A signature of circulating inflammatory proteins and development of end-stage renal disease in diabetes.
Adult
Aged
Biomarkers
/ blood
Blood Proteins
/ genetics
Cohort Studies
Diabetes Mellitus, Type 1
/ blood
Diabetes Mellitus, Type 2
/ blood
Diabetic Nephropathies
/ blood
Disease Progression
Female
Humans
Inflammation Mediators
/ blood
Kidney Failure, Chronic
/ blood
Male
Middle Aged
Prognosis
Prospective Studies
Proteomics
Receptors, Tumor Necrosis Factor
/ blood
Risk Factors
Journal
Nature medicine
ISSN: 1546-170X
Titre abrégé: Nat Med
Pays: United States
ID NLM: 9502015
Informations de publication
Date de publication:
05 2019
05 2019
Historique:
received:
13
04
2018
accepted:
07
03
2019
pubmed:
24
4
2019
medline:
11
7
2019
entrez:
24
4
2019
Statut:
ppublish
Résumé
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.
Identifiants
pubmed: 31011203
doi: 10.1038/s41591-019-0415-5
pii: 10.1038/s41591-019-0415-5
pmc: PMC6508971
mid: NIHMS1523522
doi:
Substances chimiques
Biomarkers
0
Blood Proteins
0
Inflammation Mediators
0
Receptors, Tumor Necrosis Factor
0
Types de publication
Journal Article
Research Support, N.I.H., Extramural
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
805-813Subventions
Organisme : NIDDK NIH HHS
ID : DP3 DK108220
Pays : United States
Organisme : NIDDK NIH HHS
ID : DP3 DK112177
Pays : United States
Organisme : NIDDK NIH HHS
ID : R01 DK087635
Pays : United States
Organisme : NIDDK NIH HHS
ID : P30 DK036836
Pays : United States
Organisme : NIDDK NIH HHS
ID : R01 DK076077
Pays : United States
Organisme : NIDDK NIH HHS
ID : P30 DK081943
Pays : United States
Organisme : NIDDK NIH HHS
ID : R01 DK041526
Pays : United States
Commentaires et corrections
Type : CommentIn
Type : CommentIn
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