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Microvascular injury and repair in acute human bacterial pyelonephritis
Abstract:
Acute inflammatory cell-capillary endothelial cell interactions, related to injury and repair, were investigated light and electron microscopically in acute human bacterial pyelonephritis. In inflammatory infiltrate-adjacent microvessels, the small capillaries were completely occluded by leukocyte plugs and the large capillaries were densely filled with acute inflammatory cells adhering to the endothelium. Severe damage to small and large capillaries was observed around endothelium adherent, degranulated neutrophil granulocytes containing phagocytosed bacteria. There were spaces in the endothelium, degradation of the vascular basement membrane, of the perivascular interstitial matrix and of collagen fibrils, with fibrin deposition and vessel wall fragmentation. In the small capillaries relatively distant from the interstitial infiltrates, emigration of leukocytes was frequently seen. Around the escaping cells the endothelial lining displayed occasional discontinuities, allowing leakage of vascular fluid into the interstitial space. Some small capillaries not related to the infiltrate were occluded by fibrin thrombi with apparent damage to the endothelial cells and disruption of the capillary wall. Various reparative changes were noticed in association with this change including capillary neovascularization. The findings confirm the existence of polymorphonuclear leukocyte-mediated injury of capillaries during the development of inflammatory responses in acute pyelonephritis.
Insights
In acute pyelonephritis, inflammatory cells severely damage capillaries, causing occlusion and leakage. This polymorphonuclear leukocyte-mediated injury is a key factor in kidney inflammation and repair processes.
Area of Science:
- Nephrology
- Pathology
- Microvascular Biology
Background:
- Acute pyelonephritis involves complex inflammatory cell-capillary endothelial cell interactions.
- Understanding these interactions is crucial for elucidating kidney injury and repair mechanisms.
Observation:
- Microvessels in pyelonephritis show capillaries occluded by leukocyte plugs and inflammatory cells adhering to the endothelium.
- Significant damage to capillaries, including endothelial gaps and basement membrane degradation, observed around neutrophils with phagocytosed bacteria.
- Leukocyte emigration from capillaries, vascular fluid leakage, fibrin thrombi, and capillary wall disruption were noted.
Findings:
- Polymorphonuclear leukocytes directly mediate capillary injury in acute pyelonephritis.
- Degradation of vascular basement membrane, interstitial matrix, and collagen fibrils contributes to vessel damage.
- Evidence of capillary neovascularization suggests a reparative response.
Implications:
- Highlights the critical role of leukocyte-endothelial interactions in pyelonephritis pathogenesis.
- Provides insights into microvascular damage and repair mechanisms in bacterial kidney infections.
- Suggests potential therapeutic targets for mitigating kidney damage in pyelonephritis.