Evidence map›Paper›PMID 23924517›Full record

ArticleEJNMMI research2013

Cell injury after ischemia and reperfusion in the porcine kidney evaluated by radiolabelled microspheres, sestamibi, and lactadherin.

Stine S Pedersen, Anna K Keller, Marie K Nielsen, Bente Jespersen, Lise Falborg, Jan T Rasmussen, Christian W Heegaard, Michael Rehling

Open access · goldAbstract read
In one paragraph

Article in EJNMMI research, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
0.3field-weighted citation impact, top 33% 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

2 citing papers in PubMed, 6 citations in OpenAlex.

  1. Article
  2. 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

8 authors at 2 institutions in 1 country.

Stine S PedersenInstitute of Clinical Medicine, Aarhus University, Aarhus, Denmark ; Department of Clinical Physiology and Nuclear Medicine, Aarhus University Hospital, Skejby, Denmark.
Anna K KellerInstitute of Clinical Medicine, Aarhus University, Aarhus, Denmark ; Department of Urology, Aarhus University Hospital, Skejby, Denmark.
Marie K NielsenInstitute of Clinical Medicine, Aarhus University, Aarhus, Denmark.
Bente JespersenInstitute of Clinical Medicine, Aarhus University, Aarhus, Denmark ; Department of Nephrology, Aarhus University Hospital, Skejby, Denmark.
Lise FalborgDepartment of Clinical Physiology and Nuclear Medicine, Aarhus University Hospital, Skejby, Denmark.
Jan T RasmussenProtein Chemistry Laboratory, Department of Molecular Biology and Genetics, Aarhus University, Aarhus, Denmark.
Christian W HeegaardProtein Chemistry Laboratory, Department of Molecular Biology and Genetics, Aarhus University, Aarhus, Denmark.
Michael RehlingInstitute of Clinical Medicine, Aarhus University, Aarhus, Denmark ; Department of Clinical Physiology and Nuclear Medicine, Aarhus University Hospital, Skejby, Denmark.
Aarhus University · DKAarhus University Hospital · DK

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundThe purpose of the present study was to quantify renal cell injury after ischemia and reperfusion in a pig model using (99m)Tc-lactadherin as a marker of apoptosis and (99m)Tc-sestamibi as a marker of mitochondrial dysfunction.

methodsThirty-four pigs were randomized into unilateral renal warm ischemia of 120 (WI120) or 240 min (WI240). The glomerular filtration rate (GFR) was calculated by renal clearance of (51)Cr-ethylenediaminetetraacetic acid, and apoptosis was quantified by immunohistochemical detection of caspase-3. After 240 min of reperfusion, intravenous (99m)Tc-lactadherin or (99m)Tc-sestamibi was injected simultaneously with (153)Gd microspheres into the aorta. Ex-vivo static planar images of the kidneys were acquired for determination of the differential renal function of tracer distribution using a gamma camera.

resultsIn WI120, there was no significant difference in the uptake of microspheres in the ischemic and contralateral normal kidney indicating adequate perfusion (uptake in ischemic kidney relative to the sum of uptake in both kidneys; 46% ± 12% and 51% ± 5%). In WI240, the uptake of microspheres was severely reduced in both groups (17% ± 11% and 27% ± 17%). GFR was severely reduced in the post ischemic kidney in both groups. In both groups, the uptake of lactadherin was reduced (41% ± 8%, 17% ± 13%) but not different from the uptake of (153)Gd microspheres. Caspase-3-positive cell profiles were increased in the post-ischemic kidneys (p < 0.001) and increased as the length of ischemia increased (p = 0.003). In both WI120 and WI240, the amount of (99m)Tc-sestamibi in the ischemic kidney was significantly lower than the amount of (153)Gd microspheres (40 ± 5 versus 51 ± 5 and 20 ± 11 versus 27 ± 17; p < 0.05).

conclusionsIn an established pig model with unilateral renal warm ischemia, we found significantly reduced (99m)Tc-sestamibi uptake relative to perfusion in the kidneys exposed to ischemia indicating a potential ability to detect renal ischemic and reperfusion injuries. However, apoptosis was not detected using (99m)Tc-lactadherin in the post-ischemic kidneys despite increased number of caspase-3-positive cell profiles.

trial registrationThis study is approved by the Danish Inspectorate of Animal Experiments (2010/561-1837).

Indexed as

ApoptosisCaspase-3Glomerular filtration rateIschemiaKidneyLactadherinMitochondriaPerfusionSestamibi

Identifiers

PMID23924517
PMCPMC3750402
OpenAlexW2098039612

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.