Evidence map›Paper›PMID 35408796›Full record

ReviewInternational journal of molecular sciences2022

The Role of Advanced Glycation End Products and Its Soluble Receptor in Kidney Diseases.

Mieke Steenbeke, Reinhart Speeckaert, Stéphanie Desmedt, Griet Glorieux, Joris R Delanghe, Marijn M Speeckaert

Open access · goldAbstract readReview
In one paragraph

Review in International journal of molecular sciences, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
46citing papers in PubMed, 2 pooled it
8.3field-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

46 citing papers in PubMed, 2 syntheses or guidelines pooled it, 65 citations in OpenAlex.

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  13. [Elevated advanced glycation endproducts is a risk factor for stenosis after primary arteriovenous fistula surgery].Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2025
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  17. Serum Levels of NBiomedicines · 2025
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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

6 authors at 2 institutions in 1 country.

Mieke SteenbekeNephrology Unit, Department of Internal Medicine and Pediatrics, Ghent University Hospital, 9000 Ghent, Belgium.ORCID 0000-0003-2731-7545
Reinhart SpeeckaertDepartment of Dermatology, Ghent University Hospital, 9000 Ghent, Belgium.
Stéphanie DesmedtNephrology Unit, Department of Internal Medicine and Pediatrics, Ghent University Hospital, 9000 Ghent, Belgium.ORCID 0000-0002-6846-6558
Griet GlorieuxNephrology Unit, Department of Internal Medicine and Pediatrics, Ghent University Hospital, 9000 Ghent, Belgium.ORCID 0000-0002-7641-4707
Joris R DelangheDepartment of Diagnostic Sciences, Ghent University, 9000 Ghent, Belgium.ORCID 0000-0002-5702-6792
Marijn M SpeeckaertNephrology Unit, Department of Internal Medicine and Pediatrics, Ghent University Hospital, 9000 Ghent, Belgium.ORCID 0000-0001-9183-4390
Ghent University Hospital · BEGhent University · BE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Patients with chronic kidney disease (CKD) are more prone to oxidative stress and chronic inflammation, which may lead to an increase in the synthesis of advanced glycation end products (AGEs). Because AGEs are mostly removed by healthy kidneys, AGE accumulation is a result of both increased production and decreased kidney clearance. On the other hand, AGEs may potentially hasten decreasing kidney function in CKD patients, and are independently related to all-cause mortality. They are one of the non-traditional risk factors that play a significant role in the underlying processes that lead to excessive cardiovascular disease in CKD patients. When AGEs interact with their cell-bound receptor (RAGE), cell dysfunction is initiated by activating nuclear factor kappa-B (NF-κB), increasing the production and release of inflammatory cytokines. Alterations in the AGE-RAGE system have been related to the development of several chronic kidney diseases. Soluble RAGE (sRAGE) is a decoy receptor that suppresses membrane-bound RAGE activation and AGE-RAGE-related toxicity. sRAGE, and more specifically, the AGE/sRAGE ratio, may be promising tools for predicting the prognosis of kidney diseases. In the present review, we discuss the potential role of AGEs and sRAGE as biomarkers in different kidney pathologies.

Indexed as

Cardiovascular DiseasesRenal Insufficiency, ChronicBiomarkersGlycation End Products, AdvancedHumansInflammationReceptor for Advanced Glycation End ProductsBiomarkersGlycation End Products, AdvancedReceptor for Advanced Glycation End Productsadvanced glycation end products (AGEs)chronic kidney disease (CKD)soluble receptor for AGEs (sRAGE)

Identifiers

PMID35408796
PMCPMC8998875
OpenAlexW4221087933

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.