Evidence map›Paper›PMID 39602894›Full record

ArticleKidney & blood pressure research2025

Severe Coronary Artery Calcifications in Chronic Kidney Disease Patients, Coupled with Inflammation and Bone Mineral Disease Derangement, Promote Major Adverse Cardiovascular Events through Vascular Remodeling.

Marion Morena-Carrere, Isabelle Jaussent, Leila Chenine, Anne-Marie Dupuy, Anne-Sophie Bargnoux, Hélène Leray-Moragues, Kada Klouche, Hélène Vernhet, Bernard Canaud, Jean-Paul Cristol

Abstract read
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In one paragraph

Article in Kidney & blood pressure research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
6citing 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

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

  1. Pooled it
  2. Article
  3. Article
  4. Review
  5. Article
  6. 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

10 authors.

Marion Morena-CarrerePhyMedExp, University of Montpellier, INSERM, CNRS, Department of Biochemistry and Hormonology, University Hospital Center of Montpellier, Montpellier, France.
Isabelle JaussentINM, University of Montpellier, INSERM, Montpellier, France.
Leila ChenineDepartment of Nephrology, University Hospital Center of Montpellier, Montpellier, France.
Anne-Marie DupuyDepartment of Biochemistry and Hormonology, University Hospital Center of Montpellier, Montpellier, France.
Anne-Sophie BargnouxPhyMedExp, University of Montpellier, INSERM, CNRS, Department of Biochemistry and Hormonology, University Hospital Center of Montpellier, Montpellier, France.
Hélène Leray-MoraguesCharles Mion Foundation, AIDER-Santé, Montpellier, France.
Kada KlouchePhyMedExp, University of Montpellier, INSERM, CNRS, Department of Intensive Care Medicine, University Hospital Center of Montpellier, Montpellier, France.
Hélène VernhetDepartment of Radiology, University Hospital Center of Montpellier, Montpellier, France.
Bernard CanaudUniversity of Montpellier, Nephrology, Montpellier, France.
Jean-Paul CristolPhyMedExp, University of Montpellier, INSERM, CNRS, Department of Biochemistry and Hormonology, University Hospital Center of Montpellier, Montpellier, France.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

introductionCardiovascular (CV) diseases persist as the foremost cause of morbidity/mortality among chronic kidney disease (CKD) patients. This paper examines the values of coronary artery calcification (CAC) and biomarkers of CV on major adverse CV events (MACE)/CV death in a sample of 425 non-dialysis CKD patients.

methodsAt inclusion, patients underwent chest multidetector computed tomography for CAC scoring and biomarkers of CV risk including CRP, mineral metabolism markers, fibroblast growth factor-23 (FGF-23), α-Klotho, osteoprotegerin, tartrate-resistant acid phosphatase 5b (TRAP5b), sclerostin, matrix gla protein (both dephosphorylated uncarboxylated [dp-ucMGP] and total uncarboxylated), and growth differentiation factor-15 (GDF-15) were measured. Patients were followed for a median of 3.61 years (25th-75th percentiles = 1.92-6.70).

resultsOur results reported that CAC was a major independent factor of MACE/CV mortality showing a hazard ratio of 1.71 95% (confidence interval = 1.00-2.93) after adjustment for age, gender, diabetes, and history of CV events for patients with CAC >300. Interestingly, CAC effect was further enhanced in the presence of low levels of 25(OH) vitamin D3 or α-Klotho and high levels of intact parathyroid hormone (PTH), high-sensitive C reactive protein, FGF-23, osteoprotegerin, sclerostin, dp-ucMGP, or GDF-15.

conclusionCAC constitutes a significant CV risk, further exacerbated by inflammation, hyperparathyroidism, and regulation of bone molecules implicated in calcification progression. This finding aligns with the original concept of multiple hits. Consequently, addressing the detrimental environment that fosters plaque vulnerability, reducing chronic low-grade inflammation, and normalizing mineral metabolism markers (such as vitamin D and PTH) and bone-regulating molecules may emerge as a viable therapeutic strategy.

Indexed as

Cardiovascular DiseasesChronic Kidney Disease-Mineral and Bone DisorderCoronary Artery DiseaseInflammationRenal Insufficiency, ChronicVascular CalcificationVascular RemodelingAgedBiomarkersFemaleFibroblast Growth Factor-23HumansMaleMiddle AgedBiomarkersFGF23 protein, humanFibroblast Growth Factor-23Chronic kidney diseaseCoronary artery calcificationCRPParathyroid hormoneVitamin D

Identifiers

PMID39602894
PMCPMC11844697

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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.