Evidence mapPaperPMID 41007644Full record

ReviewBiomedicines2025

Aldosterone in Chronic Kidney Disease.

Paula Polenus, Ana Đuran, Sandra Karanović Štambuk

Abstract readReview
In one paragraph

Review in Biomedicines, 2025. 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

3 authors.

Paula PolenusSchool of Medicine, University of Zagreb, 10000 Zagreb, Croatia.ORCID 0009-0003-3515-9476
Ana ĐuranDepartment of Pulmonology, University Hospital Center Split, 21000 Split, Croatia.
Sandra Karanović ŠtambukSchool of Medicine, University of Zagreb, 10000 Zagreb, Croatia.ORCID 0000-0003-2696-5305

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Chronic kidney disease (CKD) is a global health challenge, marked by significant morbidity and mortality and a rising economic burden. Despite established therapies such as renin-angiotensin system (RAS) inhibitors and SGLT2 inhibitors, a substantial residual risk of CKD progression and cardiovascular events persists. This gap is largely attributed to the sustained overactivation of the mineralocorticoid receptors by aldosterone, a key driver of renal inflammation and fibrosis. This review aims to bridge the understanding between aldosterone's intricate pathophysiology and emerging therapeutic strategies designed to address this unmet clinical need. We discuss the physiological regulation of aldosterone synthesis and secretion, the phenomenon of aldosterone breakthrough under conventional RAS blockade and the diverse mechanisms through which aldosterone mediates kidney damage. We evaluate novel non-steroidal mineralocorticoid receptor antagonists, exemplified by finerenone, which demonstrate superior safety profiles and valid efficacy in reducing renal and cardiovascular outcomes in clinical trials. Additionally, we examine aldosterone synthase inhibitors as an upstream therapeutic approach to directly reduce aldosterone production. These novel agents represent promising avenues to mitigate residual risk and improve long-term outcomes for patients with CKD.

Indexed as

aldosteronealdosterone synthase inhibitorschronic kidney diseasemineralocorticoid receptorsnon-steroidal mineralocorticoid receptor antagonists

Identifiers

PMID41007644
PMCPMC12467697

What Socratic holds

Textmetadata
LicenceCC BY
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 Socratic graph.