Evidence map›Paper›PMID 39286240›Full record

ArticleClinical kidney journal2024

Association of serum zinc with mineral stress in chronic kidney disease.

Azmat Sohail, Jakob Obereigner, Gregor Mitter, Thomas Schmid, Anna-Sofie Hofer, Gerhard Schuster, Astrid Hügl, Angelika H Dorninger, Markus Mandl, Andreas Pasch and 8 more

Abstract read
In one paragraph

Article in Clinical kidney journal, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
–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. Article
  2. Article
  3. Article
  4. 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

18 authors.

Azmat SohailInstitute for Physiology and Pathophysiology, Johannes Kepler University Linz, Linz, Austria.
Jakob ObereignerInstitute for Physiology and Pathophysiology, Johannes Kepler University Linz, Linz, Austria.
Gregor MitterInstitute for Physiology and Pathophysiology, Johannes Kepler University Linz, Linz, Austria.
Thomas SchmidAMD GmbH, Linz, Austria.
Anna-Sofie HoferDepartment of Medicine III - Nephrology, Hypertension, Transplantation Medicine, Rheumatology, Geriatrics, Ordensklinikum Linz, Linz, Austria.
Gerhard SchusterRed Cross Transfusion Service of Upper Austria, Austrian Red Cross, Linz, Austria.
Astrid HüglRed Cross Transfusion Service of Upper Austria, Austrian Red Cross, Linz, Austria.
Angelika H DorningerRed Cross Transfusion Service of Upper Austria, Austrian Red Cross, Linz, Austria.
Markus MandlInstitute for Physiology and Pathophysiology, Johannes Kepler University Linz, Linz, Austria.
Andreas PaschInstitute for Physiology and Pathophysiology, Johannes Kepler University Linz, Linz, Austria.ORCID https://orcid.org/0000-0002-7439-0748
Helmut K LacknerDivision of Physiology and Pathophysiology, Otto Loewi Research Center, Medical University of Graz, Graz, Austria.ORCID https://orcid.org/0000-0002-0159-3720
Ilona PapousekInstitute of Psychology, Biological Psychology Unit, University of Graz, Graz, Austria.ORCID https://orcid.org/0000-0002-6620-0318
Benjamin DieplingerDepartment of Laboratory Medicine, Konventhospital Barmherzige Brueder Linz and Ordensklinikum Linz, Linz, Austria.
Susanne SuessnerRed Cross Transfusion Service of Upper Austria, Austrian Red Cross, Linz, Austria.
Marlies AntlangerDepartment of Internal Medicine 2, Kepler University Hospital and Johannes Kepler University, Linz, Austria.
Daniel CejkaDepartment of Medicine III - Nephrology, Hypertension, Transplantation Medicine, Rheumatology, Geriatrics, Ordensklinikum Linz, Linz, Austria.
Ioana AlesutanInstitute for Physiology and Pathophysiology, Johannes Kepler University Linz, Linz, Austria.
Jakob VoelklInstitute for Physiology and Pathophysiology, Johannes Kepler University Linz, Linz, Austria.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Background: The excessive cardiovascular mortality of patients with chronic kidney disease (CKD) could be linked to mineral stress, the biological consequence of calcium-phosphate nanoparticle exposure. This study investigated whether zinc is associated with mineral stress markers in CKD. Methods: Results: Serum zinc concentrations and T50 were reduced, while CPP2 radius was increased in CKD patients. Serum zinc levels positively correlated with T50 and inversely correlated with CPP2 radius. In a hierarchical linear regression model, T50 was associated with age, calcium, phosphate, magnesium and albumin. Addition of zinc significantly improved prediction of the model, confirming an additional contribution of zinc to T50. Similar observations were made for the association of zinc and CPP2 radius, but spiking experiments indicated that zinc may stronger modify T50 than CPP2 radius. Also, urinary zinc excretion was increased in patients with kidney disease and correlated to T50 and CPP2 radius. Conclusions: Reduced serum zinc levels in CKD appear directly linked to lower T50 and associated with larger CPP2 radius. Further studies on the associations of zinc and mineral stress as well as putative therapeutic benefits of zinc supplementation are required.

Indexed as

calciprotein particleschronic kidney diseasemineral stressserum calcification propensityzinc

Identifiers

PMID39286240
PMCPMC11403325

What Socratic holds

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LicenceCC BY
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Registered trials

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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 Socratic graph.