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Published ahead of print on September 5, 2007
J Am Soc Nephrol 18: 2653-2660, 2007
© 2007 American Society of Nephrology
doi: 10.1681/ASN.2007010087
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BASIC RESEARCH

Mammalian Target of Rapamycin Inhibition Halts the Progression of Proteinuria in a Rat Model of Reduced Renal Mass

Fritz Diekmann*,{dagger}, Jordi Rovira*, Joaquim Carreras{ddagger}, Edgar M. Arellano*, Elisenda Bañón-Maneus*, María José Ramírez-Bajo*, Alex Gutiérrez-Dalmau*, Mercè Brunet§ and Josep M. Campistol*

Departments of * Nephrology and Renal Transplantation, {ddagger} Pathology, and § Clinical Pharmacology, Hospital Clínic, Barcelona, Spain; and {dagger} Department of Nephrology, Charité Campus Mitte, Berlin, Germany

Correspondence: Dr. Fritz Diekmann, Department of Nephrology and Renal Transplantation, Hospital Clínic, Villarroel, 170, E-08036 Barcelona, Spain. Phone: +34-932275423; Fax: +34-932275498; E-mail: fdiekman{at}clinic.ub.es

Received for publication January 22, 2007. Accepted for publication May 29, 2007.

Many kidney transplant patients experience an increase in proteinuria when converted from a calcineurin inhibitor–based regimen to one based on a mammalian target of rapamycin (mTOR) inhibitor, and preexisting proteinuria and poor renal function have been identified as risk factors for this increase. Our aim was to evaluate the effect of sirolimus, an mTOR inhibitor, on renal function and histology in a proteinuric model of reduced renal mass. Sirolimus-treated animals had approximately half as much proteinuria as vehicle-treated animals (P < 0.05), and had less glomerulosclerosis, tubular atrophy, interstitial fibrosis, and inflammation. Immunohistochemistry showed that sirolimus attenuated the increased expression of renal vascular endothelial growth factor (VEGF), as well as the expression of VEGF receptors 1 and 2. In conclusion, sirolimus halted the progression of proteinuria and structural damage in a rat model of reduced renal mass, possibly through a reduction in renal VEGF activity.




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