Evidence map›Paper›PMID 27693588›Full record

ReviewClinical immunology (Orlando, Fla.)2017

Genetics of human lupus nephritis.

Taro Iwamoto, Timothy B Niewold

Open access · greenAbstract readReview
In one paragraph

Review in Clinical immunology (Orlando, Fla.), 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
41citing papers in PubMed, 2 pooled it
4.5field-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

41 citing papers in PubMed, 2 syntheses or guidelines pooled it, 72 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Review
  4. Review
  5. Review
  6. Article
  7. Article
  8. Review
  9. Towards precision medicine for systemic lupus erythematosus and neuropsychiatric manifestations.Expert review of precision medicine and drug development · 2025
    Article
  10. Article
  11. Review
  12. Does the esv3587290 Copy Number Variation in theChildren (Basel, Switzerland) · 2024
    Article
  13. Article
  14. Article
  15. Pathogenesis of autoimmune disease.Nature reviews. Nephrology · 2023
    Review
  16. Review
  17. Review
  18. Observational
  19. The role of N6-methyladenosine (mFrontiers in medicine · 2023
    Review
  20. Article
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

2 authors at 1 institution in 1 country.

Taro IwamotoDivision of Rheumatology & Department of Immunology, Mayo Clinic, Rochester, MN 55905, USA.
Timothy B NiewoldDivision of Rheumatology & Department of Immunology, Mayo Clinic, Rochester, MN 55905, USA. Electronic address: Niewold.Timothy@mayo.edu.
Mayo Clinic in Arizona · US

Funding

Interferon Regulatory Factor 5 in Human Lupus PathogenesisR01AR065964 · NIAMS · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI NIEWOLD, TIMOTHY B · 2015 to 2018
$2.0M
Interferon Alpha as a Tool for Gene Discovery in Human LupusR01AR060861 · NIAMS · UNIVERSITY OF CHICAGO · PI NIEWOLD, TIMOTHY B · 2011 to 2015
$1.8M
The Role of IL-17 Axis in Inflammatory MyositisR01AR057781 · NIAMS · MAYO CLINIC ROCHESTER · PI NIEWOLD, TIMOTHY B, PETERSON, ERIK J · 2010 to 2014
$1.6M
NIAID NIH HHS L30 AI071651NIAMS NIH HHS R01 AR057781NIAMS NIH HHS R01 AR060861NIAMS NIH HHS R01 AR065964
6 · The paper itself

Abstract

Systemic lupus erythematosus (SLE) is an inflammatory autoimmune disease characterized by immune complex formation with multi-organ manifestations. Lupus nephritis (LN) is one of the most severe types of organ damage in SLE, and it clearly contributes to increased morbidity and mortality due to SLE. LN occurs more frequently and is more severe in non-European ancestral backgrounds, although the cause of this disparity remains largely unknown. Genetic factors play an important role in the pathogenesis of SLE. Although many SLE susceptibility genes have been identified, the genetic basis of LN is not as well understood. While some of the established general SLE susceptibility genes are associated with LN, recent discoveries highlight a number of genes with renal functions that are specifically associated with LN. Some of these genes associated with LN help to explain the disparity in the prevalence of nephritis between individuals with SLE, and also partially explain differences in LN between ancestral backgrounds. Moreover, not only the gene mutations, but also post-translational modifications seem to play important roles in the pathogenesis of LN. Overall it seems likely that a combination of general SLE susceptibility genes cooperate with LN specific risk genes to result in the genetic propensity for LN. In this review, we will outline the genetic contribution to LN and describe possible roles of LN susceptibility genes.

Indexed as

AnimalsEpigenomicsGenetic Predisposition to DiseaseHumansIncidenceLupus NephritisAPOL1GeneticsHAS2Lupus nephritisPDGFRSystemic lupus erythematosus

Identifiers

PMID27693588
PMCPMC5373939
OpenAlexW2524638166

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.