Evidence map›Paper›PMID 33081797›Full record

ReviewJournal of translational medicine2020

Contrast-induced nephropathy and oxidative stress: mechanistic insights for better interventional approaches.

Prit Kusirisin, Siriporn C Chattipakorn, Nipon Chattipakorn

Registry-linked trialAbstract readReview
In one paragraph

Review in Journal of translational medicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT04890704 (Curcuminoids Can Prevent Contrast-induced Acute Kidney Injury in Chronic Kidney Disease Patients Undergoing Elective Coronary Procedures), which is not on this map. Cited by 89 papers, 9 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
89citing papers in PubMed, 9 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.

NCT04890704 early_phase1completednot on this map

Curcuminoids Can Prevent Contrast-induced Acute Kidney Injury in Chronic Kidney Disease Patients Undergoing Elective Coronary Procedures: A Randomized Controlled Trial

TypeinterventionalSponsorBangkok Metropolitan Administration Medical College and Vajira HospitalRan2018 to 2019Enrolled96ConditionsAcute Kidney Injury, Contrast Media Toxicity, Curcuminoid, Chronic Kidney DiseasesArmsCurcuminoid, Placebo
3 · Its place in the literature

Who cites it

89 citing papers in PubMed, 9 syntheses or guidelines pooled it.

  1. Pooled it
  2. Pooled it
  3. Pooled it
  4. Pooled it
  5. Pooled it
  6. Pooled it
  7. Pooled it
  8. Pooled it
  9. Pooled it
  10. Trial
  11. Trial
  12. Trial
  13. Trial
  14. Trial
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. Article

29 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.

Prit KusirisinDivision of Nephrology, Department of Internal Medicine, Faculty of Medicine, Chiang Mai University, Chiang Mai, Thailand.
Siriporn C ChattipakornCardiac Electrophysiology Research and Training Center, Faculty of Medicine, Chiang Mai University, Chiang Mai, Thailand.
Nipon ChattipakornCardiac Electrophysiology Research and Training Center, Faculty of Medicine, Chiang Mai University, Chiang Mai, Thailand. nchattip@gmail.com.ORCID 0000-0003-3026-718X

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Contrast-induced nephropathy (CIN) or contrast-induced acute kidney injury (CI-AKI) is an iatrogenic acute kidney injury observed after intravascular administration of contrast media for intravascular diagnostic procedures or therapeutic angiographic intervention. High risk patients including those with chronic kidney disease (CKD), diabetes mellitus with impaired renal function, congestive heart failure, intraarterial intervention, higher volume of contrast, volume depletion, old age, multiple myeloma, hypertension, and hyperuricemia had increased prevalence of CIN. Although CIN is reversible by itself, some patients suffer this condition without renal recovery leading to CKD or even end-stage renal disease which required long term renal replacement therapy. In addition, both CIN and CKD have been associated with increasing of mortality. Three pathophysiological mechanisms have been proposed including direct tubular toxicity, intrarenal vasoconstriction, and excessive production of reactive oxygen species (ROS), all of which lead to impaired renal function. Reports from basic and clinical studies showing potential preventive strategies for CIN pathophysiology including low- or iso-osmolar contrast media are summarized and discussed. In addition, reports on pharmacological interventions to reduce ROS and attenuate CIN are summarized, highlighting potential for use in clinical practice. Understanding this contributory mechanism could pave ways to improve therapeutic strategies in combating CIN.

Indexed as

Acute Kidney InjuryContrast MediaHumansKidneyOxidative StressRisk FactorsContrast MediaContrast-induced nephropathyMitochondriaOxidative stressPreventionStatin

Identifiers

PMID33081797
PMCPMC7576747

What OpenQuestion holds

Textmetadata
LicenceCC BY
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 OpenQuestion graph.