Evidence map›Paper›PMID 38873847›Full record

ArticleClinical cardiology2024

Predictors of developing renal dysfunction following diagnosis of transthyretin cardiac amyloidosis.

Malcolm L McDonald, Yosef Manla, Alice Sonnino, Mileydis Alonso, Radhika K Neicheril, Alejandro Sanchez, Gabrielle Lafave, Yelenis Seijo De Armas, Antonio Lewis Camargo, Dipan Uppal and 7 more

Abstract read
In one paragraph

Article in Clinical cardiology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed, 2 pooled it
–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

7 citing papers in PubMed, 2 syntheses or guidelines pooled it.

  1. Pooled it
  2. Pooled it
  3. Review
  4. Article
  5. Article
  6. Article
  7. 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

17 authors.

Malcolm L McDonaldDepartment of Cardiovascular Disease, Heart, Vascular, and Thoracic Institute, Cleveland Clinic Florida, Weston, Florida, USA.ORCID http://orcid.org/0009-0000-6267-8114
Yosef ManlaDepartment of Cardiology, Heart, Vascular, and Thoracic Institute, Cleveland Clinic Abu Dhabi, Abu Dhabi, United Arab Emirates.
Alice SonninoDepartment of Cardiovascular Disease, Heart, Vascular, and Thoracic Institute, Cleveland Clinic Florida, Weston, Florida, USA.
Mileydis AlonsoDepartment of Cardiovascular Disease, Heart, Vascular, and Thoracic Institute, Cleveland Clinic Florida, Weston, Florida, USA.
Radhika K NeicherilDepartment of Medicine, Internal Medicine, Cleveland Clinic Florida, Weston, Florida, USA.
Alejandro SanchezDepartment of Cardiovascular Disease, Heart, Vascular, and Thoracic Institute, Cleveland Clinic Florida, Weston, Florida, USA.
Gabrielle LafaveDepartment of Cardiology, Heart, Vascular, and Thoracic Institute, Cleveland Clinic Abu Dhabi, Abu Dhabi, United Arab Emirates.
Yelenis Seijo De ArmasDepartment of Cardiovascular Disease, Heart, Vascular, and Thoracic Institute, Cleveland Clinic Florida, Weston, Florida, USA.
Antonio Lewis CamargoDepartment of Cardiovascular Disease, Heart, Vascular, and Thoracic Institute, Cleveland Clinic Florida, Weston, Florida, USA.
Dipan UppalDepartment of Cardiovascular Disease, Heart, Vascular, and Thoracic Institute, Cleveland Clinic Florida, Weston, Florida, USA.ORCID http://orcid.org/0000-0003-4187-2422
Armaan HandaDepartment of Cardiovascular Disease, Heart, Vascular, and Thoracic Institute, Cleveland Clinic Florida, Weston, Florida, USA.
David WolinskyDepartment of Cardiovascular Disease, Heart, Vascular, and Thoracic Institute, Cleveland Clinic Florida, Weston, Florida, USA.
Nina Thakkar RiveraDepartment of Cardiovascular Disease, Heart, Vascular, and Thoracic Institute, Cleveland Clinic Florida, Weston, Florida, USA.
Mauricio VelezDepartment of Cardiovascular Disease, Heart, Vascular, and Thoracic Institute, Cleveland Clinic Florida, Weston, Florida, USA.
David A BaranDepartment of Cardiovascular Disease, Heart, Vascular, and Thoracic Institute, Cleveland Clinic Florida, Weston, Florida, USA.
Jerry D EstepDepartment of Cardiovascular Disease, Heart, Vascular, and Thoracic Institute, Cleveland Clinic Florida, Weston, Florida, USA.
David SnipeliskyDepartment of Cardiovascular Disease, Heart, Vascular, and Thoracic Institute, Cleveland Clinic Florida, Weston, Florida, USA.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundIn patients with transthyretin cardiac amyloidosis (ATTR-CA), renal dysfunction is a poor prognostic indicator. Limited data are available on variables that portend worsening renal function (wRF) among ATTR-CA patients.

objectivesThis study assesses which characteristics place patients at higher risk for the development of wRF (defined as a drop of ≥10% in glomerular filtration rate [GFR]) within the first year following diagnosis of ATTR-CA.

methodsWe included patients with ATTR-CA (n = 134) evaluated between 2/2016 and 12/2022 and followed for up to 1 year at our amyloid clinic. Patients were stratified into two groups: a group with maintained renal function (mRF) and a group with wRF and compared using appropriate testing. Significant variables in the univariate analysis were included in the multivariable logistic regression model to determine characteristics associated with wRF.

resultsWithin a follow-up period of 326 ± 118 days, the median GFR% change measured -6% [-18%, +8]. About 41.8% (n = 56) had wRF, while the remainder had mRF. In addition, in patients with no prior history of chronic kidney disease (CKD), 25.5% developed de novo CKD. On multivariable logistic regression, only New York Heart Association (NYHA) class ≥III (odds ratio [OR]: 3.9, 95% confidence interval [CI]: [1.6-9.3]), history of ischemic heart disease (IHD) (OR: 0.3, 95% CI: [0.1-0.7]), and not receiving SGLT-2i (OR: 0.1, 95% CI: [0.02-0.5]) were significant predictors of wRF.

conclusionOur study demonstrated that the development of de novo renal dysfunction or wRF is common following the diagnosis of ATTR-CA. Additionally, we identified worse NYHA class and no prior history of IHD as significant predictors associated with developing wRF, while receiving SGLT-2i therapy appeared to be protective in this population.

Indexed as

Amyloid Neuropathies, FamilialRenal Insufficiency, ChronicAgedDisease ProgressionFemaleFollow-Up StudiesGlomerular Filtration RateHumansKidneyMaleMiddle AgedPrognosisRetrospective StudiesRisk AssessmentRisk FactorsTime FactorsATTRcardiac amyloidosisrenal outcomesSGLT‐2 inhibitor

Identifiers

PMID38873847
PMCPMC11176897

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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.