Pyelonephritis

Clinical features of interstitial involvement

Pyelonephritis belongs to the group of tubulointerstitial nephritis. This group of diseases is characterized by primary damage to the tubules and interstitium.

Clinically, this manifests as the absence of classical nephritic and nephrotic syndromes in the early stages. Tubule dysfunction comes to the fore:

• The kidneys' ability to concentrate urine is impaired, which clinically manifests as polyuria.
• Uncontrolled salt wasting occurs.
• The ability to excrete acids is reduced, provoking the development of metabolic acidosis.

Etiology and pathways of infection entry

In the vast majority of cases, inflammation is caused by bacteria of the normal intestinal microflora. The absolute leader is E. coli, followed by Proteus, Klebsiella, and Enterobacter. Infection penetrates the renal tissue via two pathways:

1. Ascending pathway (main). Bacteria ascend from the lower urinary tract. Normally, this is prevented by peristalsis and the antibacterial properties of the mucous membrane. However, in case of urinary stasis (due to prostate adenoma, tumors, stones, urethral stricture, or bladder atony), bacteria begin to actively multiply in the residual urine volume.
2. Hematogenous pathway (rare). Infection is seeded via the bloodstream during septicaemia or infective endocarditis. In this case, the causative agents are non-enterogenic microorganisms (e.g., staphylococci) or fungi. Risk factors include immunosuppression, a weakened patient condition, and ureteral obstruction.

The role of reflux in pathogenesis

For the development of ascending infection, the retrograde flow of urine, which delivers bacteria to the renal parenchyma, is critically important:

• Vesicoureteral reflux (VUR). Occurs due to incompetence of the valve between the ureter and the urinary bladder. Bacterial endotoxins during bladder inflammation suppress ureteral contractility, which causes or enhances the reflux of infected urine upward (this is especially common in children).
• Intrarenal reflux. This is the reflux of urine from the renal pelvis directly into the renal parenchyma through open ducts on the papillae. Anatomically, this most often occurs in the upper and lower poles, as the papillae there have flat or concave tips.

Morphology: from acute inflammation to "thyroid kidney"

Acute pyelonephritis is a purulent interstitial inflammation.

• Macroscopically circumscribed abscesses are visible in the tissue. Sometimes they merge into large wedge-shaped suppurative foci — carbuncles. In reflux, abscesses are predominantly localized at the poles of the organ.
• Microscopically the process begins with infiltration of the interstitium by neutrophils, then inflammation spreads to the tubules, causing their destruction.

Chronic pyelonephritis leads to irreversible organ remodeling.

• Macroscopically the kidneys shrink unevenly and asynchronously. Coarse corticomedullary scars, fused with dilated and deformed calyces, form on the surface (usually at the poles).
• Microscopically mononuclear infiltration and marked fibrosis are observed in the stroma. Some tubules atrophy, while others undergo compensatory dilation.

A specific histological sign of the chronic stage is the "thyroidization" phenomenon. Dilated tubules are filled with dense eosinophilic masses (colloid casts). Externally, such tissue resembles thyroid follicles, which is why the organ is macroscopically referred to as the thyroid-contracted kidney.

Briefly: answers to topical questions

Class and exam questions

What else to study on this topic

• Mechanisms of colloid cast formation in the "thyroidization" phenomenon.
• Pathogenesis of metabolic acidosis in tubulointerstitial injury.
• Clinical features and risks of asymptomatic bacteriuria.
• Effect of bacterial endotoxins on ureteral contractility.
• Differential diagnosis of renal carbuncle and isolated abscess.

Other topics in the section "Diseases of the Kidneys and Urinary Tract"

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