Evidence map›Paper›PMID 32651850›Full record

ReviewJournal of nephrology2020

AKI: an increasingly recognized risk factor for CKD development and progression.

J T Kurzhagen, S Dellepiane, V Cantaluppi, H Rabb

Abstract readReview
PubMed Publisher
In one paragraph

Review in Journal of nephrology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 130 papers, 5 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
130citing papers in PubMed, 5 pooled it
13.7field-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

130 citing papers in PubMed, 5 syntheses or guidelines pooled it, 209 citations in OpenAlex.

  1. Pooled it
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  4. Efficacy of traditional Chinese medicineFrontiers in medicine · 2024
    Pooled it
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  12. iScience · 2026
    Article
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  17. CD8Nature reviews. Cardiology · 2026
    Review
  18. Article
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  20. Kidney care at NICU discharge and follow-up recommendations for preterm infants<34 weeks.Journal of perinatology : official journal of the California Perinatal Association · 2026
    Article

70 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

4 authors at 3 institutions in 2 countries.

J T KurzhagenDivision of Nephrology, Johns Hopkins Hospital, Johns Hopkins University School of Medicine, Ross 965, 720 Rutland Ave, Baltimore, MD, 21206, USA.ORCID http://orcid.org/0000-0001-6904-0746
S DellepianeIcahn School of Medicine at Mount Sinai, New York, NY, USA.ORCID http://orcid.org/0000-0002-7133-4740
V CantaluppiNephrology and Kidney Transplantation Unit, Department of Translational Medicine, University of Piemonte Orientale (UPO), "Maggiore Della Carità" University Hospital, Novara, Italy.ORCID http://orcid.org/0000-0002-4120-3555
H RabbDivision of Nephrology, Johns Hopkins Hospital, Johns Hopkins University School of Medicine, Ross 965, 720 Rutland Ave, Baltimore, MD, 21206, USA. hrabb1@jhmi.edu.ORCID http://orcid.org/0000-0002-4761-1103
Johns Hopkins University · USIcahn School of Medicine at Mount Sinai · USUniversità degli Studi del Piemonte Orientale “Amedeo Avogadro” · IT

Funding

Dr. Werner Jackstädt-Stiftung S 134-10.117Italian Ministry of Education, University and Research (MIUR) program AGING Project
6 · The paper itself

Abstract

Acute kidney injury (AKI) is an increasing health burden with high morbidity and mortality rates worldwide. AKI is a risk factor for chronic kidney disease (CKD) development and progression to end stage renal disease (ESRD). Rapid action is required to find treatment options for AKI, plus to anticipate the development of CKD and other complications. Therefore, it is essential to understand the pathophysiology of AKI to CKD transition. Over the last several years, research has revealed maladaptive repair to be an interplay of cell death, endothelial dysfunction, tubular epithelial cell senescence, inflammatory processes and more-terminating in fibrosis. Various pathological mechanisms have been discovered and reveal targets for potential interventions. Furthermore, there have been clinical efforts measures for AKI prevention and progression including the development of novel biomarkers and prediction models. In this review, we provide an overview of pathophysiological mechanisms involved in kidney fibrosis. Furthermore, we discuss research gaps and promising therapeutic approaches for AKI to CKD progression.

Indexed as

Acute Kidney InjuryKidney Failure, ChronicRenal Insufficiency, ChronicDisease ProgressionHumansRisk FactorsAKDAKICKDMechanismsRenal fibrosis

Identifiers

PMID32651850
OpenAlexW3040982790

What OpenQuestion holds

Textmetadata
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.