Evidence map›Paper›PMID 34707157›Full record

ArticleScientific reports2021

Biomarkers of persistent renal vulnerability after acute kidney injury recovery.

Isabel Fuentes-Calvo, Cristina Cuesta, Sandra M Sancho-Martínez, Omar A Hidalgo-Thomas, María Paniagua-Sancho, Francisco J López-Hernández, Carlos Martínez-Salgado

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
1.4field-weighted citation impact, top 18% 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

7 citing papers in PubMed, 12 citations in OpenAlex.

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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

7 authors at 3 institutions in 1 country.

Isabel Fuentes-Calvo *Institute of Biomedical Research of Salamanca, IBSAL, Edificio Departamental, S-18, Campus Miguel de Unamuno, 37007, Salamanca, Spain.
Cristina Cuesta *Institute of Biomedical Research of Salamanca, IBSAL, Edificio Departamental, S-18, Campus Miguel de Unamuno, 37007, Salamanca, Spain.
Sandra M Sancho-MartínezInstitute of Biomedical Research of Salamanca, IBSAL, Edificio Departamental, S-18, Campus Miguel de Unamuno, 37007, Salamanca, Spain.
Omar A Hidalgo-ThomasInstitute of Biomedical Research of Salamanca, IBSAL, Edificio Departamental, S-18, Campus Miguel de Unamuno, 37007, Salamanca, Spain.
María Paniagua-SanchoInstitute of Biomedical Research of Salamanca, IBSAL, Edificio Departamental, S-18, Campus Miguel de Unamuno, 37007, Salamanca, Spain.
Francisco J López-HernándezInstitute of Biomedical Research of Salamanca, IBSAL, Edificio Departamental, S-18, Campus Miguel de Unamuno, 37007, Salamanca, Spain. flopezher@usal.es.
Carlos Martínez-SalgadoInstitute of Biomedical Research of Salamanca, IBSAL, Edificio Departamental, S-18, Campus Miguel de Unamuno, 37007, Salamanca, Spain. carlosms@usal.es.
Instituto de Investigación Biomédica de Salamanca · ESUniversidad de Salamanca · ESInstituto de Salud Carlos III · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Acute kidney injury (AKI) is a risk factor for new AKI episodes, chronic kidney disease, cardiovascular events and death, as renal repair may be deficient and maladaptive, and activate proinflammatory and profibrotic signals. AKI and AKI recovery definitions are based on changes in plasma creatinine, a parameter mostly associated to glomerular filtration, but largely uncoupled from renal tissue damage. The evolution of structural and functional repair has been incompletely described. We thus aimed at identifying subclinical sequelae persisting after recovery from cisplatin-induced AKI in rats. Compared to controls, after plasma creatinine recovery, post-AKI kidneys showed histological alterations and attendant susceptibility to new AKI episodes. Tubular function (assessed by the furosemide stress test, FST) also remained affected. Lingering parenchymal and functional subclinical alterations were paralleled by tapering, but abnormally high levels of urinary albumin, transferrin, insulin-like growth factor-binding protein 7 (IGFBP7), tissue inhibitor of metalloproteinases-2 (TIMP-2) and, especially, the [TIMP-2]*[IGFBP7] product. As subclinical surrogates of incomplete renal recovery, the FST and the urinary [TIMP-2]*[IGFBP7] product provide two potential diagnostic tools to monitor the sequelae and kidney vulnerability after the apparent recovery from AKI.

Indexed as

Acute Kidney InjuryAnimalsAntineoplastic AgentsBiomarkersCisplatinInsulin-Like Growth Factor Binding ProteinsKidneyMaleRatsRats, WistarTissue Inhibitor of Metalloproteinase-2Antineoplastic AgentsBiomarkersCisplatininsulin-like growth factor binding protein-related protein 1Insulin-Like Growth Factor Binding ProteinsTissue Inhibitor of Metalloproteinase-2

Identifiers

PMID34707157
PMCPMC8551194
OpenAlexW3208300720

What OpenQuestion holds

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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.