Evidence map›Paper›PMID 39466582›Full record

ArticleClinical and experimental nephrology2025

Kidney lesions and risk of cardiovascular events in biopsy-proven diabetic kidney disease with type 2 diabetes.

Miho Shimizu, Kengo Furuichi, Tadashi Toyama, Masayuki Yamanouchi, Daiki Hayashi, Akihiko Koshino, Keisuke Sako, Keisuke Horikoshi, Takahiro Yuasa, Akira Tamai and 13 more

Erratum issuedAbstract readMulticenter Study
PubMed Publisher
In one paragraph

Article in Clinical and experimental nephrology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. 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
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.

  1. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

23 authors.

Miho ShimizuDepartment of Nephrology and Rheumatology, Graduate School of Medical Sciences, Kanazawa University, 13-1 Takara-machi, Kanazawa, 920-8640, Japan. mshimizu@staff.kanazawa-u.ac.jp.ORCID http://orcid.org/0000-0002-7737-935X
Kengo FuruichiDivision of Nephrology, Kanazawa Medical University, Uchinada, Japan.
Tadashi ToyamaDepartment of Nephrology, Faculty of Medical Sciences, University of Fukui, Fukui, Japan.
Masayuki YamanouchiNephrology Center, Toranomon Hospital, Tokyo, Japan.
Daiki HayashiDepartment of Nephrology and Rheumatology, Graduate School of Medical Sciences, Kanazawa University, 13-1 Takara-machi, Kanazawa, 920-8640, Japan.
Akihiko KoshinoDepartment of Nephrology and Rheumatology, Graduate School of Medical Sciences, Kanazawa University, 13-1 Takara-machi, Kanazawa, 920-8640, Japan.
Keisuke SakoDepartment of Nephrology and Rheumatology, Graduate School of Medical Sciences, Kanazawa University, 13-1 Takara-machi, Kanazawa, 920-8640, Japan.
Keisuke HorikoshiDepartment of Nephrology and Rheumatology, Graduate School of Medical Sciences, Kanazawa University, 13-1 Takara-machi, Kanazawa, 920-8640, Japan.
Takahiro YuasaDepartment of Nephrology and Rheumatology, Graduate School of Medical Sciences, Kanazawa University, 13-1 Takara-machi, Kanazawa, 920-8640, Japan.
Akira TamaiDepartment of Nephrology and Rheumatology, Graduate School of Medical Sciences, Kanazawa University, 13-1 Takara-machi, Kanazawa, 920-8640, Japan.
Taichiro MinamiDepartment of Nephrology and Rheumatology, Graduate School of Medical Sciences, Kanazawa University, 13-1 Takara-machi, Kanazawa, 920-8640, Japan.
Megumi OshimaDepartment of Nephrology and Rheumatology, Graduate School of Medical Sciences, Kanazawa University, 13-1 Takara-machi, Kanazawa, 920-8640, Japan.
Shiori NakagawaDepartment of Nephrology and Rheumatology, Graduate School of Medical Sciences, Kanazawa University, 13-1 Takara-machi, Kanazawa, 920-8640, Japan.
Shinji KitajimaDepartment of Nephrology and Rheumatology, Graduate School of Medical Sciences, Kanazawa University, 13-1 Takara-machi, Kanazawa, 920-8640, Japan.
Ichiro MizushimaDepartment of Nephrology and Rheumatology, Graduate School of Medical Sciences, Kanazawa University, 13-1 Takara-machi, Kanazawa, 920-8640, Japan.
Akinori HaraDepartment of Hygiene and Public Health, Graduate School of Medical Sciences, Kanazawa University, Kanazawa, Japan.
Norihiko SakaiDepartment of Nephrology and Rheumatology, Graduate School of Medical Sciences, Kanazawa University, 13-1 Takara-machi, Kanazawa, 920-8640, Japan.
Kiyoki KitagawaDivision of Nephrology and Rheumatology, National Hospital Organization Kanazawa Medical Center, Kanazawa, Japan.
Mitsuhiro YoshimuraDivision of Internal Medicine, Noto General Hospital, Nanao, Japan.
Junichi HoshinoNephrology Center, Toranomon Hospital, Tokyo, Japan.
Yoshifumi UbaraNephrology Center, Toranomon Hospital, Tokyo, Japan.
Yasunori IwataDepartment of Nephrology and Rheumatology, Graduate School of Medical Sciences, Kanazawa University, 13-1 Takara-machi, Kanazawa, 920-8640, Japan.
Takashi WadaDepartment of Nephrology and Rheumatology, Graduate School of Medical Sciences, Kanazawa University, 13-1 Takara-machi, Kanazawa, 920-8640, Japan.

Funding

JSPS KAKENHI 23K06849
6 · The paper itself

Abstract

backgroundThis study assessed the association of pathological kidney lesions with cardiovascular events in biopsy-proven diabetic kidney disease (DKD) with type 2 diabetes.

methodsThis multicenter, retrospective study involved 244 patients with no previous cardiovascular events before biopsy, estimated glomerular filtration rate (eGFR) ≥ 30 mL/min/1.73 m

resultsDuring follow-up (median: 6.4 years), 43 patients experienced cardiovascular events. The baseline clinical characteristics did not differ according to cardiovascular events. The cumulative incidence of cardiovascular events was higher in patients with mesangiolysis, global glomerulosclerosis ≥ 50%, moderate/severe interstitial inflammation, and moderate/severe arteriolar hyalinosis than in those having less advanced each lesion. Fine-Gray regression models revealed that global glomerulosclerosis ≥ 50% (subdistribution hazard ratio [SHR]: 3.85; 95% confidence interval [95% CI] 1.28-11.52), moderate/severe interstitial inflammation (SHR: 2.49; 95% CI 1.18-5.29), and moderate/severe arteriolar hyalinosis (SHR: 3.51; 95% CI 1.15-10.69) were linked to increased risk of cardiovascular events, after adjusting for clinical variables including RAAS inhibitors use at baseline. Adding the severity of these lesions to clinical variables improved the predictive value for cardiovascular events.

conclusionsIn DKD with type 2 diabetes, advanced glomerulosclerosis, interstitial inflammation, and arteriolar hyalinosis were associated with cardiovascular events, adding predictive value to clinical features.

Indexed as

Cardiovascular DiseasesDiabetes Mellitus, Type 2Diabetic NephropathiesKidneyAdultAgedBiopsyFemaleGlomerular Filtration RateHumansIncidenceMaleMiddle AgedRetrospective StudiesRisk AssessmentRisk FactorsArteriolar hyalinosisCardiovascular eventsDiabetic kidney diseaseGlomerulosclerosisInterstitial inflammationType 2 diabetes mellitus

Identifiers

PMID39466582

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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.