Evidence map›Paper›PMID 25512164›Full record

ReviewClinica chimica acta; international journal of clinical chemistry2015

Urinary C-type natriuretic peptide: an emerging biomarker for heart failure and renal remodeling.

Rosita Zakeri, John C Burnett, S Jeson Sangaralingham

Abstract readReview
In one paragraph

Review in Clinica chimica acta; international journal of clinical chemistry, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing 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

10 citing papers in PubMed.

  1. Article
  2. Article
  3. Review
  4. CRRL269.Circulation research · 2019
    Article
  5. Article
  6. Article
  7. Article
  8. Review
  9. Review
  10. 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.

Rosita ZakeriCardiorenal Research Laboratory, Division of Cardiovascular Diseases, Mayo Clinic, Rochester, MN 55905, USA. Electronic address: rosita.zakeri@doctors.org.uk.
John C BurnettCardiorenal Research Laboratory, Division of Cardiovascular Diseases, Mayo Clinic, Rochester, MN 55905, USA.
S Jeson SangaralinghamCardiorenal Research Laboratory, Division of Cardiovascular Diseases, Mayo Clinic, Rochester, MN 55905, USA. Electronic address: sangaralingham.jeson@mayo.edu.

Funding

Recruitment and Phenotyping CoreP01HL076611 · NHLBI · MAYO CLINIC ROCHESTER · PI BURNETT, JOHN C · 2005 to 2015
$19.6M
INTRARENAL REGULATION OF SODIUM EXCRETIONR01HL036634 · NHLBI · MAYO CLINIC ROCHESTER · PI BURNETT, JOHN C · 1987 to 2019
$6.5M
Cardiovascular Peptides and Myocardial InfarctionR01HL083231 · NHLBI · MAYO CLINIC ROCHESTER · PI BURNETT, JOHN C, CHEN, HORNG H · 2006 to 2016
$4.6M
Mayo Clinic Center for Translational Science ActivitiesTL1RR024152 · NCRR · MAYO CLINIC ROCHESTER · PI RIZZA, ROBERT A. · 2006 to 2011
$2.5M
Mayo Clinic Center for Translational Science ActivitiesTL1TR000137 · NCATS · MAYO CLINIC ROCHESTER · PI KHOSLA, SUNDEEP · 2012 to 2015
$2.1M
PURCHASE OF A HIGH FIELD NMR SPECTROMETERS10RR002415 · NCRR · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI SHAFER, JULES ALAN · 1985 to 1985
–
NCATS NIH HHS TL1 TR000137NCRR NIH HHS TL1RR02415NCRR NIH HHS TL1 RR024152NHLBI NIH HHS P01 HL076611NHLBI NIH HHS R01 HL036634NHLBI NIH HHS R01 HL083231
6 · The paper itself

Abstract

The public health and economic burden of heart failure (HF) is staggering and the need for relevant pathophysiologic and clinical biomarkers to advance the field and improve HF therapy remains high. Renal dysfunction is common among HF patients and is associated with increased HF hospitalization and mortality. It is widely recognized that mechanisms contributing to HF pathogenesis include a complex bidirectional interaction between the kidney and heart, encompassed by the term cardiorenal syndrome (CRS). Among a new wave of urinary biomarkers germane to CRS, C-type natriuretic peptide (CNP) has emerged as an innovative biomarker of renal structural and functional impairment in HF and chronic renal disease states. CNP is a hormone, synthesized in the kidney, and is an important regulator of cell proliferation and organ fibrosis. Hypoxia, cytokines and fibrotic growth factors, which are inherent to both cardiac and renal remodeling processes, are among the recognized stimuli for CNP production and release. In this review we aim to highlight current knowledge regarding the biology and pathophysiological correlates of urinary CNP, and its potential clinical utility as a diagnostic and prognostic biomarker in HF and renal disease states.

Indexed as

BiomarkersHeart FailureHumansKidney DiseasesNatriuretic Peptide, C-TypeBiomarkersNatriuretic Peptide, C-TypeBiomarkerCardiorenal syndromeC-type natriuretic peptideHeart failureRenal remodeling

Identifiers

PMID25512164
PMCPMC4409864

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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.