of tubular expansion, some of which are filled with colloidal masses ("thyroid-like" transformation of tubules).

In later stages, there is damage to the glomeruli and blood vessels. Characteristic are the massive desolation of the tubules and their replacement by a nonspecific connective tissue. The surface of the kidney is uneven, there are multiple cicatricial retractions. Cortical layer thinned, uneven. After the acute pyelonephritis, shrinkage of the kidney does not occur, since the development of cicatricial changes is not diffuse, but focal.

The most important feature that makes it possible to differentiate pyelonephritis from other tubulointerstitial lesions of the kidneys is the mandatory involvement of the renal pelvic system in the inflammatory process.

Classification of pyelonephritis

Distinguish between acute and chronic, obstructive and non-obstructive pyelonephritis. In the prevalence of isolated one-sided and bilateral pyelonephritis.

Acute pyelonephritis can occur in the form of serous (bowl) and purulent (apostematous nephritis, carbuncle, kidney abscess, necrotic papillitis) of the inflammatory process.

Chronic pyelonephritis is a slow, periodically exacerbating bacterial inflammation, leading to irreversible changes in the calyx-pelvis system, followed by sclerosing the parenchyma and wrinkling of the kidney.

Non-obstructive pyelonephritis, unlike obstructive pyelonephritis, occurs without previous structural and functional changes in the kidneys and urinary tract.

At the heart of obstructive pyelonephritis are always factors of occlusion (blockage) of the upper urinary tract (concrements, blood clots, inflammatory detritus, organic narrowing of the ureter, reflux, etc.), accompanied by a violation of the passage of urine.

Pyelonephritis of children, pregnant and early postpartum period (gestational pyelonephritis) is allocated.

[8], [9], [10], [11]