Evidence map›Paper›PMID 29291764›Full record

ReviewSeminars in nephrology2018

Translating Knowledge Into Therapy for Acute Kidney Injury.

Mark de Caestecker, Raymond Harris

Abstract readReview
In one paragraph

Review in Seminars in nephrology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing 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

15 citing papers in PubMed.

  1. Observational
  2. The novel potential therapeutic target PSMP/MSMP promotes acute kidney injury via CCR2.Molecular therapy : the journal of the American Society of Gene Therapy · 2024
    Article
  3. Article
  4. Article
  5. Mitochondrial Pathophysiology on Chronic Kidney Disease.International journal of molecular sciences · 2022
    Review
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Dynamic signature of lymphangiogenesis during acute kidney injury and chronic kidney disease.Laboratory investigation; a journal of technical methods and pathology · 2019
    Article
  12. Review
  13. Nephron repair: powered by anaerobic energy metabolism.Annals of translational medicine · 2019
    Article
  14. Review
  15. Kidney histopathology in lethal human sepsis.Critical care (London, England) · 2018
    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

2 authors.

Mark de CaesteckerNephrology Division, Department of Medicine, Vanderbilt University Medical Center, Nashville, Tennessee. Electronic address: mark.de.caestecker@vanderbilt.edu.
Raymond HarrisNephrology Division, Department of Medicine, Vanderbilt University Medical Center, Nashville, Tennessee.

Funding

The Role of the EGF Receptor in Acute and Chronic Renal InjuryR01DK051265 · NIDDK · VANDERBILT UNIVERSITY MEDICAL CENTER · PI RAYMOND C. HARRIS, Mingzhi Zhang · 1997 to 2026
$10.1M
The role of the innate immune cell cyclooxygenase/prostaglandin system in blood pressureregulationR01DK062794 · NIDDK · VANDERBILT UNIVERSITY MEDICAL CENTER · PI RAYMOND C. HARRIS, Mingzhi Zhang · 2003 to 2026
$9.4M
The Role of renal macrophages in recovery from renal injuryR01DK095785 · NIDDK · VANDERBILT UNIVERSITY MEDICAL CENTER · PI RAYMOND C. HARRIS, Mingzhi Zhang · 2013 to 2026
$6.7M
Novel Integrated Analyses of Human Diabetic NephropathyR24DK103067 · NIDDK · VANDERBILT UNIVERSITY MEDICAL CENTER · PI CAPRIOLI, RICHARD M, DENNY, JOSHUA C. · 2014 to 2018
$6.5M
Mechanisms and therapeutic manipulation of retinoic acid signaling in Acute Kidney InjuryR01DK112688 · NIDDK · VANDERBILT UNIVERSITY MEDICAL CENTER · PI DE CAESTECKER, MARK P. · 2017 to 2020
$1.7M
NIDDK NIH HHS R01 DK051265NIDDK NIH HHS R01 DK062794NIDDK NIH HHS R01 DK095785NIDDK NIH HHS R01 DK112688NIDDK NIH HHS R24 DK103067
6 · The paper itself

Abstract

No therapies have been shown to improve outcomes in patients with acute kidney injury (AKI). Given the high morbidity and mortality associated with AKI this represents an important unmet medical need. A common feature of all of the therapeutic development efforts for AKI is that none were driven by target selection or preclinical modeling that was based primarily on human data. This is important when considering a heterogeneous and dynamic condition such as AKI, in which in the absence of more accurate molecular classifications, clinical cohorts are likely to include patients with different types of injury at different stages in the injury and repair continuum. The National Institutes of Health precision medicine initiative offers an opportunity to address this. By creating a molecular tissue atlas of AKI, defining patient subgroups, and identifying critical cells and pathways involved in human AKI, this initiative has the potential to transform our current approach to therapeutic discovery. In this review, we discuss the opportunities and challenges that this initiative presents, with a specific focus on AKI, what additional efforts will be needed to apply these discoveries to therapeutic development, and how we believe this effort might lead to the development of new therapeutics for subsets of patients with AKI.

Indexed as

Translational Research, BiomedicalAcute Kidney InjuryBiopsyClinical Trials as TopicHumansKidneyPatient SelectionPhenotypePrecision Medicineacute kidney injuryPrecision medicinetherapeutic development

Identifiers

PMID29291764
PMCPMC5894099

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.