ArticleJCI insight2025
Urine proteomic signatures of kidney function decline after hospitalization.
Article in JCI insight, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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1 citing paper in PubMed.
- New perspectives on thick ascending limb function and cell types.Kidney international · 2026Review
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16 authors.
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Abstract
backgroundUrine proteomics may provide mechanistic insights on why patients experience a higher risk of kidney function decline after hospitalization.
methodsIn 174 patients with and without acute kidney injury (AKI) from the Assessment, Serial Evaluation, and Subsequent Sequelae in AKI (ASSESS-AKI) cohort, we used Olink to profile 2783 urinary proteins collected at 3 months after hospitalization and determined their association with estimated glomerular filtration rate (eGFR) decline during median [IQR] of 5.1 [4.0 to 6.0] years follow-up. In 4 independent cohorts, including the Kidney Precision Medicine Project (KPMP), we determined whether proteins were differentially expressed with AKI. We used weighted correlation network analysis to determine proteins' cellular enrichment in the kidney transcriptome (single-cell and spatial transcriptomics) in patients with AKI receiving research kidney biopsy.
resultsWe identified 387 and 10 proteins associated with faster and slower eGFR decline, respectively, most of which were differentially expressed in patients at the time of AKI. Among these proteins, 283 (71%) were expressed by kidney cells in participants with AKI from KPMP. The expression formed 3 clusters enriched in the proximal tubule, degenerative tubule and myeloid cells, and stromal cells, and correlated with histopathological features of AKI, such as tubular injury, interstitial inflammation, and fibrosis, respectively.
conclusionUrinary proteins reflecting degenerative tubular injury, inflammation, and fibrosis are associated with eGFR decline in recently hospitalized patients.
fundingNational Institute of Diabetes and Digestive Kidney Diseases grants U01DK133081, U01DK133091, U01DK133092, U01DK133093, U01DK133095, U01DK133097, U01DK114866, U01DK114908, U01DK133090, U01DK133113, U01DK133766, U01DK133768, U01DK114907, U01DK114920, U01DK114923, U01DK114933, U24DK114886, UH3DK114926, UH3DK114861, UH3DK114915, UH3DK114937, K23DK128358, R01DK128087, and R01DK140717.
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