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 cases), less often the causative agent is Proteus spp., Klebsiella spp., Enterobacter spp., Citrobacter spp. In complicated pyelonephritis, the frequency of isolation of Escherichia coli decreases sharply, the importance of Proteus spp., Pseudomonas spp., other gram-negative bacteria, as well as gram-positive cocci increases: Staphylococcus saprophytics, Staphylococcus epidermidis, Enterococcus faecalis; fungi. Approximately 20% of patients (especially those in hospital and with a urinary catheter) have microbial associations of two or three types of bacteria, often a combination of Escherichia coli and Enterococcus faecalis. The following factors are important for the development of the inflammatory process:

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

The ability of microorganisms to adhere is due to the presence of specialized organelles - fimbriae (pili), allowing bacteria to attach to the cells of the urinary tract and move against the flow of urine. Capsular antigens (K-Ag) help suppress opsonization, phagocytosis and complement-dependent bactericidal activity of the blood. Endoplasmic antigens (O-Ag) cause an endotoxic effect, helping to reduce the peristaltic activity of the smooth muscles of the urinary tract up to its complete blockade. Uropathogenic strains include Escherichia coli strains with antigens 02, 06, 075, 04, 01. Serogroups 02 and 06 are considered the most common causative agents of chronic recurrent pyelonephritis.

The persistence of infection is facilitated by the existence of non-enveloped forms of pathogens (L-forms and protoplasts), which are not detected during routine urine culture, but retain pathogenic properties and drug resistance. Under favorable conditions, they can transform into active forms. Factors that support the vital activity of bacteria include high osmolarity and concentration of urea and ammonium salts in the renal medulla, low resistance of the renal parenchyma to infection.

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

Impaired urodynamics due to organic or functional changes that impede urine outflow create favorable conditions for the introduction and reproduction of microorganisms, increasing the likelihood of an inflammatory process. Increased intra-pelvic and intra-calyx pressure leads to compression and rupture of the thin-walled veins of the fornical zone of the calyces with direct infection from the pelvis into the venous bed of the kidney.

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Risk factors for pyelonephritis

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

• reflux at various levels (vesicoureteral, ureteropelvic);
• bladder dysfunction ("neurogenic bladder");
• kidney stone disease;
• urinary tract tumors;
• prostate adenoma;
• nephroptosis, dystopia and hypermobility of the kidneys;
• malformations of the kidneys and urinary tract (doubling, etc.);
• pregnancy;
• diabetes mellitus;
• polycystic kidney disease.

Of no small importance are the following risk factors for pyelonephritis:

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

In young women, especially great importance is attached to inflammatory diseases of the genital organs, defloration cystitis and gestational pyelonephritis.

Pyelonephritis due to urinary reflux results in rapid and extensive replacement of renal tissue with connective tissue, which contributes to the loss of renal function.

Pathomorphology of pyelonephritis

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

• interstitial stromal edema;
• neutrophilic infiltration of the renal medulla;
• perivascular lymphohistiocytic infiltration.

The most characteristic signs of chronic pyelonephritis are:

• connective tissue growths (scars);
• lymphoid and histiocytic infiltrates in the interstitium;
• areas of tubular expansion, some of which are filled with colloidal masses (“thyroid-like” transformation of the tubules).

In the late stages, there is damage to the glomeruli and blood vessels. Massive desolation of the tubules and their replacement with non-specific connective tissue are characteristic. The surface of the kidney is uneven, there are multiple cicatricial retractions. The cortex is thinned and uneven. After acute pyelonephritis, the kidney does not shrink, since the development of cicatricial changes is not diffuse, but focal.

The most important sign that allows differentiating pyelonephritis from other tubulointerstitial kidney lesions is the obligatory involvement of the renal pelvis and calyces in the inflammatory process.

Classification of pyelonephritis

A distinction is made between acute and chronic, obstructive and non-obstructive pyelonephritis. According to prevalence, unilateral and bilateral pyelonephritis are distinguished.

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

Chronic pyelonephritis is a sluggish, periodically aggravating bacterial inflammation, leading to irreversible changes in the renal pelvis and calyces system, followed by sclerosis of the parenchyma and shrinkage of the kidney.

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

Obstructive pyelonephritis is always caused by factors of occlusion (blockage) of the upper urinary tract (calculi, blood clots, inflammatory detritus, organic narrowing of the ureter, reflux, etc.), accompanied by a violation of the passage of urine.

There are pyelonephritis in childhood, pregnancy and the early postpartum period (gestational pyelonephritis).

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