RESUMEN
The SAMP1/Sku mouse is a substrain of the SAMP1 (senescence-accelerated-mouse prone 1) which exhibits renal mononuclear cell infiltration from a younger age. We hypothesized that this renal characteristic is related to the incidence of tubulointerstitial nephritis (TIN). The purpose of the present study was to evaluate the applicability of the SAMP1/Sku mouse as a murine model for TIN. TIN was experimentally induced by unilateral ureteral obstruction (UUO). The SAMP1/Sku and control ICR of both sexes received either a sham or UUO operation and were sacrificed 7 days after the operation. The kidneys of the mice were observed histopathologically, immunohistochemically and semiquantitatively. UUO kidneys showed mononuclear cell infiltration, tubular atrophy and interstitial fibrosis. In males, semiquantitative scores of mononuclear cell infiltration, tubular atrophy, and F4/80, alpha-smooth muscle actin (alpha-SMA) and transforming growth factor (TGF)-beta1 reactions were significantly higher in SAMP1/Sku than in ICR. Likewise, in females, tubular atrophy and F4/80 reaction scores were significantly higher in SAMP1/Sku than in ICR. In conclusion, induction of TIN damage by UUO was more serious in SAMP1/Sku mice than in ICR. Therefore, we propose that SAMP1/Sku mice, especially male SAMP1/Sku, have congenital risk factors for the development of TIN.
Asunto(s)
Modelos Animales de Enfermedad , Ratones Endogámicos , Nefritis Intersticial , Obstrucción Ureteral , Actinas/metabolismo , Animales , Antígenos de Diferenciación/metabolismo , Atrofia , Femenino , Fibrosis , Inmunohistoquímica , Riñón/metabolismo , Riñón/patología , Masculino , Ratones , Necrosis , Nefritis Intersticial/etiología , Factores de Riesgo , Factor de Crecimiento Transformador beta/metabolismo , Obstrucción Ureteral/complicaciones , Obstrucción Ureteral/metabolismo , Obstrucción Ureteral/patologíaRESUMEN
The kidneys of non-diabetic NOD and wild type ICR mice were examined morphometrically at 3 and 6 months of age. Kidney weights and diameter of renal corpuscles of non-diabetic NOD mice were less than those of ICR mice. No lesions were observed in glomeruli or uriniferous tubules. Renin-positive areas were more common in NOD mice than in ICR mice, but no differences were detected in the Western blot analyses.