Evidence map›Paper›PMID 18294749›Full record

ReviewToxicology2008

Biomarkers of nephrotoxic acute kidney injury.

Michael A Ferguson, Vishal S Vaidya, Joseph V Bonventre

Abstract readReview
In one paragraph

Review in Toxicology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 105 papers.

0numbers the graph read from it
0cells of the map it votes in
105citing papers in PubMed
7.8field-weighted citation impact, top 2% 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

105 citing papers in PubMed, 320 citations in OpenAlex.

  1. Trial
  2. Article
  3. Cisplatin-Induced Nephrotoxicity Attenuation byInternational journal of molecular sciences · 2026
    Article
  4. Article
  5. Review
  6. Article
  7. Article
  8. Review
  9. Review
  10. Article
  11. Article
  12. Toxicity Profile ofBiochemistry research international · 2025
    Article
  13. Nephroprotection of Wood Apple (Journal of nutrition and metabolism · 2025
    Article
  14. Article
  15. Article
  16. Article
  17. Natural Products in Renal-Associated Drug Discovery.Antioxidants (Basel, Switzerland) · 2023
    Review
  18. Review
  19. Article
  20. Review

45 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 2 institutions in 1 country.

Michael A FergusonDivision of Nephrology, Children's Hospital Boston, Hunnewell 319, Boston, MA 02115, United States. michael.ferguson@childrens.harvard.edu
Vishal S Vaidya
Joseph V Bonventre
Harvard University · USBoston Children's Hospital · US

Funding

KIDNEY INJURY MOLECULE-1 IN EPITHELIAL REPAIRR01DK072381 · NIDDK · BRIGHAM AND WOMEN'S HOSPITAL · PI BONVENTRE, JOSEPH VINCENT · 2005 to 2025
$8.6M
Mechanisms of Ischemic Kidney Injury and RepairR01DK039773 · NIDDK · MASSACHUSETTS GENERAL HOSPITAL · PI JOSEPH VINCENT BONVENTRE · 1987 to 2026
$6.2M
Mechanisms of Ischemic Kidney Injury and RepairR37DK039773 · NIDDK · MASSACHUSETTS GENERAL HOSPITAL · PI BONVENTRE, JOSEPH VINCENT · 1993 to 2021
$5.2M
Biomarkers in Acute Kidney InjuryR33DK074099 · NIDDK · BRIGHAM AND WOMEN'S HOSPITAL · PI BONVENTRE, JOSEPH VINCENT · 2007 to 2009
$1.9M
Biomarkers in Acute Kidney InjuryR21DK074099 · NIDDK · BRIGHAM AND WOMEN'S HOSPITAL · PI BONVENTRE, JOSEPH VINCENT · 2005 to 2006
$516k
Technology and Endothelial Biology of Kidney Injury Molecule-1K99ES016723 · NIEHS · BRIGHAM AND WOMEN'S HOSPITAL · PI VAIDYA, VISHAL S. · 2007 to 2007
$90k
NIDDK NIH HHS DK39773NIDDK NIH HHS DK72381NIDDK NIH HHS DK74099NIDDK NIH HHS R01 DK039773NIDDK NIH HHS R01 DK072381NIDDK NIH HHS R21 DK074099NIDDK NIH HHS R33 DK074099NIDDK NIH HHS R37 DK039773NIEHS NIH HHS K99 ES016723NIEHS NIH HHS K99 ES16723
6 · The paper itself

Abstract

Acute kidney injury (AKI) is a common condition with significant associated morbidity and mortality. Epidemiologic data suggest that a significant proportion of AKI cases is at least partially attributable to nephrotoxin exposure. This is not surprising given intrinsic renal susceptibility to toxicant-induced injury, a consequence of the unique physiologic and biochemical properties of the normally functioning kidney. A number of pathophysiologic mechanisms have been identified that mediate toxic effects on the kidney, resulting in a variety of clinical syndromes ranging from subtle changes in tubular function to fulminant renal failure. Unfortunately, standard metrics used to diagnose and monitor kidney injury, such as blood urea nitrogen and serum creatinine, are insensitive and nonspecific, resulting in delayed diagnosis and intervention. Considerable effort has been made to identify biomarkers that will allow the earlier diagnosis of AKI. Further characterization of these candidate biomarkers will clarify their utility in the setting of acute nephrotoxicity, define new diagnostic and prognostic paradigms for kidney injury, facilitate clinical trials, and lead to novel effective therapies.

Indexed as

Acute DiseaseAcute-Phase ProteinsAlbuminuriaAnimalsBiomarkersFatty Acid-Binding ProteinsHepatitis A Virus Cellular Receptor 1HumansInterleukin-18Kidney DiseasesLipocalin-2LipocalinsMembrane GlycoproteinsMolecular WeightProteinuriaProto-Oncogene ProteinsAcute-Phase ProteinsBiomarkersFatty Acid-Binding ProteinsHAVCR1 protein, humanHepatitis A Virus Cellular Receptor 1Interleukin-18LCN2 protein, humanLipocalin-2LipocalinsMembrane GlycoproteinsProto-Oncogene ProteinsReceptors, Virus

Identifiers

PMID18294749
PMCPMC4038970
OpenAlexW2070087000

What OpenQuestion holds

Textmetadata
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.