Evidence map›Paper›PMID 24854267›Full record

ArticleJournal of the American Society of Nephrology : JASN2014

HDL in children with CKD promotes endothelial dysfunction and an abnormal vascular phenotype.

Rukshana Shroff, Thimoteus Speer, Sophie Colin, Marietta Charakida, Stephen Zewinger, Bart Staels, Giulia Chinetti-Gbaguidi, Inga Hettrich, Lucia Rohrer, Francis O'Neill and 6 more

Open access · bronzeAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Journal of the American Society of Nephrology : JASN, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 71 papers.

0numbers the graph read from it
0cells of the map it votes in
71citing papers in PubMed
5.7field-weighted citation impact, top 3% 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

71 citing papers in PubMed, 121 citations in OpenAlex.

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11 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

16 authors at 6 institutions in 5 countries.

Rukshana ShroffNephrology Unit, Great Ormond Street Hospital for Children, London, United Kingdom; Vascular Physiology Unit, University College London Institute of Child Health, London, United Kingdom; Rukshana.Shroff@gosh.nhs.uk.
Thimoteus SpeerDepartment of Internal Medicine, Nephrology, and Hypertension, Saarland University Medical Centre, Homburg, Saar, Germany;
Sophie ColinFrench Institute of Health and Medical Research Joint Research Unit 1011, European Genomic Institute for Diabetes, Lille Pasteur Institute, Lille 2 University, Lille, France;
Marietta CharakidaVascular Physiology Unit, University College London Institute of Child Health, London, United Kingdom;
Stephen ZewingerDepartment of Internal Medicine, Nephrology, and Hypertension, Saarland University Medical Centre, Homburg, Saar, Germany;
Bart StaelsFrench Institute of Health and Medical Research Joint Research Unit 1011, European Genomic Institute for Diabetes, Lille Pasteur Institute, Lille 2 University, Lille, France;
Giulia Chinetti-GbaguidiFrench Institute of Health and Medical Research Joint Research Unit 1011, European Genomic Institute for Diabetes, Lille Pasteur Institute, Lille 2 University, Lille, France;
Inga HettrichDepartment of Internal Medicine, Nephrology, and Hypertension, Saarland University Medical Centre, Homburg, Saar, Germany;
Lucia RohrerInstitute of Clinical Chemistry and.
Francis O'NeillVascular Physiology Unit, University College London Institute of Child Health, London, United Kingdom;
Eve McLoughlinVascular Physiology Unit, University College London Institute of Child Health, London, United Kingdom;
David LongNephrology Unit, Great Ormond Street Hospital for Children, London, United Kingdom;
Catherine M ShanahanCardiovascular Division, King's College London, London, United Kingdom.
Ulf LandmesserCardiovascular Center, University Hospital Zurich, Zurich, Switzerland; and.
Danilo FliserDepartment of Internal Medicine, Nephrology, and Hypertension, Saarland University Medical Centre, Homburg, Saar, Germany;
John E DeanfieldVascular Physiology Unit, University College London Institute of Child Health, London, United Kingdom;
University College London · GBSaarland University · DEEuropean Genomic Institute for Diabetes · FRInstitute of Child Health · INKing's College London · GBUniversity Hospital of Zurich · CH

Funding

British Heart Foundation RG/11/14/29056Medical Research Council MC_PC_13041Medical Research Council MR/J003638/1Medical Research Council MR/K006584/1
6 · The paper itself

Abstract

Endothelial dysfunction begins in early CKD and contributes to cardiovascular mortality. HDL is considered antiatherogenic, but may have adverse vascular effects in cardiovascular disease, diabetes, and inflammatory conditions. The effect of renal failure on HDL properties is unknown. We studied the endothelial effects of HDL isolated from 82 children with CKD stages 2-5 (HDL(CKD)), who were free of underlying inflammatory diseases, diabetes, or active infections. Compared with HDL from healthy children, HDL(CKD) strongly inhibited nitric oxide production, promoted superoxide production, and increased vascular cell adhesion molecule-1 expression in human aortic endothelial cells, and reduced cholesterol efflux from macrophages. The effects on endothelial cells correlated with CKD grade, with the most profound changes induced by HDL from patients on dialysis, and partial recovery observed with HDL isolated after kidney transplantation. Furthermore, the in vitro effects on endothelial cells associated with increased aortic pulse wave velocity, carotid intima-media thickness, and circulating markers of endothelial dysfunction in patients. Symmetric dimethylarginine levels were increased in serum and fractions of HDL from children with CKD. In a longitudinal follow-up of eight children undergoing kidney transplantation, HDL-induced production of endothelial nitric oxide, superoxide, and vascular cell adhesion molecule-1 in vitro improved significantly at 3 months after transplantation, but did not reach normal levels. These results suggest that in children with CKD without concomitant disease affecting HDL function, HDL dysfunction begins in early CKD, progressing as renal function declines, and is partially reversed after kidney transplantation.

Indexed as

AdolescentArginineBiomarkersChildCholesterol, HDLCholesterol, LDLEndothelium, VascularFemaleHumansKidney TransplantationMaleNitric OxideRenal DialysisRenal Insufficiency, ChronicTriglyceridesVascular DiseasesArginineBiomarkersCholesterol, HDLCholesterol, LDLNitric Oxidesymmetric dimethylarginineTriglycerides

Identifiers

PMID24854267
PMCPMC4214534
OpenAlexW2170492758

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.