ReviewJournal of diabetes and its complications2026
Soluble Tumor Necrosis Factor Receptors (sTNFRs) as biomarkers for Diabetic Kidney Disease.
Review in Journal of diabetes and its complications, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed.
- GABA ameliorates diabetic kidney disease-induced podocyte injury via JAML-FPR2 axis-mediated suppression of macrophage infiltration.Renal failure · 2026Article
- Soluble tumor necrosis factor receptors in diabetes: risk sensing and receptor-resolved targeting.Endocrine journal · 2026Review
- Plasma Proteomics in IgA Nephropathy: From Circulating Biomarkers to Molecular Endotypes.Cells · 2026Review
- Immuno-Inflammatory Profiling and Complement Activation in Fabry Disease: A Cross-Sectional Study.International journal of molecular sciences · 2026Article
Corrections and comments
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Authors and funding
4 authors.
Funding
Abstract
Multiple biomarkers have been associated with Diabetic Kidney Disease (DKD) progression and its associated exaggerated risk for cardiovascular events and mortality. Chronic inflammation plays an important role in the progression of DKD. Tumor Necrosis Factor alpha (TNF-α) is a central proinflammatory cytokine that binds to its soluble receptor (sTNFR) and has been implicated in the pathogenesis of DKD. sTNFRs are a family of membrane proteins that regulate gene expression and activate cell death pathways. They are involved in the immune system and can bind to cytokines related to TNF. Higher levels of the type 1 (sTNFR1) and type 2 (sTNFR2) receptor have consistently been associated with progressive DKD, notably rapid GFR decline and progression to kidney failure. They offer enhanced risk prediction for progressive DKD over and above established risk markers. Higher levels of sTNFR1 and sTNFR2 also predict incident cardiovascular disease and mortality in people with diabetes. Further studies are required to define the temporal relationship between changes in circulating sTNFR levels and progression of kidney function loss. The influence of medications with kidney protective effects on sTNFR levels also requires further investigation.
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