In vitro study using human proximal tubule epithelial cell line demonstrated that high ambient glucose inhibits FXR expression and that the activation of FXR mitigates the effects of high ambient glucose to increase pro-inflammatory, pro-fibrotic mediators and extracellular matrix accumulation of collagen IV and fibronectin, which are the first step towards the development of CKD. This evidence concerns the gene NR1H4 and chronic kidney disease.