Evidence map›Paper›PMID 31551803›Full record

ReviewFrontiers in physiology2019

Chronic Kidney Disease as a Risk Factor for Heart Failure With Preserved Ejection Fraction: A Focus on Microcirculatory Factors and Therapeutic Targets.

Jens van de Wouw, Michelle Broekhuizen, Oana Sorop, Jaap A Joles, Marianne C Verhaar, Dirk J Duncker, A H Jan Danser, Daphne Merkus

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

Review in Frontiers in physiology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 56 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
56citing papers in PubMed, 2 pooled it
6.1field-weighted citation impact, top 3% 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

56 citing papers in PubMed, 2 syntheses or guidelines pooled it, 84 citations in OpenAlex.

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  13. Sexual dimorphism in animal models of heart failure with preserved ejection fraction.Journal of applied physiology (Bethesda, Md. : 1985) · 2025
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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

8 authors at 2 institutions in 1 country.

Jens van de WouwDivision of Experimental Cardiology, Department of Cardiology, Erasmus MC University Medical Center, Rotterdam, Netherlands.
Michelle BroekhuizenDivision of Experimental Cardiology, Department of Cardiology, Erasmus MC University Medical Center, Rotterdam, Netherlands.
Oana SoropDivision of Experimental Cardiology, Department of Cardiology, Erasmus MC University Medical Center, Rotterdam, Netherlands.
Jaap A JolesDepartment of Nephrology and Hypertension, University Medical Center Utrecht, Utrecht, Netherlands.
Marianne C VerhaarDepartment of Nephrology and Hypertension, University Medical Center Utrecht, Utrecht, Netherlands.
Dirk J DunckerDivision of Experimental Cardiology, Department of Cardiology, Erasmus MC University Medical Center, Rotterdam, Netherlands.
A H Jan DanserDepartment of Internal Medicine, Erasmus MC University Medical Center, Rotterdam, Netherlands.
Daphne MerkusDivision of Experimental Cardiology, Department of Cardiology, Erasmus MC University Medical Center, Rotterdam, Netherlands.
Erasmus MC · NLUniversity Medical Center Utrecht · NL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Heart failure (HF) and chronic kidney disease (CKD) co-exist, and it is estimated that about 50% of HF patients suffer from CKD. Although studies have been performed on the association between CKD and HF with reduced ejection fraction (HFrEF), less is known about the link between CKD and heart failure with preserved ejection fraction (HFpEF). Approximately, 50% of all patients with HF suffer from HFpEF, and this percentage is projected to rise in the coming years. Therapies for HFrEF are long established and considered quite successful. In contrast, clinical trials for treatment of HFpEF have all shown negative or disputable results. This is likely due to the multifactorial character and the lack of pathophysiological knowledge of HFpEF. The typical co-existence of HFpEF and CKD is partially due to common underlying comorbidities, such as hypertension, dyslipidemia and diabetes. Macrovascular changes accompanying CKD, such as hypertension and arterial stiffening, have been described to contribute to HFpEF development. Furthermore, several renal factors have a direct impact on the heart and/or coronary microvasculature and may underlie the association between CKD and HFpEF. These factors include: (1) activation of the renin-angiotensin-aldosterone system, (2) anemia, (3) hypercalcemia, hyperphosphatemia and increased levels of FGF-23, and (4) uremic toxins. This review critically discusses the above factors, focusing on their potential contribution to coronary dysfunction, left ventricular stiffening, and delayed left ventricular relaxation. We further summarize the directions of novel treatment options for HFpEF based on the contribution of these renal drivers.

Indexed as

chronic kidney diseaseheart failureHFpEFmicrocirculationtherapyvasculature

Identifiers

PMID31551803
PMCPMC6737277
OpenAlexW2967226493

What OpenQuestion 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 OpenQuestion graph.