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Vesicoureteral reflux and pyelonephritis in the monkey: a review
1Department of Urology, Tulane Regional Primate Research Center, Covington, Louisiana.
Abstract:
P-fimbriated Escherichia coli, which cause nonobstructive pyelonephritis, adhere to a specific urothelial glycolipid receptor. In either the presence or absence of reflux (in the area of turbulent urine flow) these bacteria ascend the ureter and cause a decrease in ureteral motility. Endotoxin causes peristalsis to cease, leading to ureteral dilatation and change in papillary shape, thus allowing intrarenal reflux and adherence of the bacteria to renal tubules. Bacterial infection of a refluxing ureter may cause reflux to persist. Once the bacteria reach the kidney rapid effects occur at the cellular level with activation of complement followed by granulocytic aggregation and capillary obstruction, causing renal ischemia and damage during reperfusion. In addition, during phagocytosis the respiratory burst occurs, releasing toxic oxygen molecules, which leads to renal tubular death, invasion of the interstitium, microabscess and renal scar formation, that is chronic pyelonephritis, which equates with reflux nephropathy.
Insights
P-fimbriated Escherichia coli cause pyelonephritis by adhering to urothelial receptors and ascending the ureter. Bacterial endotoxins and cellular damage lead to chronic pyelonephritis, also known as reflux nephropathy.
Area of Science:
- Urology
- Microbiology
- Nephrology
Background:
- P-fimbriated Escherichia coli are a common cause of nonobstructive pyelonephritis.
- These bacteria adhere to specific urothelial glycolipid receptors, initiating infection.
- Bacterial ascent and endotoxin effects contribute to kidney damage.
Purpose of the Study:
- To elucidate the pathogenic mechanisms of P-fimbriated Escherichia coli in pyelonephritis.
- To understand the role of bacterial factors and host responses in renal damage.
- To correlate bacterial-induced kidney injury with reflux nephropathy.
Main Methods:
- The study describes the adherence of P-fimbriated E. coli to urothelial receptors.
- It details bacterial ascent, ureteral motility changes, and endotoxin effects.
- Cellular-level events including complement activation, ischemia, and respiratory burst are discussed.
Main Results:
- P-fimbriated E. coli adhere to urothelial glycolipid receptors, leading to ureteral dysfunction.
- Endotoxin causes ureteral dilatation and intrarenal reflux, facilitating bacterial invasion of renal tubules.
- Complement activation, ischemia, and toxic oxygen molecules result in renal tubular death, microabscesses, and scarring.
Conclusions:
- P-fimbriated E. coli infection progresses from the ureter to the kidney, causing significant cellular damage.
- The described cascade of events leads to chronic pyelonephritis, equivalent to reflux nephropathy.
- Understanding these mechanisms is crucial for preventing and treating kidney scarring in pyelonephritis.