Evidence map›Paper›PMID 39989380›Full record

ArticleEuropean journal of clinical investigation2025

Circulating amyloid beta 1-40 peptide as an associate of renal function decline.

Georgios Mavraganis, Georgios Georgiopoulos, Georgios Zervas, Evmorfia Aivalioti, Dimitrios Delialis, Ioannis Petropoulos, Nikolaos Rachiotis, Christina Konstantaki, Chrysoula Moustou, Maria-Aggeliki Dimopoulou and 6 more

Abstract read
In one paragraph

Article in European journal of clinical investigation, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed, 1 pooled it
–field-weighted citation impact
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

5 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
  2. Amyloid-beta (1-40) peptide is associated with systemic metabolic health.European journal of clinical investigation · 2026
    Article
  3. Article
  4. How to measure and model cardiovascular aging.Cardiovascular research · 2025
    Review
  5. 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

16 authors.

Georgios MavraganisDepartment of Clinical Therapeutics, Alexandra Hospital, National and Kapodistrian University of Athens Medical School, Athens, Greece.
Georgios GeorgiopoulosDepartment of Clinical Therapeutics, Alexandra Hospital, National and Kapodistrian University of Athens Medical School, Athens, Greece.ORCID https://orcid.org/0000-0001-7661-5253
Georgios ZervasDepartment of Clinical Therapeutics, Alexandra Hospital, National and Kapodistrian University of Athens Medical School, Athens, Greece.
Evmorfia AivaliotiDepartment of Clinical Therapeutics, Alexandra Hospital, National and Kapodistrian University of Athens Medical School, Athens, Greece.
Dimitrios DelialisDepartment of Clinical Therapeutics, Alexandra Hospital, National and Kapodistrian University of Athens Medical School, Athens, Greece.
Ioannis PetropoulosDepartment of Clinical Therapeutics, Alexandra Hospital, National and Kapodistrian University of Athens Medical School, Athens, Greece.
Nikolaos RachiotisDepartment of Clinical Therapeutics, Alexandra Hospital, National and Kapodistrian University of Athens Medical School, Athens, Greece.
Christina KonstantakiDepartment of Clinical Therapeutics, Alexandra Hospital, National and Kapodistrian University of Athens Medical School, Athens, Greece.
Chrysoula MoustouDepartment of Clinical Therapeutics, Alexandra Hospital, National and Kapodistrian University of Athens Medical School, Athens, Greece.
Maria-Aggeliki DimopoulouDepartment of Clinical Therapeutics, Alexandra Hospital, National and Kapodistrian University of Athens Medical School, Athens, Greece.
Marco SachseDepartment of Cardiovascular Surgery, University Heart and Vascular Centre, University Medical Centre Hamburg-Eppendorf, Hamburg, Germany.
Simon Tual-ChalotBiosciences Institute, Vascular Biology and Medicine Theme, Faculty of Medical Sciences, Newcastle University, Newcastle upon Tyne, UK.ORCID https://orcid.org/0000-0002-9307-7175
Kateryna SopovaDepartment of Cardiovascular Research, Medical Faculty Mannheim, Heidelberg University, Mannheim, Germany.
Erasmia PsimmenouDepartment of Clinical Therapeutics, Alexandra Hospital, National and Kapodistrian University of Athens Medical School, Athens, Greece.
Konstantinos StellosDepartment of Cardiovascular Research, Medical Faculty Mannheim, Heidelberg University, Mannheim, Germany.ORCID https://orcid.org/0000-0002-0194-0825
Kimon StamatelopoulosDepartment of Clinical Therapeutics, Alexandra Hospital, National and Kapodistrian University of Athens Medical School, Athens, Greece.ORCID https://orcid.org/0000-0001-6444-8734

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundRecent evidence suggests that Alzheimer's amyloid-beta (1-40) (Αβ1-40), an emerging biomarker of cardiovascular disease, may be involved in the heart-brain-renal axis. We aimed to comprehensively explore the association between circulating Aβ1-40 levels and renal function and its clinical relevance.

methodsConsecutively recruited subjects in the Athens Angiometabolic Registry with measured Aβ1-40 plasma levels (n = 811) were analysed. Αβ1-40 was measured by enzyme-linked immunosorbent assay and glomerular filtration rate (GFR) was calculated using the abbreviated four-variable Modification of Diet in Renal Disease (MDRD) formula. All-cause mortality was the main clinical endpoint across a median follow-up of 47 months.

resultsCross-sectionally, a bidirectional association between Αβ1-40 [adjusted odds ratio (adjOR) = 3.67 for highest tertile of Αβ1-40 and chronic kidney disease (CKD) stage ≥3, p < .001] and CKD stage ≥3 (adjOR = 3.52 for association with highest Aβ1-40 tertile, p < .001) was observed. Longitudinally, increased Αβ1-40 at baseline was associated with decline in renal function at follow-up (adjOR for CKD stage ≥3 = 2.26, p = .033). Similarly, longitudinal changes in Aβ1-40 were inversely associated with changes in GFR (OR = .77 per 1 SD increase in Aβ1-40, p = .006). Aβ1-40 was associated with all-cause mortality, independently of traditional risk factors (hazard ratio = 1.20 per 1 SD increase in Aβ1-40, p = .016). An indirect effect of GFR on the association between Aβ1-40 and mortality (p < .05) with an estimated indirect-to-total effect ratio of .334, but not of Αβ1-40 on GFR with mortality, was observed.

conclusionsIn a population with a wide range of GFR, we found a bidirectional association between Αβ1-40 levels and renal function. The association of Αβ1-40 with all-cause mortality was partly mediated by lower GFR.

Indexed as

Amyloid beta-PeptidesPeptide FragmentsRenal Insufficiency, ChronicAgedBiomarkersCross-Sectional StudiesFemaleGlomerular Filtration RateHumansMaleMiddle AgedAmyloid beta-Peptidesamyloid beta-protein (1-40)BiomarkersPeptide Fragmentsall‐cause mortalityamyloid Αβ1‐40glomerular filtration ratekidney functionmediation analysis

Identifiers

PMID39989380
PMCPMC12011680

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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.