Journal
NATURE MEDICINE
Volume 25, Issue 5, Pages 805-+Publisher
NATURE PUBLISHING GROUP
DOI: 10.1038/s41591-019-0415-5
Keywords
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Funding
- National Institutes of Health [DK41526, DP3DK112177, DK 087635, DK108220]
- Joslin Diabetes Center [P30 DK036836]
- Novo Nordisk Foundation [NNF OC0013659]
- JDRF [5-CDA-2015-89-A-B]
- Intramural Research Program of the National Institute of Diabetes and Digestive and Kidney Diseases
- Romeo ed Enrica Invernizzi Foundation
- NATIONAL INSTITUTE OF DIABETES AND DIGESTIVE AND KIDNEY DISEASES [ZIADK069062] Funding Source: NIH RePORTER
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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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