Evidence map›Paper›PMID 29110758›Full record

ReviewSeminars in nephrology2017

APOL1 Renal Risk Variants: Fertile Soil for HIV-Associated Nephropathy.

Jeffrey B Kopp, Jurgen Heymann, Cheryl A Winkler

Open access · greenAbstract readReview
In one paragraph

Review in Seminars in nephrology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed, 1 pooled it
2.0field-weighted citation impact, top 13% 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

29 citing papers in PubMed, 1 synthesis or guideline pooled it, 39 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Review
  5. Article
  6. Review
  7. Article
  8. Characterization of immortalized human podocytes infected with lentivirus as anAmerican journal of clinical and experimental immunology · 2024
    Article
  9. Article
  10. Review
  11. Review
  12. Review
  13. Article
  14. Review
  15. Article
  16. Review
  17. Review
  18. Childhood HIV-associated nephropathy: 36 years later.Pediatric nephrology (Berlin, Germany) · 2021
    Review
  19. Article
  20. Kidney disease and APOL1.Human molecular genetics · 2021
    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

3 authors at 2 institutions in 1 country.

Jeffrey B KoppKidney Disease Section, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD. Electronic address: jbkopp@nih.gov.
Jurgen HeymannKidney Disease Section, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD.
Cheryl A WinklerBasic Research Laboratory, National Cancer Institute, National Institutes of Health, Leidos Biomedical Research, Frederick National Laboratory for Cancer Research, Frederick, MD.
National Institutes of Health · USLeidos (United States) · US

Funding

Focal Segmental Glomerulosclerosis: Genetics & MechanismsZIADK043308 · NIDDK · NATIONAL INSTITUTE OF DIABETES AND DIGESTIVE AND KIDNEY DISEASES · PI KOPP, JEFFREY BURNETT · 2009 to 2024
$15.7M
Focal segmental glomerulosclerosis: HIV-associated nephropathyZIADK043411 · NIDDK · NATIONAL INSTITUTE OF DIABETES AND DIGESTIVE AND KIDNEY DISEASES · PI HEYMANN, JURGEN · 2009 to 2024
$7.3M
Identification of Genetic Factors Associated with Infectious DiseasesZIABC010297 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI WINKLER, CHERYL · 2009 to 2022
$6.3M
Focal segmental glomerulosclerosis: HIV-associated nephropathyZ01DK043411 · NIDDK · NATIONAL INSTITUTE OF DIABETES AND DIGESTIVE AND KIDNEY DISEASES · PI KOPP, JEFFREY BURNETT · 2008 to 2008
$1.2M
FOCAL SEGMENTAL GLOMERULOSCLEROSIS--PATHOGENESIS AND TREATMENTZ01DK043308 · NIDDK · NATIONAL INSTITUTE OF DIABETES AND DIGESTIVE AND KIDNEY DISEASES · PI KOPP, JEFFREY BURNETT · 1997 to 2008
$1.0M
Intramural NIH HHS Z01 DK043308Intramural NIH HHS Z01 DK043411NCI NIH HHS HHSN261200800001E
6 · The paper itself

Abstract

Apolipoprotein L1 (APOL1) genetic variants are potent risk factors for glomerular disease, but one or more additional factors are required for expression of glomerular disease. Uncontrolled or poorly controlled human immunodeficiency virus (HIV) infection is the most potent susceptibility factor for APOL1 nephropathy that has been identified to date. APOL1 variants are associated with HIV-associated nephropathy (HIVAN), a podocyte disease, but not with HIV-immune complex disease, primarily a disease of the mesangium. The mechanism by which HIV brings out the latent glomerular disease risk remains to be defined. There are at least two classes of candidate mechanisms to explain the potent interaction between HIV-1 and APOL1. First, APOL1 variant proteins and HIV accessory proteins implicated in HIVAN may target the same or related intracellular pathways in podocytes. Recent data suggest roles for interleukin 1b and transcription factor EB. Second, features of uncontrolled HIV infection, including increased circulating factors such as interferon, may drive APOL1 gene transcription or act upon podocytes in other ways. Deeper probing of APOL1-HIV interactions may yield insights that will aid in understanding HIVAN, APOL1 nephropathy, and podocyte biology.

Indexed as

MutationAIDS-Associated NephropathyApolipoprotein L1Glomerulosclerosis, Focal SegmentalHumansHypertensionInterferonsRenal Insufficiency, ChronicRisk FactorsToll-Like Receptor 4APOL1 protein, humanApolipoprotein L1InterferonsTLR4 protein, humanToll-Like Receptor 4Chronic kidney diseaseinterferonNefVpr

Identifiers

PMID29110758
PMCPMC5745063
OpenAlexW2767112132

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.