These findings suggest that AGE-BSA, or AGEs in general, in proximal tubular cells may contribute to (I) the onset of renal fibrosis through Snai1 induction [42,43]; (II) activation of genes involved in the endothelial-to-mesenchymal transition (EMT) via elevated Ctgf mRNA expression [44]; and (III) proximal tubular cells hypertrophy via p27Kip1 [45], a mechanism previously linked to elevated glucose or increased levels of Angiotensin II. This evidence concerns the gene CDKN1B and renal fibrosis.