In studies with transgenic rats harboring human SLCO4C1, the decrease of uremic toxin (guanidino succinate, asymmetric dimethylarginine, and trans-aconitate) concentrations in plasma suggests that OATP4C1 may facilitate the excretion of uremic toxins in renal failure models and, by extension, in patients with chronic kidney disease. This evidence concerns the gene SLCO4C1 and acute kidney injury.