FMO5 and bacterial urinary tract infection: AT1R-transduced ROS formation, depending on NADPH oxidase, has also been observed in several renal cells in culture.[44] Similar observations have been made in the kidney when the endogenous RAAS was stimulated using the 2 kidney-one clip model.[45] Pro-inflammatory cytokines in a murine UTI model also affected production of OS.[46] Neutrophilic myeloperoxidase is believed to play a pivotal role in many inflammatory diseases.[47,48] Urine myeloperoxidase was increased in the murine UTI model.[49]