Evidence map›Paper›PMID 31202388›Full record

ReviewAdvances in chronic kidney disease2019

Common Mechanisms of Viral Injury to the Kidney.

Leslie A Bruggeman

Open access · greenAbstract readReview
In one paragraph

Review in Advances in chronic kidney disease, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
1.6field-weighted citation impact, top 18% 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

13 citing papers in PubMed, 19 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Article
  5. Review
  6. Review
  7. Article
  8. Article
  9. Article
  10. Review
  11. Article
  12. Viral Nephropathies, Adding SARS-CoV-2 to the List.International journal of nephrology and renovascular disease · 2021
    Review
  13. 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

1 author at 1 institution in 1 country.

Leslie A BruggemanDepartments of Inflammation & Immunity and Nephrology, Cleveland Clinic, and Case Western Reserve University School of Medicine, Cleveland, OH. Electronic address: leslie.bruggeman@case.edu.
Cleveland Clinic · US

Funding

Mechanisms of APOL1-mediated kidney diseaseR01DK108329 · NIDDK · CLEVELAND CLINIC LERNER COM-CWRU · PI BRUGGEMAN, LESLIE A, O'TOOLE, JOHN F. · 2015 to 2019
$2.0M
Kidney disease mechanisms associated with human genetic variationR01DK097836 · NIDDK · CLEVELAND CLINIC LERNER COM-CWRU · PI BRUGGEMAN, LESLIE A, O'TOOLE, JOHN F. · 2014 to 2017
$2.0M
Viral causes of idiopathic chronic kidney diseaseR21AI135434 · NIAID · CLEVELAND CLINIC LERNER COM-CWRU · PI BRUGGEMAN, LESLIE A · 2018 to 2019
$440k
Kidney disease mechanisms associated with human genetic variationR56DK097836 · NIDDK · CASE WESTERN RESERVE UNIVERSITY · PI BRUGGEMAN, LESLIE A, O'TOOLE, JOHN F. · 2012 to 2012
$198k
NIAID NIH HHS R21 AI135434NIDDK NIH HHS R01 DK097836NIDDK NIH HHS R01 DK108329NIDDK NIH HHS R56 DK097836
6 · The paper itself

Abstract

Viral infections in an immunocompetent host can cause both acute and chronic kidney diseases, either by direct damage to the infected kidney cells or as a consequence of systemic immune responses that impact the kidneys' function. Viruses have evolved mechanisms to hijack signaling pathways of the infected cell, including the mammalian target of rapamycin pathway to support viral replication, and to evade antiviral immune responses such as those mediated by miR-155 via microRNA mimetics expressed by the virus. At both the cellular and systemic levels, the host has also evolved mechanisms to counter the viral subversion strategies in the evolutionary battle for mutual survival. In the era of genomic medicine, understanding individual genetic variations that lead to differences in susceptibilities to infection and variabilities in immune responses may open new avenues for treatment, such as the recently described functions of apolipoprotein L1 risk alleles in HIV-associated nephropathy. In addition, state-of-the-art high-throughput sequencing methods have discovered new viruses as the cause for chronic diseases not previously attributed to an infection. The potential application of these methods to idiopathic kidney diseases may reveal similar occult infections by unknown viruses. Precision medicine objectives to optimize host-directed and pathogen-directed therapies for kidney diseases associated with infectious causes will only be achieved through detailed understanding of genetic susceptibility associated with immune responses and viral tropism.

Indexed as

Acute Kidney InjuryAdaptive ImmunityAIDS-Associated NephropathyApolipoprotein L1Autophagic Cell DeathCytokinesGene-Environment InteractionGenetic Predisposition to DiseaseHigh-Throughput Nucleotide SequencingHost Microbial InteractionsHumansImmune Complex DiseasesImmune EvasionImmunity, InnateMetagenomeNephritis, InterstitialApolipoprotein L1CytokinesChronic kidney diseaseGene-environment interactionsInnate immunityNext-generation sequencingViruses

Identifiers

PMID31202388
PMCPMC6578596
OpenAlexW2949314660

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.