Evidence map›Paper›PMID 32367640›Full record

ArticleFASEB journal : official publication of the Federation of American Societies for Experimental Biology2020

Inhibition of urea transporter ameliorates uremic cardiomyopathy in chronic kidney disease.

Akihiro Kuma, Xiaonan H Wang, Janet D Klein, Lin Tan, Nawazish Naqvi, Fitra Rianto, Ying Huang, Manshu Yu, Jeff M Sands

Open access · greenAbstract read
In one paragraph

Article in FASEB journal : official publication of the Federation of American Societies for Experimental Biology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
0.6field-weighted citation impact, top 37% 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

9 citing papers in PubMed, 14 citations in OpenAlex.

  1. Review
  2. A guide to uraemic toxicity.Nature reviews. Nephrology · 2026
    Review
  3. Review
  4. Article
  5. Article
  6. Article
  7. Article
  8. Urea levels and cardiovascular disease in patients with chronic kidney disease.Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association · 2022
    Article
  9. Article
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

9 authors at 2 institutions in 3 countries.

Akihiro KumaRenal Division, Department of Medicine, Emory University School of Medicine, Atlanta, GA, USA.
Xiaonan H WangRenal Division, Department of Medicine, Emory University School of Medicine, Atlanta, GA, USA.
Janet D KleinRenal Division, Department of Medicine, Emory University School of Medicine, Atlanta, GA, USA.
Lin TanDivision of Cardiology, Department of Medicine, Emory University School of Medicine, Atlanta, GA, USA.
Nawazish NaqviDivision of Cardiology, Department of Medicine, Emory University School of Medicine, Atlanta, GA, USA.
Fitra RiantoRenal Division, Department of Medicine, Emory University School of Medicine, Atlanta, GA, USA.
Ying HuangRenal Division, Department of Medicine, Emory University School of Medicine, Atlanta, GA, USA.
Manshu YuRenal Division, Department of Medicine, Emory University School of Medicine, Atlanta, GA, USA.
Jeff M SandsRenal Division, Department of Medicine, Emory University School of Medicine, Atlanta, GA, USA.
Emory University · USUniversity of Occupational and Environmental Health Japan · JP

Funding

Regulation of Renal Inner Medullary FunctionR01DK041707 · NIDDK · EMORY UNIVERSITY · PI SANDS, JEFF M · 1996 to 2017
$4.3M
NIDDK NIH HHS R01 DK041707
6 · The paper itself

Abstract

Uremic cardiomyopathy, characterized by hypertension, cardiac hypertrophy, and fibrosis, is a complication of chronic kidney disease (CKD). Urea transporter (UT) inhibition increases the excretion of water and urea, but the effect on uremic cardiomyopathy has not been studied. We tested UT inhibition by dimethylthiourea (DMTU) in 5/6 nephrectomy mice. This treatment suppressed CKD-induced hypertension and cardiac hypertrophy. In CKD mice, cardiac fibrosis was associated with upregulation of UT and vimentin abundance. Inhibition of UT suppressed vimentin amount. Left ventricular mass index in DMTU-treated CKD was less compared with non-treated CKD mice as measured by echocardiography. Nephrectomy was performed in UT-A1/A3 knockout (UT-KO) to further confirm our finding. UT-A1/A3 deletion attenuates the CKD-induced increase in cardiac fibrosis and hypertension. The amount of α-smooth muscle actin and tgf-β were significantly less in UT-KO with CKD than WT/CKD mice. To study the possibility that UT inhibition could benefit heart, we measured the mRNA of renin and angiotensin-converting enzyme (ACE), and found both were sharply increased in CKD heart; DMTU treatment and UT-KO significantly abolished these increases. Conclusion: Inhibition of UT reduced hypertension, cardiac fibrosis, and improved heart function. These changes are accompanied by inhibition of renin and ACE.

Indexed as

ActinsAnimalsCardiomegalyCardiomyopathiesFibrosisHeart VentriclesHypertensionKidneyMaleMembrane Transport ProteinsMiceMice, Inbred C57BLPeptidyl-Dipeptidase ARenal Insufficiency, ChronicRNA, MessengerTransforming Growth Factor betaActinsMembrane Transport ProteinsPeptidyl-Dipeptidase ARNA, MessengerTransforming Growth Factor betaUreaUrea Transporterscardiac fibrosiscardiovascular diseasedimethylthioureadiureticshypertrophy

Identifiers

PMID32367640
PMCPMC7302978
OpenAlexW3021721934

What OpenQuestion holds

Textmetadata
LicenceTDM
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.