Evidence map›Paper›PMID 39390382›Full record

ArticleBMC nephrology2024

Role of aldosterone in various target organ damage in patients with hypertensive emergency: a cross-sectional study.

Akihiro Miyake, Keita Endo, Koichi Hayashi, Taro Hirai, Yuki Hara, Keisuke Takano, Takehiro Horikawa, Kaede Yoshino, Masahiro Sakai, Koichi Kitamura and 4 more

Abstract read
In one paragraph

Article in BMC nephrology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing 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

2 citing papers in PubMed.

  1. Review
  2. Article
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

14 authors.

Akihiro Miyake *Department of Nephrology, Endocrinology and Diabetes, Tokyo Bay Urayasu Ichikawa Medical Center, 3-4-32 Todaijima, Urayasu, Chiba, 279-0001, Japan.
Keita Endo *Department of Nephrology, Endocrinology and Diabetes, Tokyo Bay Urayasu Ichikawa Medical Center, 3-4-32 Todaijima, Urayasu, Chiba, 279-0001, Japan.
Koichi HayashiDepartment of Nephrology, Endocrinology and Diabetes, Tokyo Bay Urayasu Ichikawa Medical Center, 3-4-32 Todaijima, Urayasu, Chiba, 279-0001, Japan.
Taro HiraiDepartment of Nephrology, Endocrinology and Diabetes, Tokyo Bay Urayasu Ichikawa Medical Center, 3-4-32 Todaijima, Urayasu, Chiba, 279-0001, Japan.
Yuki HaraDepartment of Nephrology, Endocrinology and Diabetes, Tokyo Bay Urayasu Ichikawa Medical Center, 3-4-32 Todaijima, Urayasu, Chiba, 279-0001, Japan.
Keisuke TakanoDepartment of Nephrology, Endocrinology and Diabetes, Tokyo Bay Urayasu Ichikawa Medical Center, 3-4-32 Todaijima, Urayasu, Chiba, 279-0001, Japan.
Takehiro HorikawaDepartment of Emergency and Critical Care Medicine, St Marianna University School of Medicine, Kawasaki, Kanagawa, 216-8511, Japan.
Kaede YoshinoDepartment of Nephrology, Endocrinology and Diabetes, Tokyo Bay Urayasu Ichikawa Medical Center, 3-4-32 Todaijima, Urayasu, Chiba, 279-0001, Japan.
Masahiro SakaiDepartment of Nephrology, Endocrinology and Diabetes, Tokyo Bay Urayasu Ichikawa Medical Center, 3-4-32 Todaijima, Urayasu, Chiba, 279-0001, Japan.
Koichi KitamuraDepartment of Nephrology, Endocrinology and Diabetes, Tokyo Bay Urayasu Ichikawa Medical Center, 3-4-32 Todaijima, Urayasu, Chiba, 279-0001, Japan.
Shinsuke ItoDepartment of Nephrology, Endocrinology and Diabetes, Tokyo Bay Urayasu Ichikawa Medical Center, 3-4-32 Todaijima, Urayasu, Chiba, 279-0001, Japan.
Naohiko ImaiDivision of Nephrology and Hypertension, Department of Internal Medicine, St Marianna University School of Medicine, Kawasaki, Kanagawa, 216-8511, Japan.
Shigeki FujitaniDepartment of Emergency and Critical Care Medicine, St Marianna University School of Medicine, Kawasaki, Kanagawa, 216-8511, Japan.
Toshihiko SuzukiDepartment of Nephrology, Endocrinology and Diabetes, Tokyo Bay Urayasu Ichikawa Medical Center, 3-4-32 Todaijima, Urayasu, Chiba, 279-0001, Japan. toshi-s@xj9.so-net.ne.jp.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundHypertensive emergency is a critical disease that causes multiple organ injuries. Although the renin-angiotensin-aldosterone system (RAS) is enormously activated in this disorder, whether the RAS contributes to the development of the organ damage has not been fully elucidated. This cross-sectional study was conducted to characterize the association between RAS and the organ damage in patients with hypertensive emergencies.

methodsWe enrolled 63 patients who visited our medical center with acute severe hypertension and multiple organ damage between 2012 and 2020. Hypertensive target organ damage was evaluated on admission, including severe kidney impairment (eGFR less than 30 mL/min/1.73 m

resultsAmong 63 patients, 31, 37, 43 and 8 cases manifested SKI, severe retinopathy, c-LVH and ischemic stroke, respectively. All populations with the organ injuries except cerebral infarction had higher plasma aldosterone concentrations than the remaining subset but exhibited a variable difference in systolic or diastolic blood pressure. Twenty-two patients had a triad of SKI, severe retinopathy and c-LVH, among whom 5 patients manifested TMA. Furthermore, the number of the damaged organs was correlated with plasma aldosterone levels (Spearman's coefficient = 0.50), with a strong association observed between plasma aldosterone (≥ 250 pg/mL) and 3 or more complications (odds ratio = 9.16 [95%CI: 2.76-30.35]).

conclusionIn patients with hypertensive emergencies, a higher aldosterone level not only contributed to the development of the organ damage but also was associated with the number of damaged organs in each patient.

Indexed as

AldosteroneHypertensionAgedCross-Sectional StudiesEmergenciesFemaleHeart FailureHumansHypertensive CrisisHypertensive RetinopathyHypertrophy, Left VentricularIschemic StrokeMaleMiddle AgedMultiple Organ FailureRenal InsufficiencyAldosteroneAldosteroneCardiac hypertrophyeGFRHypertensive emergencyKidneyRetinopathyThrombotic microangiopathy

Identifiers

PMID39390382
PMCPMC11468402

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LicenceCC BY-NC-ND
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Registered trials

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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.