The activation of the VDR promoted the reduction in the renal microvasculature disturbances by attenuating the TGF-β1/Smad2/3-dependent and downregulation of Ang-2 and AT1 expression, regulating the Angs/Tie-2 and VEGF/VEGFR2 axes, which presents disturbances in ADR-induced nephropathy in rats. This evidence concerns the gene SMAD2 and kidney disorder.