Clinical Features of Interstitial Involvement
Pyelonephritis belongs to the group of tubulointerstitial nephritides. This group of diseases is characterized by primary injury to the tubules and interstitium.
Clinically, this manifests as an absence of classic nephritic and nephrotic syndromes in the early stages. Tubular dysfunction comes to the forefront:
- The kidney's ability to concentrate urine is impaired, clinically manifested as polyuria.
- Uncontrolled salt wasting occurs.
- Acid excretion capacity decreases, provoking the development of metabolic acidosis.
Etiology and Routes of Infection
In the overwhelming majority of cases, the cause of inflammation is bacteria from the normal intestinal microflora. The undisputed leader is E. coli, followed by Proteus, Klebsiella, and Enterobacter. Infection enters the renal tissue via two main routes:
- Ascending pathway (primary). Bacteria ascend from the lower urinary tract. Normally, peristalsis and the antibacterial properties of the mucosa prevent this. However, during urinary stasis (due to prostate enlargement, tumors, calculi, urethral stricture, or bladder atonia), bacteria begin to multiply rapidly in the residual urine volume.
- Hematogenous pathway (rare). Infection is seeded via the bloodstream during septicaemia or infective endocarditis. In this case, the causative agents are non-enteric microorganisms (e.g., staphylococci) or fungi. Risk factors include immunosuppression, a weakened patient state, and ureteral obstruction.
Role of Reflux in Pathogenesis
For ascending infection to develop, retrograde urine flow is critical, delivering bacteria to the renal parenchyma:
- Vesicoureteral reflux (VUR). Occurs due to incompetence of the valve mechanism between the ureter and the urinary bladder. Bacterial endotoxins during bladder inflammation suppress ureteral contractility, which induces or enhances the retrograde flow of infected urine (especially common in children).
- Intrarenal reflux. This is the retrograde flow of urine from the renal pelvis directly into the renal parenchyma through open ducts at the papillae. Anatomically, this most frequently 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 presents as suppurative interstitial inflammation.
- Macroscopically, discrete abscesses are visible in the tissue. Sometimes they coalesce into large wedge-shaped areas of suppuration—carbuncles. In the presence of reflux, these foci are localized predominantly at the poles of the organ.
- Microscopically, the process begins with neutrophil infiltration of the interstitium, followed by the spread of inflammation to the tubules, causing their destruction.
Chronic pyelonephritis leads to irreversible structural remodeling of the organ.
- Macroscopically, the kidneys shrink unevenly and asynchronously. On the surface (usually at the poles), coarse corticomedullary scars form, fused with dilated and deformed calyces.
- Microscopically, the stroma shows mononuclear infiltration and pronounced fibrosis. Some tubules atrophy, while others undergo compensatory dilation.
A specific histological sign of the chronic stage is the 'thyroidization' phenomenon. Dilated tubules become filled with dense eosinophilic masses (colloid casts). Externally, such tissue resembles thyroid follicles, leading to the macroscopic term thyroid-like shrunken kidney.