Evidence map›Paper›PMID 39577983›Full record

ArticleKidney international2024

Has APOL1 kidney disease treatment been hiding in plain sight?

Opeyemi A Olabisi

Abstract readComment
PubMed Publisher
In one paragraph

Article in Kidney international, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact
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

0 citing papers in PubMed.

No citing paper in PubMed yet.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

1 author.

Opeyemi A OlabisiDepartment of Medicine, Division of Nephrology and Duke Molecular Physiology Institute, Duke University School of Medicine, Durham, North Carolina, USA. Electronic address: Opeyemi.olabisi@duke.edu.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Two coding variants of APOL1 account for much of the excess risk of focal segmental glomerulosclerosis in people of recent West African ancestry. There is an unmet need of treatment for apolipoprotein L1 kidney disease. In this issue, Sula Karreci et al. reported that lisinopril reduced proteinuria and glomerulosclerosis in a mouse model of apolipoprotein L1-induced focal segmental glomerulosclerosis, in a genotype-specific manner. By contrast, hydralazine and dapagliflozin had no effect. This study highlights the potential therapeutic utility of angiotensin-converting enzyme inhibitor in apolipoprotein L1 kidney disease.

Indexed as

Angiotensin-Converting Enzyme InhibitorsApolipoprotein L1Glomerulosclerosis, Focal SegmentalAnimalsApolipoproteinsDisease Models, AnimalHumansLipoproteins, HDLLisinoprilMiceProteinuriaAngiotensin-Converting Enzyme InhibitorsAPOL1 protein, humanApolipoprotein L1ApolipoproteinsLipoproteins, HDLLisinopril

Identifiers

PMID39577983

What OpenQuestion holds

Textmetadata
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.