Evidence map›Paper›PMID 33481059›Full record

ReviewJournal of molecular medicine (Berlin, Germany)2021

Vascular pathologies in chronic kidney disease: pathophysiological mechanisms and novel therapeutic approaches.

Philip Düsing, Andreas Zietzer, Philip Roger Goody, Mohammed Rabiul Hosen, Christian Kurts, Georg Nickenig, Felix Jansen

Open access · hybridAbstract readReview
In one paragraph

Review in Journal of molecular medicine (Berlin, Germany), 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 139 papers, 6 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
139citing papers in PubMed, 6 pooled it
19.3field-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

139 citing papers in PubMed, 6 syntheses or guidelines pooled it, 208 citations in OpenAlex.

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  4. Intravenous sodium thiosulphate for vascular calcification of hemodialysis patients-a systematic review and meta-analysis.Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association · 2023
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79 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

7 authors at 1 institution in 1 country.

Philip DüsingHeart Center, Department of Medicine II, University Hospital Bonn, University of Bonn, Venusberg-Campus 1, 53127, Bonn, Germany.
Andreas ZietzerHeart Center, Department of Medicine II, University Hospital Bonn, University of Bonn, Venusberg-Campus 1, 53127, Bonn, Germany.
Philip Roger GoodyHeart Center, Department of Medicine II, University Hospital Bonn, University of Bonn, Venusberg-Campus 1, 53127, Bonn, Germany.
Mohammed Rabiul HosenHeart Center, Department of Medicine II, University Hospital Bonn, University of Bonn, Venusberg-Campus 1, 53127, Bonn, Germany.
Christian KurtsInstitute of Experimental Immunology, University Hospital Bonn, University of Bonn, Venusberg-Campus 1, Bonn, 53127, Germany.
Georg NickenigHeart Center, Department of Medicine II, University Hospital Bonn, University of Bonn, Venusberg-Campus 1, 53127, Bonn, Germany.
Felix JansenHeart Center, Department of Medicine II, University Hospital Bonn, University of Bonn, Venusberg-Campus 1, 53127, Bonn, Germany. felix.jansen@ukbonn.de.ORCID 0000-0001-6962-5330
University of Bonn · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cardiovascular disease (CVD) is a major cause of death in patients with chronic kidney disease (CKD). Both conditions are rising in incidence as well as prevalence, creating poor outcomes for patients and high healthcare costs. Recent data suggests CKD to be an independent risk factor for CVD. Accumulation of uremic toxins, chronic inflammation, and oxidative stress have been identified to act as CKD-specific alterations that increase cardiovascular risk. The association between CKD and cardiovascular mortality is markedly influenced through vascular alterations, in particular atherosclerosis and vascular calcification (VC). While numerous risk factors promote atherosclerosis by inducing endothelial dysfunction and its progress to vascular structural damage, CKD affects the medial layer of blood vessels primarily through VC. Ongoing research has identified VC to be a multifactorial, cell-mediated process in which numerous abnormalities like mineral dysregulation and especially hyperphosphatemia induce a phenotype switch of vascular smooth muscle cells to osteoblast-like cells. A combination of pro-calcifying stimuli and an impairment of inhibiting mechanisms like fetuin A and vitamin K-dependent proteins like matrix Gla protein and Gla-rich protein leads to mineralization of the extracellular matrix. In view of recent studies, intercellular communication pathways via extracellular vesicles and microRNAs represent key mechanisms in VC and thereby a promising field to a deeper understanding of the involved pathomechanisms. In this review, we provide an overview about pathophysiological mechanisms connecting CKD and CVD. Special emphasis is laid on vascular alterations and more recently discovered molecular pathways which present possible new therapeutic targets.

Indexed as

AnimalsAtherosclerosisCardio-Renal SyndromeDisease Models, AnimalEndothelium, VascularExtracellular VesiclesHeart Disease Risk FactorsHumansIncidenceInflammationMiceMicroRNAsMyocytes, Smooth MuscleRatsRenal Insufficiency, ChronicTunica MediaMicroRNAsMirn142 microRNA, mouseVitamin K 1AtherosclerosisChronic kidney diseaseCoronary artery diseaseVascular calcification

Identifiers

PMID33481059
PMCPMC7900031
OpenAlexW3124003341

What OpenQuestion 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 OpenQuestion graph.