Another clinical finding in support of this is the dysfunction of OATs in patients with severe renal dysfunction (creatinine clearance (CrCl) < 30 mL/min), who demonstrated decreased renal clearance of sulfate conjugate of morinidazole (substrate for OAT1 and OAT3) and glucuronide conjugates (substrates for OAT3) [18]. This evidence concerns the gene SLC22A8 and Abnormal renal physiology.