Evidence map›Paper›PMID 30590482›Full record

ReviewEndocrine reviews2019

Genetics of Human Primary Hypertension: Focus on Hormonal Mechanisms.

Worapaka Manosroi, Gordon H Williams

Open access · bronzeAbstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Endocrine reviews, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 64 papers, 4 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
64citing papers in PubMed, 4 pooled it
3.9field-weighted citation impact, top 5% 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

64 citing papers in PubMed, 4 syntheses or guidelines pooled it, 148 citations in OpenAlex.

  1. Pooled it
  2. Efficacy and Safety of Radiofrequency-Based Renal Denervation on Resistant Hypertensive Patients: A Systematic Review and Meta-analysis.High blood pressure & cardiovascular prevention : the official journal of the Italian Society of Hypertension · 2024
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4 more citing papers are in PubMed but not listed here.

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 1 institution in 2 countries.

Worapaka ManosroiDivision of Endocrinology, Diabetes, and Hypertension, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts.
Gordon H WilliamsDivision of Endocrinology, Diabetes, and Hypertension, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts.
Brigham and Women's Hospital · US

Funding

Salt Sensitive Hypertension and StriatinR01HL144779 · NHLBI · BRIGHAM AND WOMEN'S HOSPITAL · PI WILLIAMS, GORDON H · 2019 to 2022
$3.3M
Striatin, Aldosterone and HypertensionR56HL114765 · NHLBI · BRIGHAM AND WOMEN'S HOSPITAL · PI WILLIAMS, GORDON H · 2018 to 2018
$838k
NHLBI NIH HHS R01 HL144779NHLBI NIH HHS R56 HL114765
6 · The paper itself

Abstract

Increasingly, primary hypertension is being considered a syndrome and not a disease, with the individual causes (diseases) having a common sign-an elevated blood pressure. To determine these causes, genetic tools are increasingly employed. This review identified 62 proposed genes. However, only 21 of them met our inclusion criteria: (i) primary hypertension, (ii) two or more supporting cohorts from different publications or within a single publication or one supporting cohort with a confirmatory genetically modified animal study, and (iii) 600 or more subjects in the primary cohort; when including our exclusion criteria: (i) meta-analyses or reviews, (ii) secondary and monogenic hypertension, (iii) only hypertensive complications, (iv) genes related to blood pressure but not hypertension per se, (v) nonsupporting studies more common than supporting ones, and (vi) studies that did not perform a Bonferroni or similar multiassessment correction. These 21 genes were organized in a four-tiered structure: distant phenotype (hypertension); intermediate phenotype [salt-sensitive (18) or salt-resistant (0)]; subintermediate phenotypes under salt-sensitive hypertension [normal renin (4), low renin (8), and unclassified renin (6)]; and proximate phenotypes (specific genetically driven hypertensive subgroup). Many proximate hypertensive phenotypes had a substantial endocrine component. In conclusion, primary hypertension is a syndrome; many proposed genes are likely to be false positives; and deep phenotyping will be required to determine the utility of genetics in the treatment of hypertension. However, to date, the positive genes are associated with nearly 50% of primary hypertensives, suggesting that in the near term precise, mechanistically driven treatment and prevention strategies for the specific primary hypertension subgroups are feasible.

Indexed as

Endocrine SystemGenetic Predisposition to DiseaseAnimalsFemaleHumansHypertensionMalePolymorphism, Single Nucleotide

Identifiers

PMID30590482
PMCPMC6936319
OpenAlexW2905827573

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.