Evidence map›Paper›PMID 32060481›Full record

ReviewNature reviews. Nephrology2020

Targeting the progression of chronic kidney disease.

Marta Ruiz-Ortega, Sandra Rayego-Mateos, Santiago Lamas, Alberto Ortiz, Raul R Rodrigues-Diez

Registry-linked trialAbstract readReview
PubMed Publisher
In one paragraph

Review in Nature reviews. Nephrology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT06501222 (The Renal Protective Effects of Remote Ischemic Preconditioning in Patients With Chronic Kidney Disease), which is not on this map. Cited by 536 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
536citing papers in PubMed, 1 pooled it
64.0field-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.

NCT06501222 narecruitingnot on this mapstarted 2024, after this paper: background citation

The Renal Protective Effects of Remote Ischemic Preconditioning in Patients With Chronic Kidney Disease: Randomized, Parallel-controlled, proof-of Concept Trial

TypeinterventionalSponsorYuanjun YangRan2024 to 2027Enrolled114ConditionsChronic Kidney DiseasesArmsRemote ischemic conditioning
3 · Its place in the literature

Who cites it

536 citing papers in PubMed, 1 synthesis or guideline pooled it, 931 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Article
  4. Review
  5. Review
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Magnesium Attenuates Renal Senescence and Fibrosis With Reduced DNA Damage Response and H3K4me3 Enrichment at the p16FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026
    Article
  13. Review
  14. Article
  15. Article
  16. Current issues in molecular biology · 2026
    Article
  17. Article
  18. A practical toolbox for modelling fibrosis in vitro.Nature biomedical engineering · 2026
    Review
  19. Article
  20. Article

476 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 at 4 institutions in 1 country.

Marta Ruiz-OrtegaCellular and Molecular Biology in Renal and Vascular Pathology Laboratory, IIS-Fundación Jiménez Díaz-Universidad Autónoma Madrid, Madrid, Spain. mruizo@fjd.es.ORCID http://orcid.org/0000-0002-1495-6535
Sandra Rayego-MateosRed de Investigación Renal (REDINREN), Madrid, Spain.
Santiago LamasRed de Investigación Renal (REDINREN), Madrid, Spain.
Alberto OrtizRed de Investigación Renal (REDINREN), Madrid, Spain.ORCID http://orcid.org/0000-0002-9805-9523
Raul R Rodrigues-DiezCellular and Molecular Biology in Renal and Vascular Pathology Laboratory, IIS-Fundación Jiménez Díaz-Universidad Autónoma Madrid, Madrid, Spain.
Hospital Universitario Fundación Jiménez Díaz · ESCentro de Biología Molecular Severo Ochoa · ESInstituto de Investigación Biomédica de Lleida · ESSpanish Clinical Research Network · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Chronic kidney disease (CKD) is a devastating condition that is reaching epidemic levels owing to the increasing prevalence of diabetes mellitus, hypertension and obesity, as well as ageing of the population. Regardless of the underlying aetiology, CKD is slowly progressive and leads to irreversible nephron loss, end-stage renal disease and/or premature death. Factors that contribute to CKD progression include parenchymal cell loss, chronic inflammation, fibrosis and reduced regenerative capacity of the kidney. Current therapies have limited effectiveness and only delay disease progression, underscoring the need to develop novel therapeutic approaches to either stop or reverse progression. Preclinical studies have identified several approaches that reduce fibrosis in experimental models, including targeting cytokines, transcription factors, developmental and signalling pathways and epigenetic modulators, particularly microRNAs. Some of these nephroprotective strategies are now being tested in clinical trials. Lessons learned from the failure of clinical studies of transforming growth factor β1 (TGFβ1) blockade underscore the need for alternative approaches to CKD therapy, as strategies that target a single pathogenic process may result in unexpected negative effects on simultaneously occurring processes. Additional promising avenues include preventing tubular cell injury and anti-fibrotic therapies that target activated myofibroblasts, the main collagen-producing cells.

Indexed as

Disease ProgressionHumansRenal Insufficiency, Chronic

Identifiers

PMID32060481
OpenAlexW3006609143

What Socratic holds

Textmetadata
Read underepoch 390

Registered trials

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 Socratic graph.