Evidence map›Paper›PMID 39290459›Full record

ArticleJournal of extracellular biology2024

Urinary extracellular vesicles as a monitoring tool for renal damage in patients not meeting criteria for chronic kidney disease.

Miriam Anfaiha-Sanchez, Aranzazu Santiago-Hernandez, Juan Antonio Lopez, Nerea Lago-Baameiro, Maria Pardo, Ariadna Martin-Blazquez, Jesus Vazquez, Gema Ruiz-Hurtado, Maria G Barderas, Julian Segura and 3 more

Abstract read
In one paragraph

Article in Journal of extracellular biology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

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

6 citing papers in PubMed.

  1. Review
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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

13 authors.

Miriam Anfaiha-SanchezImmunology Department Instituto de Investigación Sanitaria Fundación Jiménez Díaz-UAM Madrid Spain.
Aranzazu Santiago-HernandezImmunology Department Instituto de Investigación Sanitaria Fundación Jiménez Díaz-UAM Madrid Spain.
Juan Antonio LopezLaboratory of Cardiovascular Proteomics CNIC Madrid Spain.
Nerea Lago-BaameiroIDIS-Hospital Clínico Universitario Santiago de Compostela Spain.
Maria PardoIDIS-Hospital Clínico Universitario Santiago de Compostela Spain.
Ariadna Martin-BlazquezImmunology Department Instituto de Investigación Sanitaria Fundación Jiménez Díaz-UAM Madrid Spain.
Jesus VazquezLaboratory of Cardiovascular Proteomics CNIC Madrid Spain.
Gema Ruiz-HurtadoCardiorenal Translational Laboratory Institute of Research Imas12 Hospital Universitario 12 de Octubre Madrid Spain.
Maria G BarderasDepartment of Vascular Physiopathology Hospital Nacional de Parapléjicos Toledo Spain.
Julian SeguraCardiorenal Translational Laboratory Institute of Research Imas12 Hospital Universitario 12 de Octubre Madrid Spain.
Luis M RuilopeCardiorenal Translational Laboratory Institute of Research Imas12 Hospital Universitario 12 de Octubre Madrid Spain.
Marta Martin-LorenzoImmunology Department Instituto de Investigación Sanitaria Fundación Jiménez Díaz-UAM Madrid Spain.
Gloria Alvarez-LlamasImmunology Department Instituto de Investigación Sanitaria Fundación Jiménez Díaz-UAM Madrid Spain.ORCID https://orcid.org/0000-0002-3313-721X

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Background: Current definition of chronic kidney disease (CKD) identifies only advanced stages, but effective management demands early detection. Urinary albumin-to-creatinine ratio (ACR) 30 mg/g is a cut-off point for CKD clinical diagnosis. Patients with lower values (normoalbuminuria) and eGFR > 60 mL/min/1.73 m Methods: Hypertensive patients were classified in control group (C) with ACR < 10 mg/g, and high-normal group (HN) with ACR 10-30 mg/g. Isolated uEVs were characterized by western blotting and electron microscopy and the protein cargo was analyzed by untargeted proteomics (LC-MS/MS) in a first discovery cohort. Protein confirmation was performed in a different cohort by ExoView. Immunohistochemistry of human kidney biopsies was also performed to evaluate the potential of uEVs to reflect renal damage. Results: HN albuminuria does not affect the uEVs concentration, size, or tetraspanin profile. Among >6200 uEVs proteins identified, 43 define a panel significantly altered in HN patients without variation in urine, mostly annotated in the tubule (39 out of 43). The tubular transporter long-chain fatty acid transport protein 2 (SLC27A2) and the apical membrane protein amnionless (AMN) confirmed their alteration in HN patients evidencing impaired tubular reabsorption. SLC27A2 showed tubular expression and significantly reduced levels in patients with diagnostic criteria for CKD. Conclusions: Alterations in the EV-mediated molecular profile are evident before pathological ACR levels are reached. Direct quantitation of SLC27A2 and AMN in uEVs helps identifying normoalbuminuric subjects with higher cardiorenal risk in early monitoring of CKD.

Indexed as

albuminuriaAMNcardiovascular riskchronic kidney diseaseExoViewextracellular vesiclesFATP2proteomicsSLC27A2

Identifiers

PMID39290459
PMCPMC11406310

What Socratic holds

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LicenceCC BY-NC-ND
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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.