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Abstract: FR-PO971

Lubiprostone Inhibits Progression of Renal Failure via Intestinal Microbiome

Session Information

Category: CKD (Non-Dialysis)

  • 2302 CKD (Non-Dialysis): Clinical, Outcomes, and Trials


  • Watanabe, Shun, Tohoku Daigaku, Sendai, Miyagi, Japan
  • Nakayama, Masaaki, St. Luke's International Hospital, Chuo-ku, Tokyo, Japan
  • Yokoo, Takashi, Tokyo Jikeikai Ika Daigaku Igakubu Igakuka Jinzo Koketsuatsu Naikagaku, Minato-ku, Tokyo, Japan
  • Sanada, Satoru, Japan Community Health Care Organization Sendai Hospital, Sendai, Miyagi, Japan
  • Asanuma, Katsuhiko, Chiba Daigaku, Chiba, Chiba, Japan
  • Suzuki, Yusuke, Juntendo Daigaku, Bunkyo-ku, Tokyo, Japan
  • Konta, Tsuneo, Yamagata Daigaku, Yamagata, Yamagata, Japan
  • Abe, Takaaki, Tohoku Daigaku, Sendai, Miyagi, Japan

The gut microbiota and chronic kidney disease (CKD) are believed to be closely interrelated. We previously reported that the administration of the chronic constipation treatment drug lubiprostone (Lubi) in a mouse model of renal failure suppressed the accumulation of uremic toxins in the body during renal failure and demonstrated a renal protective effect. Based on these findings, we hypothesized that Lubi could be a potential novel treatment for kidney diseases.


The objective of this study was to investigate the effects of Lubi on the suppression of uremic toxin accumulation and disease progression in patients with renal failure.
The trial design was randomized, double-blind, placebo-controlled, multicenter collaborative, and exploratory physician-initiated.
A total of 118 patients with CKD Stage 3b were assigned to the placebo group (33 patients), 8 μg group (35 patients), or 16 μg group (50 patients), and the trial was conducted at eight domestic facilities from 2017 to 2020.
The primary outcome was the change in plasma indoxyl sulfate (IS) levels from baseline to 24 weeks after the start of the trial. The secondary outcomes included changes in uremic toxins (phenyl sulfate, p-cresyl sulfate, trimethylamine N-oxide) and eGFR.
Statistical analysis involved conducting ANCOVA analysis with the eGFR value at allocation and the baseline values of each evaluation item as covariates, followed by post hoc testing using Dunnett's method.


The change in IS levels was as follows: placebo group: 0.13±0.15 μg/ml, 8 μg group: 0.091±0.15 μg/ml, 16 μg group: 0.13±0.13 μg/ml (least squares mean ± standard error), and no significant differences were observed. However, the change in eGFR was as follows: placebo group: -1.55±0.65 ml/min/1.73m2, 8 μg group: -0.34±0.66 ml/min/1.73m2, 16 μg group: 0.37±0.54 ml/min/1.73m2, with a significant difference observed between the placebo and 16 μg groups (p-value = 0.0457).


While Lubi 16 μg did not improve uremic toxin levels, it improved eGFR, thereby generating new evidence for the treatment of CKD. In the future, we plan to analyze metabolites and the gut microbiota from the samples obtained in this trial to explore the mechanism of the inhibitory effect of Lubi on the progression of renal failure and search for new targets for renal failure treatment.