Evidence map›Paper›PMID 31925537›Full record

ReviewPediatric nephrology (Berlin, Germany)2021

Mitochondrial DNA mutations in renal disease: an overview.

Larissa P Govers, Hakan R Toka, Ali Hariri, Stephen B Walsh, Detlef Bockenhauer

Open access · hybridAbstract readReview
In one paragraph

Review in Pediatric nephrology (Berlin, Germany), 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed
3.7field-weighted citation impact, top 6% 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

38 citing papers in PubMed, 69 citations in OpenAlex.

  1. Article
  2. Integrative Approaches to Treating Cellular Senescence in Kidney Disease.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026
    Review
  3. Review
  4. Article
  5. Associations of Blood Mitochondrial DNA Quality and Quantity with Risk of Kidney Function Decline.Clinical journal of the American Society of Nephrology : CJASN · 2026
    Article
  6. Article
  7. Article
  8. Article
  9. Extrarenal manifestations in inherited kidney diseases.Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association · 2025
    Review
  10. Review
  11. Review
  12. Article
  13. Genes · 2024
    Article
  14. Genetic determinants of renal scarring in children with febrile UTI.Pediatric nephrology (Berlin, Germany) · 2024
    Article
  15. Article
  16. Review
  17. Review
  18. Review
  19. Article
  20. 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

5 authors at 3 institutions in 2 countries.

Larissa P GoversDepartment of Renal Medicine, University College London, London, UK.
Hakan R TokaManatee Kidney Diseases Consultants, Bradenton, USA.
Ali HaririClinical Development, Sanofi Rare Disease, Boston, USA.
Stephen B WalshDepartment of Renal Medicine, University College London, London, UK.
Detlef BockenhauerDepartment of Renal Medicine, University College London, London, UK. d.bockenhauer@ucl.ac.uk.ORCID 0000-0001-5878-941X
University College London · GBBoston University · USGreat Ormond Street Hospital for Children NHS Foundation Trust · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Kidneys have a high energy demand to facilitate the reabsorption of the glomerular filtrate. For this reason, renal cells have a high density of mitochondria. Mitochondrial cytopathies can be the result of a mutation in both mitochondrial and nuclear DNA. Mitochondrial dysfunction can lead to a variety of renal manifestations. Examples of tubular manifestations are renal Fanconi Syndrome, which is often found in patients diagnosed with Kearns-Sayre and Pearson's marrow-pancreas syndrome, and distal tubulopathies, which result in electrolyte disturbances such as hypomagnesemia. Nephrotic syndrome can be a glomerular manifestation of mitochondrial dysfunction and is typically associated with focal segmental glomerular sclerosis on histology. Tubulointerstitial nephritis can also be seen in mitochondrial cytopathies and may lead to end-stage renal disease. The underlying mechanisms of these cytopathies remain incompletely understood; therefore, current therapies focus mainly on symptom relief. A better understanding of the molecular disease mechanisms is critical in order to improve treatments.

Indexed as

MutationDNA, MitochondrialHumansKearns-Sayre SyndromeMitochondriaMitochondrial MyopathiesNephritis, InterstitialDNA, MitochondrialDistal tubulopathiesMitochondrial DNANephrotic syndromeRenal diseaseRenal Fanconi syndromeTubulointerstitial nephritis

Identifiers

PMID31925537
PMCPMC7701126
OpenAlexW2999618498

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.