Evidence map›Paper›PMID 33632272›Full record

ReviewRadiation oncology (London, England)2021

Radiation-induced kidney toxicity: molecular and cellular pathogenesis.

Richard Klaus, Maximilian Niyazi, Bärbel Lange-Sperandio

Open access · goldAbstract readReview
In one paragraph

Review in Radiation oncology (London, England), 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 80 papers.

0numbers the graph read from it
0cells of the map it votes in
80citing papers in PubMed
14.1field-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

80 citing papers in PubMed, 141 citations in OpenAlex.

  1. Review
  2. Kidney disease and transplantation in childhood cancer survivors.Pediatric nephrology (Berlin, Germany) · 2026
    Review
  3. Article
  4. Article
  5. Article
  6. Article
  7. Radiomitigators: Breakthroughs in Post-Radiation Recovery.Antioxidants (Basel, Switzerland) · 2026
    Review
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Review
  15. Review
  16. Article
  17. Article
  18. Review
  19. Article
  20. Article

20 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

3 authors at 3 institutions in 1 country.

Richard KlausDivision of Pediatric Nephrology, Department of Pediatrics, Dr. v. Hauner Children's Hospital, University Hospital, LMU Munich, Lindwurmstr. 4, 80337, Munich, Germany.
Maximilian NiyaziDepartment of Radiation Oncology, University Hospital, LMU Munich, Munich, Germany.
Bärbel Lange-SperandioDivision of Pediatric Nephrology, Department of Pediatrics, Dr. v. Hauner Children's Hospital, University Hospital, LMU Munich, Lindwurmstr. 4, 80337, Munich, Germany. baerbel.lange-sperandio@med.uni-muenchen.de.ORCID http://orcid.org/0000-0001-8898-3459
LMU Klinikum · DELudwig-Maximilians-Universität München · DEUniversity Children's Hospital Tübingen · DE

Funding

Deutsche Forschungsgemeinschaft (DE) La1257/5-1
6 · The paper itself

Abstract

Radiation nephropathy (RN) is a kidney injury induced by ionizing radiation. In a clinical setting, ionizing radiation is used in radiotherapy (RT). The use and the intensity of radiation therapy is limited by normal-tissue damage including kidney toxicity. Different thresholds for kidney toxicity exist for different entities of RT. Histopathologic features of RN include vascular, glomerular and tubulointerstitial damage. The different molecular and cellular pathomechanisms involved in RN are not fully understood. Ionizing radiation causes double-stranded breaks in the DNA, followed by cell death including apoptosis and necrosis of renal endothelial, tubular and glomerular cells. Especially in the latent phase of RN oxidative stress and inflammation have been proposed as putative pathomechanisms, but so far no clear evidence was found. Cellular senescence, activation of the renin-angiotensin-aldosterone-system and vascular dysfunction might contribute to RN, but only limited data is available. Several signalling pathways have been identified in animal models of RN and different approaches to mitigate RN have been investigated. Drugs that attenuate cell death and inflammation or reduce oxidative stress and renal fibrosis were tested. Renin-angiotensin-aldosterone-system blockade, anti-apoptotic drugs, statins, and antioxidants have been shown to reduce the severity of RN. These results provide a rationale for the development of new strategies to prevent or reduce radiation-induced kidney toxicity.

Indexed as

AnimalsCellular SenescenceDNA DamageFibrosisHumansHypertension, RenovascularInflammationKidneyOxidative StressRadiation InjuriesRadiotherapyRenin-Angiotensin SystemCellular senescenceDNA damageRadiation nephropathyRadiotherapyRenal fibrosisRenal inflammationTotal body irradiation

Identifiers

PMID33632272
PMCPMC7905925
OpenAlexW3129744915

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.