Evidence map›Paper›PMID 29930940›Full record

ReviewFrontiers in medicine2018

Molecular Mechanisms of Injury in HIV-Associated Nephropathy.

Samuel J Rednor, Michael J Ross

Open access · goldAbstract readReview
In one paragraph

Review in Frontiers in medicine, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
1.7field-weighted citation impact, top 17% 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

31 citing papers in PubMed, 50 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
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  7. Review
  8. Article
  9. Article
  10. An Update on Viral Infection-Associated Collapsing Glomerulopathy.Advances in kidney disease and health · 2024
    Review
  11. Article
  12. Article
  13. Article
  14. Review
  15. Review
  16. Article
  17. Article
  18. Review
  19. Renal Considerations in COVID-19: Biology, Pathology, and Pathophysiology.ASAIO journal (American Society for Artificial Internal Organs : 1992) · 2021
    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

2 authors at 2 institutions in 1 country.

Samuel J RednorDivision of Nephrology, Albert Einstein College of Medicine/Montefiore Medical Center, Bronx, NY, United States.
Michael J RossDivision of Nephrology, Albert Einstein College of Medicine/Montefiore Medical Center, Bronx, NY, United States.
Albert Einstein College of Medicine · USMontefiore Medical Center · US

Funding

Novel mechanisms of antiretroviral protection against HIV-related kidney diseasesR01DK101338 · NIDDK · ICAHN SCHOOL OF MEDICINE AT MOUNT SINAI · PI ROSS, MICHAEL J · 2014 to 2018
$1.9M
The role of APOL1 polymorphisms in promoting HIV-related kidney injuryR01DK108346 · NIDDK · ICAHN SCHOOL OF MEDICINE AT MOUNT SINAI · PI ROSS, MICHAEL J · 2015 to 2019
$1.6M
NIDDK NIH HHS R01 DK101338NIDDK NIH HHS R01 DK108346
6 · The paper itself

Abstract

HIV-associated nephropathy (HIVAN) is an important cause of secondary focal glomerulosclerosis that occurs primarily in persons of African ancestry with advanced HIV disease. Although HIVAN is characterized by severe proteinuria and rapid progression to end stage renal disease without treatment, the phenotype is markedly attenuated by treatment with antiretroviral medications. HIV infection of glomerular and tubular epithelial cells and subsequent viral gene expression is a key contributor to HIVAN pathogenesis and the kidney can serve as reservoir for HIV strains that differ those in blood. HIV gene expression in renal epithelial cells leads to dysregulation of cellular pathways including cell cycle, inflammation, cell death, and cytoskeletal homeostasis. Polymorphisms in the APOL1 gene explain the marked predilection of HIVAN to occur in persons of African descent and HIVAN. Since HIVAN has the strongest association with APOL1 genotype of any of the APOL1-associated nephropathies, studies to determine the mechanisms by which HIV and APOL1 risk variants together promote kidney injury hold great promise to improve our understanding of the pathogenesis of APOL1-mediated kidney diseases.

Indexed as

AIDSAPOL1chronic kidney diseaseHIVHIV-associated nephropathypodocyteproteinuriarenal tubular epithelial cell

Identifiers

PMID29930940
PMCPMC5999756
OpenAlexW2805353634

What OpenQuestion holds

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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.