Intrauterine food restriction as a determinant of nephrosclerosis

Intrauterine food restriction as a determinant of nephrosclerosis

Autor Lucas, SRR Google Scholar
Miraglia, S. M. Google Scholar
Gil, F. Z. Google Scholar
Coimbra, T. M. Google Scholar
Instituição Fac Med Ribeirao Preto
Universidade Federal de São Paulo (UNIFESP)
Resumo We previously showed that 8-month-old rats subjected to a 50% intrauterine food restriction had a decreased number of nephrons with increased glomerular diameter, which suggests compensatory hypertrophy, Hypertrophy could be the early event of glomerular damage. in this study, we extended our investigation and performed functional, morphological, and immunohistochemical evaluations in 3- and 18-month-old rats that underwent a 50% intrauterine food restriction (RT3 and RT18, respectively) and age-matched control rats (C3 and C18, respectively). Our findings showed that glomerular filtration rate was significant decreased in RT18 rats (2.42 +/- 0.15 mL/min/kg; n = 28; P < 0.05) compared with C18 control rats (4.19 +/- 0.10 ml/min/kg; P < 0.05) and the percentage of glomeruli with sclerosis was greater in RT18 rats (13.01% +/- 2.95%; n = 9; P < 0.01) than in C18 rats (2.71% +/- 0.35%; n = 6), RT18 rats also showed more intense tubulointerstitial lesions and immunohistochemical alterations in the renal cortex. Immunohistochemical studies showed increased fibronectin and desmin expression in glomeruli and tubulointerstitium and increased vimentin and Lu-smooth muscle actin in the tubulointerstitial area from the renal cortex of RT18 rats (P < 0.05), Desmin was also increased at the edge of glomeruli from RT18 rats, suggesting podocyte injury. Our data show that when food restriction is imposed during pregnancy, permanent damage occurs in the kidney of the offspring. Glomerular lesions were more severe than the tubulointerstitial damage in these animals. (C) 2001 by the National Kidney Foundation, Inc.
Assunto food restriction
glomerular hypertrophy
tubulointerstitial lesions
Idioma Inglês
Data 2001-03-01
Publicado em American Journal of Kidney Diseases. Philadelphia: W B Saunders Co, v. 37, n. 3, p. 467-476, 2001.
ISSN 0272-6386 (Sherpa/Romeo, fator de impacto)
Editor W B Saunders Co
Extensão 467-476
Direito de acesso Acesso restrito
Tipo Artigo
Web of Science WOS:000167495600002

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