ArticleKidney medicine2024
Circulating Protein and Metabolite Correlates of Histologically Confirmed Diabetic Kidney Disease.
Article in Kidney medicine, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers, 1 of them a synthesis that pooled it.
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Who cites it
5 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Global research landscape and trends of metabolomics in diabetic kidney disease: focus on immunometabolic interactions.Frontiers in clinical diabetes and healthcare · 2026Pooled it
- The landscape of allele-specific expression in human kidneys.Science advances · 2026Article
- Metabolomic Signatures of Inflammation in Chronic Kidney Disease.Kidney medicine · 2026Article
- Pathology-Anchored Biomarker Research Progress for the Early Diagnosis of Diabetic Kidney Disease: From Pathological Association to Early Validation.Biomedicines · 2026Review
- Circulating Testican-2 and MGT5A are Markers of Membranous Nephropathy.Kidney international reports · 2026Article
Corrections and comments
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Authors and funding
10 authors.
Funding
Abstract
Rationale & Objective: Diabetic kidney disease (DKD) is one of the leading causes of end-stage kidney disease globally. We aim to identify proteomic and metabolomic correlates of histologically confirmed DKD that may improve our understanding of its pathophysiology. Study Design: A cross-sectional study. Setting & Participants: A total of 434 Boston Kidney Biopsy Cohort participants. Predictors: Histopathological diagnosis of DKD on biopsy. Outcomes: Proteins and metabolites associated with DKD. Analytical Approach: We performed linear regression to identify circulating proteins and metabolites associated with a histopathological diagnosis of DKD (n = 81) compared with normal or thin basement membrane (n = 27), and other kidney diseases without diabetes (n = 279). Pathway enrichment analysis was used to explore biological pathways enriched in DKD. Identified proteins were assessed for their discriminative ability in cases of DKD versus a distinct set of 48 patients with diabetes but other kidney diseases. Results: After adjusting for age, sex, estimated glomerular filtration, and albuminuria levels, there were 8 proteins and 1 metabolite that differed between DKD and normal/thin basement membrane, and 84 proteins and 11 metabolites that differed between DKD and other kidney diseases without diabetes. Five proteins were significant in both comparisons: C-type mannose receptor 2, plexin-A1, plexin-D1, renin, and transmembrane glycoprotein NMB. The addition of these proteins improved discrimination over clinical variables alone of a histopathological diagnosis of DKD on biopsy among patients with diabetes (change in area under the curve 0.126; Limitations: A cross-sectional approach and lack of an external validation cohort. Conclusions: Distinct proteins and biological pathways are correlated with a histopathological diagnosis of DKD.
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