Evidence map›Paper›PMID 31590461›Full record

ReviewInternational journal of molecular sciences2019

Molecular Mechanisms of the Acute Kidney Injury to Chronic Kidney Disease Transition: An Updated View.

Francesco Guzzi, Luigi Cirillo, Rosa Maria Roperto, Paola Romagnani, Elena Lazzeri

Abstract readReview
In one paragraph

Review in International journal of molecular sciences, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 92 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
92citing papers in PubMed, 1 pooled it
–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

92 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
  2. Article
  3. Apoptotic Bodies in Kidney Disease: Orchestrators of Inflammation, Fibrosis, and Repair.Journal of the American Society of Nephrology : JASN · 2026
    Review
  4. Article
  5. Article
  6. Article
  7. A macrophage-endothelial cell axis in kidney diseases.International urology and nephrology · 2026
    Review
  8. Article
  9. Review
  10. Review
  11. Article
  12. Epigenetic memories induced by hypoxia in AKI-to-CKD transition.Clinical and experimental nephrology · 2025
    Review
  13. Review
  14. Review
  15. Review
  16. Review
  17. Article
  18. Article
  19. Review
  20. Article

32 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

5 authors.

Francesco GuzziExcellence Centre for Research, Transfer and High Education for the development of DE NOVO Therapies (DENOTHE), University of Florence, 50139 Florence, Italy. francesco.guzzi@gmail.com.ORCID 0000-0003-0788-5078
Luigi CirilloNephrology and Dialysis Unit, Meyer Children's University Hospital, 50139 Florence, Italy. cirlui89@gmail.com.
Rosa Maria RopertoNephrology and Dialysis Unit, Meyer Children's University Hospital, 50139 Florence, Italy. rosa.roperto@meyer.it.
Paola RomagnaniExcellence Centre for Research, Transfer and High Education for the development of DE NOVO Therapies (DENOTHE), University of Florence, 50139 Florence, Italy. paola.romagnani@unifi.it.
Elena LazzeriExcellence Centre for Research, Transfer and High Education for the development of DE NOVO Therapies (DENOTHE), University of Florence, 50139 Florence, Italy. elena.lazzeri@unifi.it.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Increasing evidence has demonstrated the bidirectional link between acute kidney injury (AKI) and chronic kidney disease (CKD) such that, in the clinical setting, the new concept of a unified syndrome has been proposed. The pathophysiological reasons, along with the cellular and molecular mechanisms, behind the ability of a single, acute, apparently self-limiting event to drive chronic kidney disease progression are yet to be explained. This acute injury could promote progression to chronic disease through different pathways involving the endothelium, the inflammatory response and the development of fibrosis. The interplay among endothelial cells, macrophages and other immune cells, pericytes and fibroblasts often converge in the tubular epithelial cells that play a central role. Recent evidence has strengthened this concept by demonstrating that injured tubules respond to acute tubular necrosis through two main mechanisms: The polyploidization of tubular cells and the proliferation of a small population of self-renewing renal progenitors. This alternative pathophysiological interpretation could better characterize functional recovery after AKI.

Indexed as

Acute Kidney InjuryAnimalsCell ProliferationCell Self RenewalDisease ProgressionFibrosisHumansRenal Insufficiency, ChronicSignal Transductionacute kidney injurychronic kidney diseasepolyploidizationrenal progenitors

Identifiers

PMID31590461
PMCPMC6801733

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.