Evidence map›Paper›PMID 28090081›Full record

ReviewNature reviews. Nephrology2017

Metabolic reprogramming and tolerance during sepsis-induced AKI.

Hernando Gómez, John A Kellum, Claudio Ronco

Abstract readReview
In one paragraph

Review in Nature reviews. Nephrology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 119 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
119citing papers in PubMed, 1 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

119 citing papers in PubMed, 1 synthesis or guideline pooled it.

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59 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.

Hernando GómezCenter for Critical Care Nephrology, Department of Critical Care Medicine, University of Pittsburgh, School of Medicine, Room 604 Scaife Hall, 3550 Terrace Street, Pittsburgh, Pennsylvania 15261, USA.
John A KellumCenter for Critical Care Nephrology, Department of Critical Care Medicine, University of Pittsburgh, School of Medicine, Room 604 Scaife Hall, 3550 Terrace Street, Pittsburgh, Pennsylvania 15261, USA.
Claudio RoncoDepartment of Nephrology, Dialysis and Transplantation, San Bortolo Hospital, International Renal Research Institute of Vicenza, Viale Rodolfi 37, 36100 Vicenza, Italy.

Funding

Pittsburgh Career Development Program in Emergency Medicine ResearchK12HL109068 · NHLBI · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI CALLAWAY, CLIFTON W., YEALY, DONALD M · 2011 to 2015
$3.1M
The role of energy regulation in the epithelial cell response to sepsis and the origin of multiple organ dysfuntionK08GM117310 · NIGMS · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI GOMEZ DANIES, HERNANDO · 2016 to 2018
$560k
NHLBI NIH HHS K12 HL109068NIGMS NIH HHS K08 GM117310
6 · The paper itself

Abstract

The host defence against infection is an adaptive response in which several mechanisms are deployed to decrease the pathogen load, limit tissue injury and restore homeostasis. In the past few years new evidence has suggested that the ability of the immune system to limit the microbial burden - termed resistance - might not be the only defence mechanism. In fact, the capacity of the host to decrease its own susceptibility to inflammation- induced tissue damage - termed tolerance - might be as important as resistance in determining the outcome of the infection. Metabolic adaptations are central to the function of the cellular immune response. Coordinated reprogramming of metabolic signalling enables cells to execute resistance and tolerance pathways, withstand injury, steer tissue repair and promote organ recovery. During sepsis-induced acute kidney injury, early reprogramming of metabolism can determine the extent of organ dysfunction, progression to fibrosis, and the development of chronic kidney disease. Here we discuss the mechanisms of tolerance that act in the kidney during sepsis, with particular attention to the role of metabolic responses in coordinating these adaptive strategies. We suggest a novel conceptual model of the cellular and organic response to sepsis that might lead to new avenues for targeted, organ-protective therapies.

Indexed as

Acute Kidney InjuryAnimalsHumansImmune ToleranceRenal Insufficiency, ChronicSepsis

Identifiers

PMID28090081
PMCPMC5508527

What OpenQuestion holds

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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.