Evidence mapPaperPMID 36749631Full record

Trial reportJCI insight2023

Mineralocorticoid receptor antagonism in diabetes reduces albuminuria by preserving the glomerular endothelial glycocalyx.

Michael Crompton, Joanne K Ferguson, Raina D Ramnath, Karen L Onions, Anna S Ogier, Monica Gamez, Colin J Down, Laura Skinner, Kitty H Wong, Lauren K Dixon and 10 more

Open access · goldAbstract readRandomized Controlled Trial
In one paragraph

Trial report in JCI insight, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
11.7field-weighted citation impact, top 1% 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

21 citing papers in PubMed, 58 citations in OpenAlex.

  1. Trial
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  20. Diabetic Nephropathy and Gaseous Modulators.Antioxidants (Basel, Switzerland) · 2023
    Review
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

20 authors at 5 institutions in 4 countries.

Michael CromptonBristol Renal, Translational Health Sciences, Bristol Medical School, University of Bristol, Bristol, United Kingdom.
Joanne K FergusonBristol Renal, Translational Health Sciences, Bristol Medical School, University of Bristol, Bristol, United Kingdom.
Raina D RamnathBristol Renal, Translational Health Sciences, Bristol Medical School, University of Bristol, Bristol, United Kingdom.
Karen L OnionsBristol Renal, Translational Health Sciences, Bristol Medical School, University of Bristol, Bristol, United Kingdom.
Anna S OgierBristol Renal, Translational Health Sciences, Bristol Medical School, University of Bristol, Bristol, United Kingdom.
Monica GamezBristol Renal, Translational Health Sciences, Bristol Medical School, University of Bristol, Bristol, United Kingdom.
Colin J DownBristol Renal, Translational Health Sciences, Bristol Medical School, University of Bristol, Bristol, United Kingdom.
Laura SkinnerBristol Renal, Translational Health Sciences, Bristol Medical School, University of Bristol, Bristol, United Kingdom.
Kitty H WongBristol Renal, Translational Health Sciences, Bristol Medical School, University of Bristol, Bristol, United Kingdom.
Lauren K DixonBristol Renal, Translational Health Sciences, Bristol Medical School, University of Bristol, Bristol, United Kingdom.
Judit SutakPathology Department, Southmead Hospital, Bristol, United Kingdom.
Steven J HarperSchool of Physiology, Pharmacology & Neuroscience, University of Bristol, Bristol, United Kingdom.
Paola PontrelliDivision of Nephrology, Dialysis and Transplantation, Department of Emergency and Organ Transplantation, Aldo Moro University of Bari, Bari, Italy.
Loreto GesualdoDivision of Nephrology, Dialysis and Transplantation, Department of Emergency and Organ Transplantation, Aldo Moro University of Bari, Bari, Italy.
Hiddo L HeerspinkDepartment of Clinical Pharmacology, University Medical Center Groningen, University of Groningen, The Netherlands.
Robert D TotoDepartment of Clinical Sciences, The University of Texas Southwestern Medical Center, Dallas, Texas, USA.
Gavin I WelshBristol Renal, Translational Health Sciences, Bristol Medical School, University of Bristol, Bristol, United Kingdom.
Rebecca R FosterBristol Renal, Translational Health Sciences, Bristol Medical School, University of Bristol, Bristol, United Kingdom.
Simon C SatchellBristol Renal, Translational Health Sciences, Bristol Medical School, University of Bristol, Bristol, United Kingdom.
Matthew J ButlerBristol Renal, Translational Health Sciences, Bristol Medical School, University of Bristol, Bristol, United Kingdom.
University of Bristol · GBUniversity of Bari Aldo Moro · ITSouthmead Hospital · GBThe University of Texas Southwestern Medical Center · USUniversity Medical Center Groningen · NL

Funding

British Heart Foundation FS/CRTF/22/24361British Heart Foundation PG/15/81/31740British Heart Foundation PG/20/10187British Heart Foundation PG/22/11121Medical Research Council MR/M018237/1Medical Research Council MR/T031921/1Medical Research Council MR/W024187/1
6 · The paper itself

Abstract

The glomerular endothelial glycocalyx (GEnGlx) forms the first part of the glomerular filtration barrier. Previously, we showed that mineralocorticoid receptor (MR) activation caused GEnGlx damage and albuminuria. In this study, we investigated whether MR antagonism could limit albuminuria in diabetes and studied the site of action. Streptozotocin-induced diabetic Wistar rats developed albuminuria, increased glomerular albumin permeability (Ps'alb), and increased glomerular matrix metalloproteinase (MMP) activity with corresponding GEnGlx loss. MR antagonism prevented albuminuria progression, restored Ps'alb, preserved GEnGlx, and reduced MMP activity. Enzymatic degradation of the GEnGlx negated the benefits of MR antagonism, confirming their dependence on GEnGlx integrity. Exposing human glomerular endothelial cells (GEnC) to diabetic conditions in vitro increased MMPs and caused glycocalyx damage. Amelioration of these effects confirmed a direct effect of MR antagonism on GEnC. To confirm relevance to human disease, we used a potentially novel confocal imaging method to show loss of GEnGlx in renal biopsy specimens from patients with diabetic nephropathy (DN). In addition, patients with DN randomized to receive an MR antagonist had reduced urinary MMP2 activity and albuminuria compared with placebo and baseline levels. Taken together, our work suggests that MR antagonists reduce MMP activity and thereby preserve GEnGlx, resulting in reduced glomerular permeability and albuminuria in diabetes.

Indexed as

Diabetes MellitusDiabetic NephropathiesAlbuminuriaAnimalsEndothelial CellsGlycocalyxHumansMineralocorticoid Receptor AntagonistsRatsRats, WistarReceptors, MineralocorticoidMineralocorticoid Receptor AntagonistsReceptors, MineralocorticoidChronic kidney diseaseDiabetesEndocrinologyGlycobiologyNephrology

Identifiers

PMID36749631
PMCPMC10077489
OpenAlexW4319332817

What Socratic holds

Textmetadata
LicenceCC BY
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 Socratic graph.