Evidence map›Paper›PMID 40468989›Full record

ArticleKidney research and clinical practice2026

Integrated genomics and metabolomics to identify cause-specific biomarkers for chronic kidney disease in a Korean population.

Min Woo Kang, Ji-Eun Kim, Jihyun Kang, Seonmi Kim, JooYong Park, Sohyun Bae, Yon Su Kim, Ji-Yeob Choi, Joo-Youn Cho, Seung Seok Han

Abstract read
In one paragraph

Article in Kidney research and clinical practice, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing 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

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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

3 citing papers in PubMed.

  1. Systemic Proteome Profiling to Differentiate Primary Glomerular Diseases.Journal of the American Society of Nephrology : JASN · 2026
    Article
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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

10 authors.

Min Woo KangDepartment of Internal Medicine, Seoul National University College of Medicine, Seoul, Republic of Korea.
Ji-Eun KimInstitute of Health Policy and Management, Seoul National University Medical Research Center, Seoul, Republic of Korea.
Jihyun KangDepartment of Clinical Pharmacology and Therapeutics, Seoul National University College of Medicine, Seoul, Republic of Korea.
Seonmi KimDepartment of Internal Medicine, Seoul National University College of Medicine, Seoul, Republic of Korea.
JooYong ParkDepartment of Big Data Medical Convergence, Eulji University, Seongnam, Republic of Korea.
Sohyun BaeDepartment of Internal Medicine, Seoul National University College of Medicine, Seoul, Republic of Korea.
Yon Su KimDepartment of Internal Medicine, Seoul National University College of Medicine, Seoul, Republic of Korea.
Ji-Yeob ChoiInstitute of Health Policy and Management, Seoul National University Medical Research Center, Seoul, Republic of Korea.
Joo-Youn ChoDepartment of Clinical Pharmacology and Therapeutics, Seoul National University College of Medicine, Seoul, Republic of Korea.
Seung Seok HanDepartment of Internal Medicine, Seoul National University College of Medicine, Seoul, Republic of Korea.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundThe heterogeneity of chronic kidney disease (CKD) and fragmented analysis methods hinder the precise identification of novel biomarkers. We addressed this challenge using two independent cohorts to integrate genomics and metabolomics, aiming to identify cause-specific biomarkers for CKD in the Korean population.

methodsA longitudinal genome-wide association study using the Cox proportional hazards model was conducted using the Ansan and Ansung cohort. To validate these genomic biomarkers and integrate them with plasma metabolomics biomarkers, we utilized a hospital-based biopsy cohort to identify cause-specific CKD biomarkers. Within the biopsy cohort, we analyzed four disease subsets, including type 2 diabetic kidney disease (DKD), hypertensive nephropathy (HN), immunoglobulin A nephropathy (IgAN), and membranous nephropathy (MN), and compared them with healthy individuals. Significant single nucleotide polymorphisms(SNPs) and metabolites for each CKD subset were identified through logistic regression and correlation-based network analyses. Subsequently, we analyzed the risk of disease progression associated with the identified pairs.

resultsA total of 448 variants associated with CKD occurrence were identified, with significant differences in several genetic variants and metabolites observed among patients with DKD, HN, IgAN, and MN compared to healthy individuals. Among 36 SNP-metabolite pairs, those involing FOXB1 and ZFP42 were associated with DKD, whereas pairs involving MMRN1 and SYNJ2 were linked to MN. Notably, the rs1025170 variant in FOXB1 and tyrosine pair was correlated with DKD progression.

conclusionIntegrating genomics and metabolomics across independent cohorts enables the discovery of cause-specific biomarkers for the occurrence and progression of CKD in the Korean population.

Indexed as

Chronic renal insufficiencyDiabetic nephropathiesGenome-wide association studyGlomerulonephritisHypertensive nephropathyMetabolomics

Identifiers

PMID40468989
PMCPMC12824508

What Socratic holds

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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 Socratic graph.