Evidence map›Paper›PMID 31082862›Full record

ReviewCurrent opinion in nephrology and hypertension2019

Ten years in: APOL1 reaches beyond the kidney.

Joshua S Waitzman, Jennie Lin

Open access · greenAbstract readReview
In one paragraph

Review in Current opinion in nephrology and hypertension, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
0.1field-weighted citation impact, top 50% 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

1 citing paper in PubMed, 1 citations in OpenAlex.

  1. 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.

Joshua S WaitzmanDivision of Nephrology and Hypertension.
Jennie LinDivision of Nephrology and Hypertension.
Hypertension Institute · USRenal Research Institute · US

Funding

Modulation of Macrophage Function through Alternative Splicing in Cardiometabolic DiseasesK08HL135348 · NHLBI · UNIVERSITY OF PENNSYLVANIA · PI LIN, JENNIE J · 2017 to 2020
$657k
NHLBI NIH HHS K08 HL135348
6 · The paper itself

Abstract

purpose of reviewAPOL1 nephropathy risk variants drive most of the excess risk of chronic kidney disease (CKD) seen in African Americans, but whether the same risk variants account for excess cardiovascular risk remains unclear. This mini-review highlights the controversies in the APOL1 cardiovascular field. RECENT

findingsIn the past 10 years, our understanding of how APOL1 risk variants contribute to renal cytotoxicity has increased. Some of the proposed mechanisms for kidney disease are biologically plausible for cells and tissues relevant to cardiovascular disease (CVD), but cardiovascular studies published since 2014 have reported conflicting results regarding APOL1 risk variant association with cardiovascular outcomes. In the past year, several studies have also contributed conflicting results from different types of study populations. SUMMARY: Heterogeneity in study population and study design has led to differing reports on the role of APOL1 nephropathy risk variants in CVD. Without consistently validated associations between these risk variants and CVD, mechanistic studies for APOL1's role in cardiovascular biology lag behind.

Indexed as

Apolipoprotein L1Cardiovascular DiseasesGenotypeHumansRenal Insufficiency, ChronicAPOL1 protein, humanApolipoprotein L1

Identifiers

PMID31082862
PMCPMC7340511
OpenAlexW2945111020

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.