Evidence map›Paper›PMID 34043882›Full record

ArticleJournal of diabetes investigation2021

Plasma heparin cofactor II activity is inversely associated with albuminuria and its annual deterioration in patients with diabetes.

Tomoyo Hara, Ryoko Uemoto, Akiko Sekine, Yukari Mitsui, Shiho Masuda, Kiyoe Kurahashi, Sumiko Yoshida, Toshiki Otoda, Tomoyuki Yuasa, Akio Kuroda and 10 more

Open access · goldAbstract read
In one paragraph

Article in Journal of diabetes investigation, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
0.6field-weighted citation impact, top 33% 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

6 citing papers in PubMed, 6 citations in OpenAlex.

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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

20 authors at 3 institutions in 1 country.

Tomoyo HaraDepartment of Hematology, Endocrinology and Metabolism, Tokushima University Graduate School of Biomedical Sciences, Tokushima, Japan.
Ryoko UemotoDepartment of Community Medicine and Medical Science, Tokushima University Graduate School of Biomedical Sciences, Tokushima, Japan.
Akiko SekineDepartment of Community Medicine and Medical Science, Tokushima University Graduate School of Biomedical Sciences, Tokushima, Japan.
Yukari MitsuiDepartment of Hematology, Endocrinology and Metabolism, Tokushima University Graduate School of Biomedical Sciences, Tokushima, Japan.
Shiho MasudaDepartment of Hematology, Endocrinology and Metabolism, Tokushima University Graduate School of Biomedical Sciences, Tokushima, Japan.
Kiyoe KurahashiDepartment of Hematology, Endocrinology and Metabolism, Tokushima University Graduate School of Biomedical Sciences, Tokushima, Japan.
Sumiko YoshidaDepartment of Hematology, Endocrinology and Metabolism, Tokushima University Graduate School of Biomedical Sciences, Tokushima, Japan.
Toshiki OtodaDepartment of Community Medicine and Medical Science, Tokushima University Graduate School of Biomedical Sciences, Tokushima, Japan.
Tomoyuki YuasaDepartment of Community Medicine and Medical Science, Tokushima University Graduate School of Biomedical Sciences, Tokushima, Japan.
Akio KurodaDiabetes Therapeutics and Research Center, Institute of Advanced Medical Sciences, Tokushima University, Tokushima, Japan.ORCID https://orcid.org/0000-0003-2147-6844
Yasumasa IkedaDepartment of Pharmacology, Tokushima University Graduate School of Biomedical Sciences, Tokushima, Japan.
Itsuro EndoDepartment of Bioregulatory Sciences, Tokushima University Graduate School of Biomedical Sciences, Tokushima, Japan.
Soichi HondaMinami Municipal National Insurance Hospital, Minami-cho, Japan.
Katsuhiko YoshimotoDepartment of Medical Pharmacology, Tokushima University Graduate School of Biomedical Sciences, Tokushima, Japan.
Akira KondoKondo Naika Hospital, Tokushima, Japan.
Toshiaki TamakiAnan Medical Center, Anan, Japan.
Toshio MatsumotoFujii Memorial Institute of Medical Sciences, Tokushima University, Tokushima, Japan.
Munehide MatsuhisaDiabetes Therapeutics and Research Center, Institute of Advanced Medical Sciences, Tokushima University, Tokushima, Japan.ORCID https://orcid.org/0000-0003-4624-939X
Masahiro AbeDepartment of Hematology, Endocrinology and Metabolism, Tokushima University Graduate School of Biomedical Sciences, Tokushima, Japan.
Ken-Ichi AiharaDepartment of Community Medicine and Medical Science, Tokushima University Graduate School of Biomedical Sciences, Tokushima, Japan.ORCID https://orcid.org/0000-0001-8906-0920
Tokushima University · JPAnan National College of Technology · JPSapporo Minami Hospital · JP

Funding

Japan Society for the Promotion of Science KAKENHI 19K08680Nippon Boehringer Ingelheim Co., Ltd.Ono Pharmaceutical Co., Ltd.Teijin Pharma Ltd.
6 · The paper itself

Abstract

AIMS/

introductionThrombin exerts various pathophysiological functions by activating protease-activated receptors (PARs). Recent data have shown that PARs influence the development of glomerular diseases including diabetic kidney disease (DKD) by regulating inflammation. Heparin cofactor II (HCII) specifically inactivates thrombin; thus, we hypothesized that low plasma HCII activity correlates with DKD development, as represented by albuminuria. MATERIALS AND

methodsPlasma HCII activity and spot urine biomarkers, including albumin and liver-type fatty acid-binding protein (L-FABP), were determined as the urine albumin-to-creatinine ratio (uACR) and the urine L-FABP-to-creatinine ratio (uL-FABPCR) in 310 Japanese patients with diabetes mellitus (176 males and 134 females). The relationships between plasma HCII activities and those DKD urine biomarkers were statistically evaluated. In addition, the relationship between plasma HCII activities and annual uACR changes was statistically evaluated for 201/310 patients (115 males and 86 females).

resultsThe mean plasma HCII activity of all participants was 93.8 ± 17.7%. Multivariate-regression analysis including confounding factors showed that plasma HCII activity independently contributed to the suppression of the uACR and log-transformed uACR values (P = 0.036 and P = 0.006, respectively) but not uL-FABPCR (P = 0.541). In addition, plasma HCII activity significantly and inversely correlated with annual uACR and log-transformed uACR increments after adjusting for confounding factors (P = 0.001 and P = 0.014, respectively).

conclusionsThe plasma HCII activity was inversely and specifically associated with glomerular injury in patients with diabetes. The results suggest that HCII can serve as a novel predictive factor for early-stage DKD development, as represented by albuminuria.

Indexed as

AdultAgedAlbuminsAlbuminuriaBiomarkersCreatinineDiabetes Mellitus, Type 1Diabetes Mellitus, Type 2Diabetic NephropathiesFatty Acid-Binding ProteinsFemaleHeparin Cofactor IIHumansMaleMiddle AgedReceptors, Proteinase-ActivatedAlbuminsBiomarkersCreatinineFABP1 protein, humanFatty Acid-Binding ProteinsHeparin Cofactor IIReceptors, Proteinase-ActivatedSERPIND1 protein, humanThrombinAlbuminuriaHeparin cofactor IIProtease-Activated Receptors

Identifiers

PMID34043882
PMCPMC8668075
OpenAlexW3165520388

What OpenQuestion holds

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LicenceCC BY-NC
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Registered trials

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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.