Pediatric Nephrology

, Volume 21, Issue 8, pp 1082–1092 | Cite as

Compensatory renal growth protects mice against Shiga toxin 2-induced toxicity

  • Gabriela Verónica CameranoEmail author
  • Oscar David Bustuoabad
  • Roberto Pablo Meiss
  • Sonia Alejandra Gómez
  • Gabriela Cristina Fernández
  • Martín Amadeo Isturiz
  • Marina Sandra Palermo
  • Graciela Isabel Dran
Original Article


Uninephrectomy (Unx) is followed by the compensatory renal growth (CRG) of the remaining kidney. Previous evidence has shown that during CRG, renal tissue is resistant to a variety of pathologies. We tested the hypothesis that the functional changes that take place during CRG could attenuate Shiga toxin (Stx) toxicity in a mouse model of Stx2-induced hemolytic uremic syndrome (HUS). The participation of nitric oxide (NO) was analyzed. After CRG induction with Unx, mice were exposed to a lethal dose of Stx2, and the degree of renal damage and mortality was measured. Stx2 effects on the growth, renal blood flow (RBF) and NO synthase (NOS) intrarenal expression in the remaining kidney were then studied. The induction of CRG strongly prevented Stx2-mediated mortality and renal damage. Administration of the NOS inhibitor NG-nitro-L-arginine methyl ester (L-NAME) during CRG partially impaired the protection. Both Stx2 and L-NAME interfered with the hypertrophic and hyperplastic responses to Unx, as well as with the increase in RBF. In intact mice, Stx2 decreased renal perfusion, inhibited endothelial NOS basal expression and enhanced inducible NOS expression; all of these effects were attenuated by prior Unx. It is concluded that during CRG mice are highly protected against Stx2 toxicity and lethality. The protective capacity of CRG could be related to the enhancement of renal perfusion and preservation of eNOS renal expression, counterbalancing two major pathogenic mechanisms of Stx2.


Uninephrectomy Compensatory renal growth Shiga toxin Hemolytic uremic syndrome 



We thank Dr. Carlos Amorena, University of San Martin Bs. As., for his critical review of the manuscript, and Vet. Hector Costa for excellent technical assistance. This work was supported by grants from Consejo Nacional de Investigaciones Científicas y Técnicas (CONICET), Fundación “Alberto J. Roemmers” and Agencia Nacional de Promoción Científica y Tecnológica, Argentina.


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Copyright information

© IPNA 2006

Authors and Affiliations

  • Gabriela Verónica Camerano
    • 1
    • 4
    Email author
  • Oscar David Bustuoabad
    • 1
  • Roberto Pablo Meiss
    • 2
  • Sonia Alejandra Gómez
    • 3
  • Gabriela Cristina Fernández
    • 3
  • Martín Amadeo Isturiz
    • 3
  • Marina Sandra Palermo
    • 3
  • Graciela Isabel Dran
    • 1
  1. 1.Sección Medicina ExperimentalAcademia Nacional de MedicinaBuenos AiresArgentina
  2. 2.Departamento de Patología, Centro de Estudios OncológicosAcademia Nacional de MedicinaBuenos AiresArgentina
  3. 3.Sección InmunologíaAcademia Nacional de MedicinaBuenos AiresArgentina
  4. 4.División Medicina Experimental, ILEX,Academia Nacional de MedicinaBuenos AiresArgentina

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