“…They commented that the origin of GSA was unknown but suggested that it would be expected to arise from failure of transamidination and described that uremic patients excrete substantially more GSA than control subjects. In the previous study [22,26], GAA was decreased in 24-h urine samples from uremic patients, since urine production would be impaired in a substantial portion of the kidney. It was reported that GSA and GAA are localized in the inner medulla and cortex of the kidney, respectively [27].…”