Evidence map›Paper›PMID 25525179›Full record

ArticleJournal of the American Society of Nephrology : JASN2015

Alteration of the Intestinal Environment by Lubiprostone Is Associated with Amelioration of Adenine-Induced CKD.

Eikan Mishima, Shinji Fukuda, Hisato Shima, Akiyoshi Hirayama, Yasutoshi Akiyama, Yoichi Takeuchi, Noriko N Fukuda, Takehiro Suzuki, Chitose Suzuki, Akinori Yuri and 5 more

Open access · bronzeAbstract read
In one paragraph

Article in Journal of the American Society of Nephrology : JASN, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 111 papers.

0numbers the graph read from it
0cells of the map it votes in
111citing papers in PubMed
6.8field-weighted citation impact, top 2% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

111 citing papers in PubMed, 188 citations in OpenAlex.

  1. Trial
  2. Science advances · 2023
    Trial
  3. Contribution of 'clinically negligible' residual kidney function to clearance of uremic solutes.Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association · 2020
    Trial
  4. Review
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  18. The Gut-Kidney Axis in Chronic Kidney Diseases.Diagnostics (Basel, Switzerland) · 2024
    Review
  19. Review
  20. Article

51 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

15 authors at 3 institutions in 2 countries.

Eikan MishimaDivision of Nephrology, Endocrinology, and Vascular Medicine and Tohoku Medical Megabank Organization, Tohoku University, Sendai, Japan;
Shinji FukudaInstitute for Advanced Biosciences, Keio University, Tsuruoka, Japan; RIKEN Center for Integrative Medical Sciences, Yokohama, Japan;
Hisato ShimaDivision of Nephrology, Endocrinology, and Vascular Medicine and.
Akiyoshi HirayamaInstitute for Advanced Biosciences, Keio University, Tsuruoka, Japan;
Yasutoshi AkiyamaDivision of Nephrology, Endocrinology, and Vascular Medicine and Tohoku Medical Megabank Organization, Tohoku University, Sendai, Japan;
Yoichi TakeuchiDivision of Nephrology, Endocrinology, and Vascular Medicine and.
Noriko N FukudaInstitute for Advanced Biosciences, Keio University, Tsuruoka, Japan;
Takehiro SuzukiDivision of Nephrology, Endocrinology, and Vascular Medicine and.
Chitose SuzukiDivision of Nephrology, Endocrinology, and Vascular Medicine and.
Akinori YuriLaboratory of Oncology, Pharmacy Practice and Sciences, Tohoku University Graduate School of Pharmaceutical Sciences, Sendai, Japan; and.
Koichi KikuchiDepartment of Clinical Biology and Hormonal Regulation, Tohoku University Graduate School of Medicine, Sendai, Japan;
Yoshihisa TomiokaLaboratory of Oncology, Pharmacy Practice and Sciences, Tohoku University Graduate School of Pharmaceutical Sciences, Sendai, Japan; and.
Sadayoshi ItoDivision of Nephrology, Endocrinology, and Vascular Medicine and.
Tomoyoshi SogaInstitute for Advanced Biosciences, Keio University, Tsuruoka, Japan;
Takaaki AbeDivision of Nephrology, Endocrinology, and Vascular Medicine and Department of Clinical Biology and Hormonal Regulation, Tohoku University Graduate School of Medicine, Sendai, Japan; Department of Medical Science, Tohoku University Graduate School of Biomedical Engineering, Sendai, Japan takaabe@med.tohoku.ac.jp.
Center for Vascular Biology Research · USTohoku University · JPKeio University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The accumulation of uremic toxins is involved in the progression of CKD. Various uremic toxins are derived from gut microbiota, and an imbalance of gut microbiota or dysbiosis is related to renal failure. However, the pathophysiologic mechanisms underlying the relationship between the gut microbiota and renal failure are still obscure. Using an adenine-induced renal failure mouse model, we evaluated the effects of the ClC-2 chloride channel activator lubiprostone (commonly used for the treatment of constipation) on CKD. Oral administration of lubiprostone (500 µg/kg per day) changed the fecal and intestinal properties in mice with renal failure. Additionally, lubiprostone treatment reduced the elevated BUN and protected against tubulointerstitial damage, renal fibrosis, and inflammation. Gut microbiome analysis of 16S rRNA genes in the renal failure mice showed that lubiprostone treatment altered their microbial composition, especially the recovery of the levels of the Lactobacillaceae family and Prevotella genus, which were significantly reduced in the renal failure mice. Furthermore, capillary electrophoresis-mass spectrometry-based metabolome analysis showed that lubiprostone treatment decreased the plasma level of uremic toxins, such as indoxyl sulfate and hippurate, which are derived from gut microbiota, and a more recently discovered uremic toxin, trans-aconitate. These results suggest that lubiprostone ameliorates the progression of CKD and the accumulation of uremic toxins by improving the gut microbiota and intestinal environment.

Indexed as

AdenineAlprostadilAnimalsChloride Channel AgonistsDisease ProgressionDrug Evaluation, PreclinicalGastrointestinal TractKidney Failure, ChronicLubiprostoneMaleMice, Inbred C57BLMicrobiotaRandom AllocationUremiaAdenineAlprostadilChloride Channel AgonistsLubiprostoneCKDgastrointestinal medicationsintestineuremia

Identifiers

PMID25525179
PMCPMC4520171
OpenAlexW2122843838

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.