Pyelonephritis provokes growth retardation and apoptosis in infant rat renal cortex.
Kidney Int
; 51(6): 1855-62, 1997 Jun.
Article
em En
| MEDLINE
| ID: mdl-9186875
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.
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Coleções:
01-internacional
Contexto em Saúde:
6_ODS3_enfermedades_notrasmisibles
Base de dados:
MEDLINE
Assunto principal:
Pielonefrite
/
Apoptose
/
Transtornos do Crescimento
/
Córtex Renal
/
Animais Recém-Nascidos
Limite:
Animals
Idioma:
En
Revista:
Kidney Int
Ano de publicação:
1997
Tipo de documento:
Article