Evidence map›Paper›PMID 38716349›Full record

ArticleInternational journal of clinical and experimental pathology2024

Protective effect of ischaemic preconditioning on acute and chronic renal damage following ischaemia reperfusion injury: characterisation of fibrosis development after inflammation resolution.

Charlotte Vm Brown, Gilda Pino-Chavez, Aeliya Zaidi, Irina Grigorieva, Emma Woods, Robert Steadman, Rafael Chavez, Soma Meran, Usman Khalid

Abstract read
In one paragraph

Article in International journal of clinical and experimental pathology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing 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

4 citing papers in PubMed.

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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

9 authors.

Charlotte Vm BrownWales Kidney Research Unit (WKRU), Division of Infection and Immunity, School of Medicine, Cardiff University Cardiff CF14 4XN, UK.
Gilda Pino-ChavezWales Kidney Research Unit (WKRU), Division of Infection and Immunity, School of Medicine, Cardiff University Cardiff CF14 4XN, UK.
Aeliya ZaidiWales Kidney Research Unit (WKRU), Division of Infection and Immunity, School of Medicine, Cardiff University Cardiff CF14 4XN, UK.
Irina GrigorievaWales Kidney Research Unit (WKRU), Division of Infection and Immunity, School of Medicine, Cardiff University Cardiff CF14 4XN, UK.
Emma WoodsWales Kidney Research Unit (WKRU), Division of Infection and Immunity, School of Medicine, Cardiff University Cardiff CF14 4XN, UK.
Robert SteadmanWales Kidney Research Unit (WKRU), Division of Infection and Immunity, School of Medicine, Cardiff University Cardiff CF14 4XN, UK.
Rafael ChavezWales Kidney Research Unit (WKRU), Division of Infection and Immunity, School of Medicine, Cardiff University Cardiff CF14 4XN, UK.
Soma MeranWales Kidney Research Unit (WKRU), Division of Infection and Immunity, School of Medicine, Cardiff University Cardiff CF14 4XN, UK.
Usman KhalidWales Kidney Research Unit (WKRU), Division of Infection and Immunity, School of Medicine, Cardiff University Cardiff CF14 4XN, UK.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectivesAcute Kidney Injury (AKI) and Chronic Kidney Disease (CKD) are increasingly recognised as one disease continuum, rather than distinct entities, and are associated with a huge burden to healthcare services. The leading cause of AKI worldwide is Ischaemia Reperfusion Injury (IRI), most commonly seen in clinical settings of sepsis-driven hypotension. Ischaemic Preconditioning (IPC) is a strategy aimed at reducing the deleterious effects of IRI. The objectives of this study were to demonstrate an efficacious

methodsA rat model of bilateral kidney IRI was used: Male Lewis rats (n=84) were assigned to IRI, sham or IPC. In IRI, renal pedicles were clamped for 45 minutes. IPC groups underwent pulsatile IPC prior to IRI. Kidneys were retrieved at 24 hours, 48 hours, 7 days, 14 days and 28 days, and assessed histologically.

resultsIRI led to marked AKI (24-48 h) and renal fibrosis development by 28 days. IPC attenuated this damage, with 66% less fibrosis. Interestingly, at 14-days, the histological appearance of both IRI and IPC kidneys was rather similar, potentially representing an important transitional point at which kidneys commit to either fibrosis or recovery. This may provide a suitable inflexion point for introduction of novel anti-fibrotic therapies.

conclusionsIn conclusion, we have characterised a model of kidney injury from acute to chronic phases, allowing detailed mechanistic understanding and which can be manipulated by effective treatment strategies such as IPC.

Indexed as

acute kidney injury (AKI)Ischaemia reperfusion injury (IRI)ischaemic preconditioning (IPC)renal fibrosis

Identifiers

PMID38716349
PMCPMC11070433

What OpenQuestion holds

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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.