Evidence map›Paper›PMID 26208584›Full record

ReviewPediatric nephrology (Berlin, Germany)2016

Tubular atrophy in the pathogenesis of chronic kidney disease progression.

Jeffrey R Schelling

Open access · greenAbstract readReview
In one paragraph

Review in Pediatric nephrology (Berlin, Germany), 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 104 papers.

0numbers the graph read from it
0cells of the map it votes in
104citing papers in PubMed
4.1field-weighted citation impact, top 6% 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

104 citing papers in PubMed, 155 citations in OpenAlex.

  1. GLP-1 receptor agonists-a potential therapy for chronic kidney disease?Clinical science (London, England : 1979) · 2026
    Review
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Review
  15. Article
  16. Article
  17. Rac1 promotes proximal tubule kidney repair by coupling the actin cytoskeleton to mitochondrial function.Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  18. Article
  19. Article
  20. Review

44 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

1 author at 1 institution in 1 country.

Jeffrey R SchellingDepartment of Medicine, Case Western Reserve University, Cleveland, OH, USA. jeffrey.schelling@case.edu.
MetroHealth Medical Center · US

Funding

Limited Competition for the Continuation of the Chronic Renal Insufficiency CohorU01DK061021 · NIDDK · CASE WESTERN RESERVE UNIVERSITY · PI RAHMAN, MAHBOOB · 2001 to 2025
$17.3M
Mechanisms of tubular atrophy in renal diseaseR01DK067528 · NIDDK · CASE WESTERN RESERVE UNIVERSITY · PI SCHELLING, JEFFREY R · 2005 to 2025
$7.1M
NIDDK NIH HHS 2R01 DK067528NIDDK NIH HHS 2U01 DK061021NIDDK NIH HHS R01 DK067528NIDDK NIH HHS U01 DK061021
6 · The paper itself

Abstract

The longstanding focus in chronic kidney disease (CKD) research has been on the glomerulus, which is sensible because this is where glomerular filtration occurs, and a large proportion of progressive CKD is associated with significant glomerular pathology. However, it has been known for decades that tubular atrophy is also a hallmark of CKD and that it is superior to glomerular pathology as a predictor of glomerular filtration rate decline in CKD. Nevertheless, there are vastly fewer studies that investigate the causes of tubular atrophy, and fewer still that identify potential therapeutic targets. The purpose of this review is to discuss plausible mechanisms of tubular atrophy, including tubular epithelial cell apoptosis, cell senescence, peritubular capillary rarefaction and downstream tubule ischemia, oxidative stress, atubular glomeruli, epithelial-to-mesenchymal transition, interstitial inflammation, lipotoxicity and Na(+)/H(+) exchanger-1 inactivation. Once a a better understanding of tubular atrophy (and interstitial fibrosis) pathophysiology has been obtained, it might then be possible to consider tandem glomerular and tubular therapeutic strategies, in a manner similar to cancer chemotherapy regimens, which employ multiple drugs to simultaneously target different mechanistic pathways.

Indexed as

AnimalsAtrophyDisease Models, AnimalDisease ProgressionEpithelial CellsFibrosisHumansKidney TubulesRenal CirculationRenal Insufficiency, ChronicSignal TransductionApoptosisChronic kidney diseaseInterstitial fibrosisLipotoxicityNHE1

Identifiers

PMID26208584
PMCPMC4726480
OpenAlexW2025914300

What OpenQuestion holds

Textmetadata
LicenceTDM
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.