Evidence map›Paper›PMID 30925515›Full record

ReviewCurrent opinion in nephrology and hypertension2019

Recent advances in acute kidney injury and its consequences and impact on chronic kidney disease.

Anna Zuk, Joseph V Bonventre

Abstract readReview
In one paragraph

Review in Current opinion in nephrology and hypertension, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.

0numbers the graph read from it
0cells of the map it votes in
39citing 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

39 citing papers in PubMed.

  1. Trial
  2. Urinary UDP-sugars provide actionable prediction of acute kidney injury in cardiac surgery patients.American journal of physiology. Heart and circulatory physiology · 2026
    Article
  3. Review
  4. Article
  5. Magnetic resonance imaging of renal oxygenation.Nature reviews. Nephrology · 2025
    Review
  6. Role of local complement activation in kidney fibrosis and repair.The Journal of clinical investigation · 2025
    Review
  7. Article
  8. Improving Processes of Care after Acute Kidney Injury.Journal of the American Society of Nephrology : JASN · 2025
    Article
  9. Article
  10. Review
  11. Article
  12. Article
  13. Review
  14. Review
  15. Nephron-SpecificInternational journal of biological sciences · 2024
    Article
  16. Proximal TubularInternational journal of molecular sciences · 2023
    Article
  17. Review
  18. Article
  19. Article
  20. Review
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.

Anna ZukResearch and Development, Akebia Therapeutics, Inc, Cambridge.
Joseph V BonventreDepartment of Medicine, Harvard Medical School.

Funding

KIDNEY INJURY MOLECULE-1 IN EPITHELIAL REPAIRR01DK072381 · NIDDK · BRIGHAM AND WOMEN'S HOSPITAL · PI BONVENTRE, JOSEPH VINCENT · 2005 to 2025
$8.6M
Mechanisms of Ischemic Kidney Injury and RepairR37DK039773 · NIDDK · MASSACHUSETTS GENERAL HOSPITAL · PI BONVENTRE, JOSEPH VINCENT · 1993 to 2021
$5.2M
NIDDK NIH HHS R01 DK072381NIDDK NIH HHS R37 DK039773
6 · The paper itself

Abstract

purpose of reviewAcute kidney injury (AKI) remains a major unmet medical need and associates with high morbidity, mortality, and healthcare costs. Among survivors, long-term outcomes of AKI can include development of chronic kidney disease (CKD) or progression of preexisting CKD. In this review, we focus on ongoing efforts by the AKI community to understand the human AKI to CKD continuum, with an emphasis on the cellular stress responses that underlie AKI and the maladaptive responses that persist in the acute-to-chronic phase. The emphasis is on work that has been published in the past year in this rapidly expanding field. RECENT

findingsRecent studies in preclinical models highlight the importance of mitochondrial dysfunction, cell death, and inflammation on the underlying pathogenesis of AKI. These pathogenic mechanisms can resolve with adaptive kidney repair but persist in maladaptive repair that leads to progressive chronic disease. The complexity and interconnections of these pathways involve cross-talk between the tubular epithelium, endothelium, and interstitial compartments. SUMMARY: Approaches which lessen or counteract these cellular responses represent novel strategies to prevent AKI and stop or slow down the progression to CKD.

Indexed as

Acute Kidney InjuryDisease ProgressionHumansKidneyRenal Insufficiency, Chronic

Identifiers

PMID30925515
PMCPMC7020661

What OpenQuestion holds

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Registered trials

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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.