Evidence map›Paper›PMID 26351984›Full record

ArticleArquivos brasileiros de cardiologia2015

Human Tissue Kallikrein Activity in Angiographically Documented Chronic Stable Coronary Artery Disease.

Estêvão Lanna Figueiredo, Carolina Antunes Magalhães, Karlyse Claudino Belli, Ari Mandil, José Carlos Faria Garcia, Rosanã Aparecida Araújo, Amintas Fabiano de Souza Figueiredo, Lucia Campos Pellanda

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In one paragraph

Article in Arquivos brasileiros de cardiologia, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact, top 97% 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

1 citing paper in PubMed, 2 citations in OpenAlex.

  1. 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

8 authors at 4 institutions in 2 countries.

Estêvão Lanna FigueiredoDepartamento de Cardiologia, Hospital Lifecenter, Belo Horizonte, MG, Brazil.
Carolina Antunes MagalhãesDepartamento de Análises Clínicas e Toxicológicas, Faculdade de Farmácia, Universidade Federal de Minas Gerais, Belo Horizonte, MG, Brazil.
Karlyse Claudino BelliDivisão de Cardiologia, Laboratório de Pesquisa de Patofisiologia do Exercício, Hospital de Clínicas de Porto Alegre, Porto Alegre, RS, Brazil.
Ari MandilDepartamento de Hemodinâmica, Hospital Lifecenter, Belo Horizonte, MG, Brazil.
José Carlos Faria GarciaDepartamento de Hemodinâmica, Hospital Lifecenter, Belo Horizonte, MG, Brazil.
Rosanã Aparecida AraújoDepartamento de Hemodinâmica, Hospital Lifecenter, Belo Horizonte, MG, Brazil.
Amintas Fabiano de Souza FigueiredoDepartamento de Análises Clínicas e Toxicológicas, Faculdade de Farmácia, Universidade Federal de Minas Gerais, Belo Horizonte, MG, Brazil.
Lucia Campos PellandaPrograma de Pós-Graduação em Cardiologia, Fundação Universitária de Cardiologia, Porto Alegre, RS, Brazil.
Lifecenter Hospital · BRUniversidade Federal de Minas Gerais · BRDuke University · USUniversidade Federal de Ciências da Saúde de Porto Alegre · BR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundHuman tissue kallikrein (hK1) is a key enzyme in the kallikrein-kinin system (KKS). hK1-specific amidase activity is reduced in urine samples from hypertensive and heart failure (HF) patients. The pathophysiologic role of hK1 in coronary artery disease (CAD) remains unclear.

objectiveTo evaluate hK1-specific amidase activity in the urine of CAD patientsMethods:Sixty-five individuals (18-75 years) who underwent cardiac catheterism (CATH) were included. Random midstream urine samples were collected immediately before CATH. Patients were classified in two groups according to the presence of coronary lesions: CAD (43 patients) and non-CAD (22 patients). hK1 amidase activity was estimated using the chromogenic substrate D-Val-Leu-Arg-Nan. Creatinine was determined using Jaffé's method. Urinary hK1-specific amidase activity was expressed as µM/(min · mg creatinine) to correct for differences in urine flow rates.

resultsUrinary hK1-specific amidase activity levels were similar between CAD [0.146 µM/(min ·mg creatinine)] and non-CAD [0.189 µM/(min . mg creatinine)] patients (p = 0.803) and remained similar to values previously reported for hypertensive patients [0.210 µM/(min . mg creatinine)] and HF patients [0.104 µM/(min . mg creatinine)]. CAD severity and hypertension were not observed to significantly affect urinary hK1-specific amidase activity.

conclusionCAD patients had low levels of urinary hK1-specific amidase activity, suggesting that renal KKS activity may be reduced in patients with this disease.

Indexed as

AdolescentAdultAgedAmidohydrolasesBiomarkersCoronary Artery DiseaseCreatinineCross-Sectional StudiesFemaleHeart FailureHumansHypertensionKallikrein-Kinin SystemMaleMiddle AgedReference ValuesAmidohydrolasesBiomarkersCreatinineTissue Kallikreins

Identifiers

PMID26351984
PMCPMC4651403
OpenAlexW1667238395

What OpenQuestion holds

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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.