Evidence mapPaperPMID 40403103Full record

ReviewCirculation research2025

Renal-Cardiac Crosstalk in the Pathogenesis and Progression of Heart Failure.

Heidi Noels, Emiel P C van der Vorst, Sébastien Rubin, Amber Emmett, Nikolaus Marx, Maciej Tomaszewski, Joachim Jankowski

Abstract readReview
In one paragraph

Review in Circulation research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.

0numbers the graph read from it
0cells of the map it votes in
36citing 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

36 citing papers in PubMed.

  1. Article
  2. Review
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  5. Cardiac Biomarkers in Chronic Kidney Disease: Signal or Noise?Clinical journal of the American Society of Nephrology : CJASN · 2026
    Review
  6. Article
  7. Review
  8. Review
  9. Review
  10. Article
  11. Article
  12. High-potency statins are associated with reduced osteoporosis but increased fracture risk in CKD patients: a multi-center retrospective study.Osteoporosis international : a journal established as result of cooperation between the European Foundation for Osteoporosis and the National Osteoporosis Foundation of the USA · 2026
    Article
  13. Review
  14. Article
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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

7 authors.

Heidi NoelsInstitute for Molecular Cardiovascular Research (H.N., E.P.C.v.d.V., J.J.), Uniklinik RWTH Aachen, RWTH Aachen University, Germany.ORCID 0000-0003-3053-6984
Emiel P C van der VorstInstitute for Molecular Cardiovascular Research (H.N., E.P.C.v.d.V., J.J.), Uniklinik RWTH Aachen, RWTH Aachen University, Germany.ORCID 0000-0001-5771-6278
Sébastien RubinL'Institut national de la santé et de la recherche médicale (INSERM), BMC, U1034, University of Bordeaux, Pessac, France (S.R.).ORCID 0000-0002-1246-0712
Amber EmmettFaculty of Medicine, Biology and Health, Division of Cardiovascular Sciences, The University of Manchester, United Kingdom (A.E., M.T.).ORCID 0000-0003-3894-3453
Nikolaus MarxDepartment of Internal Medicine I-Cardiology, Angiology and Internal Intensive Care Medicine (N.M.), RWTH Aachen University, Germany.ORCID 0000-0001-6141-634X
Maciej TomaszewskiFaculty of Medicine, Biology and Health, Division of Cardiovascular Sciences, The University of Manchester, United Kingdom (A.E., M.T.).ORCID 0000-0001-8215-6567
Joachim JankowskiInstitute for Molecular Cardiovascular Research (H.N., E.P.C.v.d.V., J.J.), Uniklinik RWTH Aachen, RWTH Aachen University, Germany.ORCID 0000-0002-4528-2967

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Chronic kidney disease (CKD) represents a global health issue with a high socioeconomic impact. Beyond a progressive decline of kidney function, patients with CKD are at increased risk of cardiovascular diseases, including heart failure (HF) and sudden cardiac death. HF in CKD can manifest both as HF with reduced ejection fraction and HF with preserved ejection fraction, with the latter further increasing in relative importance in the more advanced stages of CKD. Typical cardiac remodeling characteristics in uremic cardiomyopathy include left ventricular hypertrophy, myocardial fibrosis, cardiac electrical dysregulation, capillary rarefaction, and microvascular dysfunction, which are triggered by increased cardiac preload, cardiac afterload, and preload and afterload-independent factors. The pathophysiological mechanisms underlying cardiac remodeling in CKD are multifactorial and include neurohormonal activation (with increased activation of the renin-angiotensin-aldosterone system, the sympathetic nervous system, and mineralocorticoid receptor signaling), cardiac steroid activation, mitochondrial dysfunction, inflammation, innate immune activation, and oxidative stress. Furthermore, disturbances in cardiac metabolism and calcium homeostasis, macrovascular and microvascular dysfunction, increased cellular profibrotic responses, the accumulation of uremic retention solutes, and mineral and bone disorders also contribute to cardiovascular disease and HF in CKD. Here, we review the current knowledge of HF in CKD, including the clinical characteristics and pathophysiological mechanisms revealed in animal studies. We also elaborate on the detrimental impact of comorbidities of CKD on HF using hypertension as an example and discuss the clinical characteristics of hypertensive heart disease and the genetic predisposition. Overall, this review aims to increase the understanding of HF in CKD to support future research and clinical translational approaches for improved diagnosis and therapy of this vulnerable patient population.

Indexed as

Heart FailureKidneyRenal Insufficiency, ChronicAnimalsDisease ProgressionHumansRenin-Angiotensin SystemVentricular Remodelingcardiovascular diseasesheart failurehypertensioninflammationmetabolism

Identifiers

PMID40403103
PMCPMC12105978

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.