Evidence map›Paper›PMID 25165721›Full record

ReviewBioMed research international2014

Pathophysiology of cisplatin-induced acute kidney injury.

Abdullah Ozkok, Charles L Edelstein

Open access · hybridAbstract readReview
In one paragraph

Review in BioMed research international, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 379 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
379citing papers in PubMed, 1 pooled it
22.2field-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

379 citing papers in PubMed, 1 synthesis or guideline pooled it, 683 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Article
  4. Review
  5. Review
  6. Article
  7. Article
  8. Review
  9. Article
  10. Kidney disease and transplantation in childhood cancer survivors.Pediatric nephrology (Berlin, Germany) · 2026
    Review
  11. Review
  12. Article
  13. Article
  14. Cisplatin-Induced Nephrotoxicity Attenuation byInternational journal of molecular sciences · 2026
    Article
  15. Molecules (Basel, Switzerland) · 2026
    Article
  16. Article
  17. Article
  18. Review
  19. Erythropoietin and Ferulic Acid Loaded on FeApplied biochemistry and biotechnology · 2026
    Article
  20. Article

319 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

2 authors at 1 institution in 1 country.

Abdullah OzkokDivision of Renal Diseases and Hypertension, University of Colorado at Denver, P.O. Box C281, 12700 East 19th Avenue, Aurora, CO 80262, USA.
Charles L EdelsteinDivision of Renal Diseases and Hypertension, University of Colorado at Denver, P.O. Box C281, 12700 East 19th Avenue, Aurora, CO 80262, USA.
University of Colorado Denver · US

Funding

The IL-33/CD4 T cell/CXCL1 System in Acute Kidney InjuryI01BX001737 · VA · VA EASTERN COLORADO HEALTH CARE SYSTEM · PI EDELSTEIN, CHARLES LOUIS · 2013 to 2016
–
BLRD VA I01 BX001737
6 · The paper itself

Abstract

Cisplatin and other platinum derivatives are the most widely used chemotherapeutic agents to treat solid tumors including ovarian, head and neck, and testicular germ cell tumors. A known complication of cisplatin administration is acute kidney injury (AKI). The nephrotoxic effect of cisplatin is cumulative and dose-dependent and often necessitates dose reduction or withdrawal. Recurrent episodes of AKI may result in chronic kidney disease. The pathophysiology of cisplatin-induced AKI involves proximal tubular injury, oxidative stress, inflammation, and vascular injury in the kidney. There is predominantly acute tubular necrosis and also apoptosis in the proximal tubules. There is activation of multiple proinflammatory cytokines and infiltration of inflammatory cells in the kidney. Inhibition of the proinflammatory cytokines TNF-α or IL-33 or depletion of CD4+ T cells or mast cells protects against cisplatin-induced AKI. Cisplatin also causes endothelial cell injury. An understanding of the pathogenesis of cisplatin-induced AKI is important for the development of adjunctive therapies to prevent AKI, to lessen the need for dose decrease or drug withdrawal, and to lessen patient morbidity and mortality.

Indexed as

Acute Kidney InjuryKidney Tubules, ProximalAntineoplastic AgentsCisplatinFemaleHumansInterleukin-33InterleukinsMaleNeoplasms, Germ Cell and EmbryonalOxidative StressTumor Necrosis Factor-alphaAntineoplastic AgentsCisplatinIL33 protein, humanInterleukin-33InterleukinsTNF protein, humanTumor Necrosis Factor-alpha

Identifiers

PMID25165721
PMCPMC4140112
OpenAlexW2114889530

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.