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Pyelonephritis provokes growth retardation and apoptosis in infant rat renal cortex
E Serlachius1, B Sundelin, A C Eklöf
1Department of Woman and Child Health, Karolinska Institute, Stockholm, Sweden.
Insights
Childhood pyelonephritis can cause kidney damage by reducing cell proliferation and increasing apoptosis in renal cells. This study in rats reveals mechanisms contributing to parenchymal loss after urinary tract infections.
Area of Science:
- Nephrology
- Pediatric Nephrology
- Infectious Diseases
Background:
- Childhood pyelonephritis frequently leads to renal scarring and hypoplastic kidneys.
- Understanding the mechanisms of cortical lesions in pyelonephritis is crucial for preventing long-term kidney damage.
Purpose of the Study:
- To investigate the cellular mechanisms underlying renal cortical lesions in a rat model of childhood pyelonephritis.
- To examine the impact of infection on cell proliferation and apoptosis in the kidney cortex.
Main Methods:
- Induction of urinary tract infection using a nephropathogenic E. coli strain in three-week-old rats.
- Histopathological examination, immunohistochemistry for proliferating cell nuclear antigen (PCNA), and 3H-thymidine autoradiography to assess cell proliferation and apoptosis.
Main Results:
- Marked leukocyte infiltration observed in the renal medulla and the cortical zone adjacent to the pelvis.
- Significant decrease in proximal tubular cell proliferation (PCNA immunoreactivity and mitotic response) during the first four days post-infection.
- Transient increase in apoptotic cortical cells observed four days after infection, with no increase at ten days.
Conclusions:
- Inhibition of cell proliferation and enhanced apoptosis are key cellular events contributing to renal parenchymal loss in pyelonephritis.
- These findings provide insights into the pathogenesis of kidney damage following childhood urinary tract infections.
Abstract:
Childhood pyelonephritis is a common cause of renal cortical scarring and hypoplastic kidneys. To understand the mechanisms underlying the cortical lesions, urinary tract infection was induced in three-week-old rats by an intravesical infusion of E. coli, type 06 K13 HL a rat nephropathogenic strain. Four days after infection, histopathological examination showed marked infiltration of leukocytes in the medullary tissue adjoining the calyces and pelvis. In the cortex, signs of inflammation were found only in the cortical zone adjacent to the pelvis. No cells indicative of inflammation were observed in other parts of the cortex. Immunohistochemistry for endogenous proliferating cell nuclear antigen (PCNA) demonstrated a marked decrease in immunoreactivity in proximal tubular (PT) cells. The mitotic response of PT cells, assessed by 3H-thymidine autoradiography, showed a highly significant decrease during the first four days after induction of the infection. Four days after infection, a transient increase in apoptotic cells was observed in cortical cells outside the inflammatory areas. No increase in apoptotic cells was detected in the cortex 10 days after infection. Only a few apoptotic cells were detected in the control kidneys. In conclusion, the data indicate that inhibition of cell proliferation and enhancement of apoptosis may contribute to the renal parenchymal loss after childhood pyelonephritis.