The results of the present study demonstrate that 25OHD3 can activate VDR in uremic conditions, and agree with previous results showing similar results in animals with normal renal function.[21] It has been shown that uremic milieu contains toxins that block the binding of activated VDR with VDRE in the promoter of target genes.[22] Thus, inhibition of VDR target gene expression by uremia can partially explain the resistance to 1,25(OH)2D3 observed in CKD. Here, VDR is linked to uremia.