Evidence map›Paper›PMID 26561643›Full record

ReviewJournal of the American Society of Nephrology : JASN2016

Inflammation in AKI: Current Understanding, Key Questions, and Knowledge Gaps.

Hamid Rabb, Matthew D Griffin, Dianne B McKay, Sundararaman Swaminathan, Peter Pickkers, Mitchell H Rosner, John A Kellum, Claudio Ronco, Acute Dialysis Quality Initiative Consensus XIII Work Group

Abstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Journal of the American Society of Nephrology : JASN, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 355 papers, 4 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
355citing papers in PubMed, 4 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.

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

355 citing papers in PubMed, 4 syntheses or guidelines pooled it.

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  9. Urinary UDP-sugars provide actionable prediction of acute kidney injury in cardiac surgery patients.American journal of physiology. Heart and circulatory physiology · 2026
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295 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

9 authors.

Hamid RabbDivision of Nephrology, Department of Medicine, Johns Hopkins University, Baltimore, Maryland; hrabb1@jhmi.edu.
Matthew D GriffinRegenerative Medicine Institute, School of Medicine, College of Medicine Nursing and Health Sciences, National University of Ireland, Galway, Ireland;
Dianne B McKayDivision of Nephrology and Hypertension, Department of Medicine, University of California, San Diego, La Jolla, California;
Sundararaman SwaminathanDivision of Nephrology, University of Virginia School of Medicine, Charlottesville, Virginia;
Peter PickkersDepartment of Intensive Care Medicine, Radboud University Medical Center, Nijmegen, The Netherlands;
Mitchell H RosnerDivision of Nephrology, University of Virginia School of Medicine, Charlottesville, Virginia;
John A KellumCenter for Critical Care Nephrology and Department of Critical Care Medicine, University of Pittsburgh, Pittsburgh, Pennsylvania; and.
Claudio RoncoDepartment of Nephrology Dialysis and Transplantation, Saint Bortolo Hospital and the International Renal Research Institute, Vicenza, Italy.
Acute Dialysis Quality Initiative Consensus XIII Work Group

Funding

KIDNEY INJURY MOLECULE-1 IN EPITHELIAL REPAIRR01DK072381 · NIDDK · BRIGHAM AND WOMEN'S HOSPITAL · PI BONVENTRE, JOSEPH VINCENT · 2005 to 2025
$8.6M
NIDDK NIH HHS R01 DK072381
6 · The paper itself

Abstract

Inflammation is a complex biologic response that is essential for eliminating microbial pathogens and repairing tissue after injury. AKI associates with intrarenal and systemic inflammation; thus, improved understanding of the cellular and molecular mechanisms underlying the inflammatory response has high potential for identifying effective therapies to prevent or ameliorate AKI. In the past decade, much knowledge has been generated about the fundamental mechanisms of inflammation. Experimental work in small animal models has revealed many details of the inflammatory response that occurs within the kidney after typical causes of AKI, including insights into the molecular signals released by dying cells, the role of pattern recognition receptors, the diverse subtypes of resident and recruited immune cells, and the phased transition from destructive to reparative inflammation. Although this expansion of the basic knowledge base has increased the number of mechanistically relevant targets of intervention, progress in developing therapies that improve AKI outcomes by modulation of inflammation remains slow. In this article, we summarize the most important recent developments in understanding the inflammatory mechanisms of AKI, highlight key limitations of the commonly used animal models and clinical trial designs that may prevent successful clinical application, and suggest priority approaches for research toward clinical translation in this area.

Indexed as

Acute Kidney InjuryAnimalsDisease Models, AnimalHumansInflammationKidneyacute renal failureclinical nephrologyimmunologypathophysiology ofrenal disease and progression

Identifiers

PMID26561643
PMCPMC4731128

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.