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A signature of circulating inflammatory proteins and development of end-stage renal disease in diabetes.

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TLDR
These findings provide strong evidence that KRIS proteins contribute to the inflammatory process underlying end-stage renal disease development in both types of diabetes, and point to new therapeutic targets and new prognostic tests to identify subjects at risk of end-Stage renal disease.
Abstract
Chronic inflammation is postulated to be involved in the development of end-stage renal disease in diabetes, but which specific circulating inflammatory proteins contribute to this risk remain unknown. To study this, we examined 194 circulating inflammatory proteins in subjects from three independent cohorts with type 1 and type 2 diabetes. In each cohort, we identified an extremely robust kidney risk inflammatory signature (KRIS), consisting of 17 proteins enriched in tumor necrosis factor-receptor superfamily members, that was associated with a 10-year risk of end-stage renal disease. All these proteins had a systemic, non-kidney source. Our prospective study findings provide strong evidence that KRIS proteins contribute to the inflammatory process underlying end-stage renal disease development in both types of diabetes. These proteins point to new therapeutic targets and new prognostic tests to identify subjects at risk of end-stage renal disease, as well as biomarkers to measure responses to treatment of diabetic kidney disease.

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Targeting the progression of chronic kidney disease

TL;DR: The authors review drivers of fibrogenesis, including epithelial cell injury, inflammation, regeneration pathways and factors that promote the AKI-to-CKD transition, and discuss direct targeting of fibrotic pathways and therapeutic approaches that have reportedly decreased kidney fibrosis in preclinical and/or clinical studies.
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The single-cell transcriptomic landscape of early human diabetic nephropathy

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Mitochondrial Damage and Activation of the STING Pathway Lead to Renal Inflammation and Fibrosis

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Innate immunity in diabetic kidney disease.

TL;DR: The authors discuss the mechanisms by which innate immune pathways might contribute to DKD as well as the therapeutic potential of targeting these pathways.
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