Role of interleukin-13 on the development of minimal change nephrotic syndrome - A novel animal model

Abstract

IL-13 has been implicated in the pathogenesis of minimal change nephrotic syndrome (MCNS). This study aimed to investigate the role of IL-13 on the development of proteinuria and expression of podocyte-related genes associated with nephrotic syndrome. IL-13 was overexpressed in Wistar rats through transfection of a mammalian expression vector cloned with the rat IL-13 gene by in-vivo electroporation. The IL-13 transfected rats (n=41) showed significant proteinuria, hypoalbuminemia and hypercholesterolemia when compared to control rats (n=17). No significant histological changes were observed in the glomeruli of IL-13- transfected rats except effacement of podocyte foot processes. Glomerular gene and protein expression was significantly upregulated for B7-1 and IL-4RI?, but downregulated for nephrin, podocin and dystroglycan in IL-13-transfected rats compared to controls. In conclusion, overexpression of IL-13 causes podocyte injury and induces minimal change-like nephropathy in rat.