Evidence map›Paper›PMID 31055583›Full record

ReviewNephron2019

Metabolic Stress Resistance in Acute Kidney Injury: Evidence for a PPAR-Gamma-Coactivator-1 Alpha-Nicotinamide Adenine Dinucleotide Pathway.

Samir M Parikh

Open access · bronzeAbstract readReview
In one paragraph

Review in Nephron, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
1.8field-weighted citation impact, top 15% 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

11 citing papers in PubMed, 18 citations in OpenAlex.

  1. Review
  2. Article
  3. Nicotinamide Riboside, a Promising Vitamin BMolecules (Basel, Switzerland) · 2023
    Review
  4. Article
  5. Polarization of Microglia and Its Therapeutic Potential in Sepsis.International journal of molecular sciences · 2022
    Review
  6. Review
  7. Nicotinamide and acute kidney injury.Clinical kidney journal · 2021
    Article
  8. Article
  9. Article
  10. Article
  11. Review
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

1 author at 1 institution in 1 country.

Samir M ParikhDivision of Nephrology and Center for Vascular Biology Research, Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, Massachusetts, USA, sparikh1@bidmc.harvard.edu.
Beth Israel Deaconess Medical Center · US

Funding

UAB-UCSD O'Brien Core Center for Acute Kidney Injury ResearchP30DK079337 · NIDDK · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI AGARWAL, ANUPAM · 2008 to 2022
$18.3M
The Aging Kidney: Chronic Injury, Impaired Functions and Clinical OutcomesR01AG027002 · NIA · TUFTS MEDICAL CENTER · PI PARIKH, SAMIR M, SARNAK, MARK J · 2005 to 2022
$7.3M
Tie2-driven vascular control in critical illnessR35HL139424 · NHLBI · UT SOUTHWESTERN MEDICAL CENTER · PI PARIKH, SAMIR M · 2018 to 2024
$6.4M
Mitochondrial Biogenesis in Kidney DiseaseR01DK095072 · NIDDK · UT SOUTHWESTERN MEDICAL CENTER · PI Samir M Parikh · 2012 to 2026
$5.3M
NHLBI NIH HHS R35 HL139424NIA NIH HHS R01 AG027002NIDDK NIH HHS P30 DK079337NIDDK NIH HHS R01 DK095072
6 · The paper itself

Abstract

Acute kidney injury (AKI) is estimated to affect 3-10% of all hospitalized adults in the United States, making it one of the most common inpatient diagnoses. Despite this staggering incidence, most individuals exposed to AKI stressors, such as intravenous radiocontrast or cardiopulmonary bypass, do not develop AKI. In fact, whereas animal models of ischemia, sepsis, or nephrotoxicity suggest near-uniform responses to stressors, the natural history of stressed patients is highly heterogeneous. Recent studies of mitochondrial perturbations underlying experimental and human AKI suggest a conserved metabolic contribution to this variance. The renal tubule is only second to the heart in terms of mitochondrial abundance, reflecting the exquisite need for fuel combustion to generate the energy for active solute transport. The homeostasis of nicotinamide adenine dinucleotide (NAD+), a requisite coenzyme in oxidative metabolism, may be an important determinant of the renal response to AKI stressors. This mini-review highlights recent studies implicating NAD+ dysregulation in experimental and human AKI and summarizes findings from a pilot randomized trial to augment NAD+ among at-risk individuals.

Indexed as

Stress, PhysiologicalAcute Kidney InjuryAnimalsHumansMitochondriaPeroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alphaRandomized Controlled Trials as TopicPeroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alphaPPARGC1A protein, humanAcute kidney injuryAcute renal failureMitochondriaNiacinamideNicotinamideNicotinamide adenine dinucleotideQuinolinateTubuleVitamin B3

Identifiers

PMID31055583
PMCPMC6821556
OpenAlexW2944807739

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.