The limitations of this study are as follows, first, the study period was short to assess the change of eGFR from baseline to the final visit. Second, ACR was used instead of measuring the urinary albumin excretion, because 24 h urine collection would have been difficult in outpatients; this study was conducted as a multicenter study, and the ACR has been shown previously to be positively correlated with the urinary albumin excretion [26]. Also, the ACR was not calculated

by the levels of albumin and creatinine in the first morning void urine. Third, we did not measure the true GFR and ambulatory blood pressure monitoring, because of the difficulty in performing these measurements in the outpatient setting. In the next step, we consider that additional clinical studies are needed to validate the effect on albuminuria of selleck chemicals llc topiroxostat in patients with high albuminuria levels, because the percent change of the ACR from the baseline to the final visit in this study was set as a secondary endpoint and the baseline level of ACR was not sufficiently higher in the both groups. Also, it is important

to clarify the maximum effect on albuminuria in clinical BAY 80-6946 datasheet practice, its time relationship, and dose-responsiveness. In conclusion, the results of this study demonstrated that treatment with topiroxostat effectively reduced the serum urate levels in Japanese hyperuricemic patients with renal impairment, with or without gout. In addition, topiroxostat also exhibited the potential to decrease the albuminuria in these patients, although further clinical studies are needed to validate its efficacy. Acknowledgments We are grateful to the investigators, local study coordinators, PAK5 and patients for their

valuable contributions to this study; Yoshimi Ogawa, employee of Sanwa Kagaku Kenkyusho co., ltd. (SKK), for contribution to the study designs; Hiroya Hashimoto, employee of SKK, for statistical programming support; and Ryusuke Sakamoto, employee of SKK for medical writing support. This study was funded by SKK. Conflict of interest TH was an advisor to SKK regarding this study and received honoraria from SKK. IH’s laboratory has received research subsidies from SKK. The other authors have declared that no conflict of interest exists. Open AccessThis article is distributed under the terms of the Creative Commons Attribution License which permits any use, distribution, and reproduction in any medium, provided the original author(s) and the source are credited. References 1. Zhu Y, Pandya BJ, Choi HK. Comorbidities of gout and hyperuricemia in the US general population: NHANES 2007–2008. Am J Med. 2012;125:679–87.PubMedCrossRef 2. Iseki K, Oshiro S, Tozawa M, et al. Significance of hyperuricemia on the early detection of renal OTX015 cell line failure in a cohort of screened subjects. Hypertens Res. 2001;24:691–7.PubMedCrossRef 3. Chonchol M, Shlipak MG, Katz R, Sarnak M, et al.