Evidence map›Paper›PMID 33340240›Full record

ReviewThe FEBS journal2021

APOL1 risk variants and the development of HIV-associated nephropathy.

Rohan Goyal, Pravin C Singhal

Open access · greenAbstract readReview
In one paragraph

Review in The FEBS journal, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed, 3 pooled it
1.7field-weighted citation impact, top 15% 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

20 citing papers in PubMed, 3 syntheses or guidelines pooled it, 24 citations in OpenAlex.

  1. Pooled it
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  11. Characterization of immortalized human podocytes infected with lentivirus as anAmerican journal of clinical and experimental immunology · 2024
    Article
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  15. A glimpse into the future of systemic lupus erythematosus.Therapeutic advances in musculoskeletal disease · 2022
    Review
  16. The Pathology Lesion Patterns of Podocytopathies: How and why?Frontiers in cell and developmental biology · 2022
    Review
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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.

Rohan GoyalSUNY Downstate Health Sciences University, New York, NY, USA.
Pravin C SinghalInstitute of Molecular Medicine, Feinstein Institute for Medical Research and Zucker School of Medicine at Hofstra-Northwell, Manhasset, NY, USA.ORCID 0000-0002-6898-358X
Feinstein Institute for Medical Research · USSUNY Downstate Health Sciences University · US

Funding

Epigenetic factors and HIV-associated NephropathyR01DK098074 · NIDDK · FEINSTEIN INSTITUTE FOR MEDICAL RESEARCH · PI SINGHAL, PRAVIN C · 2013 to 2016
$2.5M
APOL1 in Diabetic PodocytopathyR01DK118017 · NIDDK · FEINSTEIN INSTITUTE FOR MEDICAL RESEARCH · PI SINGHAL, PRAVIN C · 2018 to 2021
$2.0M
NIDDK NIH HHS R01 DK098074NIDDK NIH HHS R01 DK118017
6 · The paper itself

Abstract

HIV-associated nephropathy (HIVAN) remains a concern among untreated HIV patients, notably of African descent, as patients can reach end-stage renal disease within 3 years. Two variants (G1 and G2) of the APOL1 gene, common in African populations to protect against African sleeping sickness, have been associated with an increased risk of several glomerular disorders including HIVAN, hypertension-attributed chronic kidney disease, and idiopathic focal segmental glomerulosclerosis and are accordingly named renal risk variants (RRVs). This review examines the mechanisms by which APOL1 RRVs drive glomerular injury in the setting of HIV infection and their potential application to patient management. Innate antiviral mechanisms activated by chronic HIV infection, especially those involving type 1 interferons, are of particular interest as they have been shown to upregulate APOL1 expression. Additionally, the downregulation of miRNA 193a (a repressor of APOL1) is also associated with the upregulation of APOL1. Interestingly, glomerular damage affected by APOL1 RRVs is caused by both loss- and gain-of-function changes in the protein, explicitly characterizing these effects. Their intracellular localization offers a further understanding of the nuances of APOL1 variant effects in promoting renal disease. Finally, although APOL1 variants have been recognized as a critical genetic player in mediating kidney disease, there are significant gaps in their application to patient management for screening, diagnosis, and treatment.

Indexed as

AIDS-Associated NephropathyApolipoprotein L1Genetic VariationGlomerulosclerosis, Focal SegmentalHIV InfectionsHumansKidneyMicroRNAsRisk FactorsAPOL1 protein, humanApolipoprotein L1MicroRNAsMIRN193 microRNA, humanApolipoprotein (Apo)L1collapsing FSGSHIVANparietal epithelial cellspodocytes

Identifiers

PMID33340240
PMCPMC8213861
OpenAlexW3116460564

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.