Scientific findings have shown that increases in IS concentrations which occur from the beginning of CKD progression are capable of activating the deposition of fibroblasts via the HSP90 depletion pathway or TGF-β1 induction mediators, and similar gene matrices against decapentaplegic (SMAD3), contributing to renal fibrosis, thus increasing the pro-inflammatory phenotype and progressing to renal degradation (Shimizu et al., 2013). This evidence concerns the gene TGFB1 and renal fibrosis.