Evidence map›Paper›PMID 26804019›Full record

ReviewNature reviews. Nephrology2016

Mitochondrial dysfunction in inherited renal disease and acute kidney injury.

Francesco Emma, Giovanni Montini, Samir M Parikh, Leonardo Salviati

Open access · greenAbstract readReview
In one paragraph

Review in Nature reviews. Nephrology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 231 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
231citing papers in PubMed, 2 pooled it
16.4field-weighted citation impact, top 1% 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

231 citing papers in PubMed, 2 syntheses or guidelines pooled it, 374 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Trial
  4. Review
  5. Article
  6. Review
  7. Proteinuria in adolescence.Pediatric nephrology (Berlin, Germany) · 2026
    Review
  8. Review
  9. Review
  10. CaAntibodies (Basel, Switzerland) · 2026
    Article
  11. Article
  12. Observational
  13. When rare diseases do not appear as a single entity.Advances in laboratory medicine · 2026
    Article
  14. Article
  15. Review
  16. Article
  17. Review
  18. Review
  19. Article
  20. Review

171 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

4 authors at 4 institutions in 2 countries.

Francesco EmmaDivision of Nephrology and Dialysis, Ospedale Pediatrico Bambino Gesù-IRCCS, Piazza Sant'Onofrio 4, 00165 Rome, Italy.
Giovanni MontiniPediatric Nephrology and Dialysis Unit, Department of Clinical Sciences and Community Health, University of Milan, Fondazione IRCCS Ca' Granda - Ospedale Maggiore Policlinico, Via della Commenda 9, Milano, Italy.
Samir M ParikhDivision of Nephrology and Center for Vascular Biology Research, Beth Israel Deaconess Medical Center and Harvard Medical School, 330 Brookline Avenue, Boston, Massachusetts 02215, USA.
Leonardo SalviatiClinical Genetics Unit, Department of Woman and Child Health, University of Padova, Via Giustiniani 3, 35128, Padova, Italy.
Bambino Gesù Children's Hospital · ITBeth Israel Deaconess Medical Center · USUniversity of Milan · ITUniversity of Padua · IT

Funding

Mitochondrial Biogenesis in Kidney DiseaseR01DK095072 · NIDDK · UT SOUTHWESTERN MEDICAL CENTER · PI Samir M Parikh · 2012 to 2026
$5.3M
NIDDK NIH HHS R01 DK095072NIDDK NIH HHS R01‑DK0950972
6 · The paper itself

Abstract

Mitochondria are increasingly recognized as key players in genetic and acquired renal diseases. Most mitochondrial cytopathies that cause renal symptoms are characterized by tubular defects, but glomerular, tubulointerstitial and cystic diseases have also been described. For example, defects in coenzyme Q10 (CoQ10) biosynthesis and the mitochondrial DNA 3243 A>G mutation are important causes of focal segmental glomerulosclerosis in children and in adults, respectively. Although they sometimes present with isolated renal findings, mitochondrial diseases are frequently associated with symptoms related to central nervous system and neuromuscular involvement. They can result from mutations in nuclear genes that are inherited according to classic Mendelian rules or from mutations in mitochondrial DNA, which are transmitted according to more complex rules of mitochondrial genetics. Diagnosis of mitochondrial disorders involves clinical characterization of patients in combination with biochemical and genetic analyses. In particular, prompt diagnosis of CoQ10 biosynthesis defects is imperative because of their potentially reversible nature. In acute kidney injury (AKI), mitochondrial dysfunction contributes to the physiopathology of tissue injury, whereas mitochondrial biogenesis has an important role in the recovery of renal function. Potential therapies that target mitochondrial dysfunction or promote mitochondrial regeneration are being developed to limit renal damage during AKI and promote repair of injured tissue.

Indexed as

Acute Kidney InjuryAlkyl and Aryl TransferasesAnimalsDNA, MitochondrialHumansKearns-Sayre SyndromeKidney DiseasesMitochondriaMitochondrial MyopathiesMutationOxidative PhosphorylationReactive Oxygen SpeciesUbiquinoneAlkyl and Aryl Transferasescoenzyme Q10DNA, Mitochondrialprenyl diphosphate synthase, subunit 2, humanReactive Oxygen SpeciesUbiquinone

Identifiers

PMID26804019
PMCPMC5469549
OpenAlexW2264921308

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.