Therefore, we hypothesized that (i) dose-dependent competition between furosemide and selected PBUTs (IS, Kyn, PCS, IAA, and KA) for OAT1 and/or OAT3 leads to higher serum free UT concentrations in furosemide-treated patients with CKD than in those not treated with furosemide, and (ii) this difference is independent of other determinants of UT concentrations, such as the eGFR (Figure 1). This evidence concerns the gene SLC22A6 and chronic kidney disease.