Evidence map›Paper›PMID 34063052›Full record

ReviewLife (Basel, Switzerland)2021

Chronic Kidney Disease as a Systemic Inflammatory Syndrome: Update on Mechanisms Involved and Potential Treatment.

Francesca Tinti, Silvia Lai, Annalisa Noce, Silverio Rotondi, Giulia Marrone, Sandro Mazzaferro, Nicola Di Daniele, Anna Paola Mitterhofer

Open access · goldAbstract readReview
In one paragraph

Review in Life (Basel, Switzerland), 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 63 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
63citing papers in PubMed, 2 pooled it
9.7field-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

63 citing papers in PubMed, 2 syntheses or guidelines pooled it, 93 citations in OpenAlex.

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3 more citing papers are in PubMed but not listed here.

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

8 authors at 2 institutions in 1 country.

Francesca TintiDepartment of Translational and Precision Medicine, Sapienza University of Rome, Viale dell'Università 37, 00185 Rome, Italy.ORCID 0000-0001-8867-3979
Silvia LaiDepartment of Translational and Precision Medicine, Sapienza University of Rome, Viale dell'Università 37, 00185 Rome, Italy.ORCID 0000-0002-7199-2954
Annalisa NoceDepartment of Systems Medicine, Nephrology and Dialysis Unit, University of Rome Tor Vergata, via Montpellier 1, 00133 Rome, Italy.ORCID 0000-0003-1310-3730
Silverio RotondiDepartment of Translational and Precision Medicine, Sapienza University of Rome, Viale dell'Università 37, 00185 Rome, Italy.
Giulia MarroneDepartment of Systems Medicine, Nephrology and Dialysis Unit, University of Rome Tor Vergata, via Montpellier 1, 00133 Rome, Italy.ORCID 0000-0002-5854-2086
Sandro MazzaferroDepartment of Translational and Precision Medicine, Sapienza University of Rome, Viale dell'Università 37, 00185 Rome, Italy.ORCID 0000-0003-3071-1893
Nicola Di DanieleDepartment of Systems Medicine, Nephrology and Dialysis Unit, University of Rome Tor Vergata, via Montpellier 1, 00133 Rome, Italy.
Anna Paola MitterhoferDepartment of Systems Medicine, Nephrology and Dialysis Unit, University of Rome Tor Vergata, via Montpellier 1, 00133 Rome, Italy.ORCID 0000-0002-0132-386X
Sapienza University of Rome · ITUniversity of Rome Tor Vergata · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Chronic kidney disease (CKD) is characterized by manifestations and symptoms involving systemic organs and apparatus, associated with elevated cardiovascular morbidity and mortality, bone disease, and other tissue involvement. Arterial hypertension (AH), diabetes mellitus (DM), and dyslipidemia, with glomerular or congenital diseases, are the traditional risk factors recognized as the main causes of progressive kidney dysfunction evolving into uremia. Acute kidney injury (AKI) has recently been considered an additional risk factor for the worsening of CKD or the development of CKD de novo. Evidence underlies the role of systemic inflammation as a linking factor between AKI and CKD, recognizing the role of inflammation in AKI evolution to CKD. Moreover, abnormal increases in oxidative stress (OS) and inflammatory status in CKD seem to exert an important pathogenetic role, with significant involvement in the clinical management of this condition. With our revision, we want to focus on and update the inflammatory mechanisms responsible for the pathologic conditions associated with CKD, with particular attention on the development of AKI and AKI-CKD de novo, the alteration of calcium-phosphorus metabolism with bone disease and CKD-MBD syndrome, the status of malnutrition and malnutrition-inflammation complex syndrome (MICS) and protein-energy wasting (PEW), uremic sarcopenia, the status of OS, and the different inflammatory pathways, highlighting a new approach to CKD. The depth comprehension of the mechanisms underlying the development of inflammation in CKD may present new possible therapeutic approaches in CKD and hopefully improve the management of correlated morbidities and provide a reduction in associated mortality.

Indexed as

acute kidney injurychronic kidney diseasecytokinefibroblast growth factor 23inflammationinterleukin-6malnutritionmineral bone diseaseoxidative stresssarcopenia

Identifiers

PMID34063052
PMCPMC8147921
OpenAlexW3157888397

What OpenQuestion 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 OpenQuestion graph.