Evidence map›Paper›PMID 19715538›Full record

ReviewCurrent drug targets2009

Immune mechanisms and novel pharmacological therapies of acute kidney injury.

Amandeep Bajwa, Gilbert R Kinsey, Mark D Okusa

Open access · greenAbstract readReview
In one paragraph

Review in Current drug targets, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.

0numbers the graph read from it
0cells of the map it votes in
37citing papers in PubMed
2.5field-weighted citation impact, top 10% 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

37 citing papers in PubMed, 77 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Review
  14. Peptidyl arginine deiminase-4 exacerbates ischemic AKI by finding NEMO.American journal of physiology. Renal physiology · 2019
    Article
  15. Article
  16. Regulatory T cells in acute and chronic kidney diseases.American journal of physiology. Renal physiology · 2018
    Review
  17. Article
  18. Article
  19. Novel Therapies for Acute Kidney Injury.Kidney international reports · 2017
    Review
  20. Article
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 1 institution in 1 country.

Amandeep BajwaCenter for Immunity, Inflammation and Regenerative Medicine, University of Virginia Health System, Charlottesville, 22908, USA.
Gilbert R Kinsey
Mark D Okusa
University of Virginia · US

Funding

Sphingolipids in Acute Kidney Injury and Disease ProgressionR01DK085259 · NIDDK · UNIVERSITY OF VIRGINIA · PI OKUSA, MARK DOUGLAS · 2010 to 2023
$5.0M
Leukocyte Trafficking in Acute Renal FailureR01DK062324 · NIDDK · UNIVERSITY OF VIRGINIA CHARLOTTESVILLE · PI OKUSA, MARK DOUGLAS · 2003 to 2016
$4.4M
Kidney Disease and InflammationT32DK072922 · NIDDK · UNIVERSITY OF VIRGINIA · PI OKUSA, MARK DOUGLAS · 2006 to 2020
$2.6M
ADENOSINE AND RENAL INJURYR01DK056223 · NIDDK · UNIVERSITY OF VIRGINIA CHARLOTTESVILLE · PI OKUSA, MARK DOUGLAS · 2000 to 2009
$1.9M
Lysophosphatidic Acid Receptors and Acute Renal FailureR01DK065957 · NIDDK · UNIVERSITY OF VIRGINIA CHARLOTTESVILLE · PI OKUSA, MARK DOUGLAS · 2004 to 2007
$1.3M
Immune Mechanisms in Kidney Ischemic PreconditioningF32DK083185 · NIDDK · UNIVERSITY OF VIRGINIA · PI KINSEY, GILBERT R · 2009 to 2010
$59k
NIDDK NIH HHS F32 DK083185NIDDK NIH HHS R01 DK056223NIDDK NIH HHS R01 DK062324NIDDK NIH HHS R01 DK065957NIDDK NIH HHS R01 DK085259NIDDK NIH HHS R01 DK56223NIDDK NIH HHS R01 DK62324NIDDK NIH HHS T32 DK072922
6 · The paper itself

Abstract

Ischemia-reperfusion injury (IRI) is a major cause of acute kidney injury (AKI) and both innate and adaptive immunity contribute to the pathogenesis. Kidney resident cells promote inflammation after IRI by increasing endothelial cell adhesion molecule expression and vascular permeability. Kidney epithelial cells bind complement and express toll-like receptors and resident and infiltrating cells produce cytokines/chemokines. Early activation of kidney dendritic cells (DCs) initiates a cascade of events leading to accumulation of interferon-gamma-producing neutrophils, infiltrating macrophages, CD4(+) T cells, B cells and invariant natural killer T (NKT) cells. Recent studies from our laboratory now implicate the IL23/IL17 pathway in kidney IRI. Following the initial early phase of inflammation, the late phase involves infiltration of anti-inflammatory cells including regulatory T cells, alternatively activated macrophages and stem cells leading to attenuation of inflammation and initiation of repair. Based upon these immune mechanisms of injury, recent studies hold promise for novel drug therapies. These pharmacological agents have been shown to reduce inflammation or cytotoxicity in rodent models of AKI and some show early promise in clinical trials. This review summarizes recent advances to further our understanding of the immune mechanisms of AKI and potential pharmacological therapies.

Indexed as

Acute Kidney InjuryAnimalsAnti-Inflammatory AgentsCell SurvivalDisease Models, AnimalHumansInflammationReperfusion InjuryAnti-Inflammatory Agents

Identifiers

PMID19715538
PMCPMC2941672
OpenAlexW2158674216

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.