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A Signature of Circulating Inflammatory Proteins and Development of End Stage Renal Disease in Diabetes

Chronic inflammation is postulated to be involved in development of end stage renal disease (ESRD) in diabetes, but which specific circulating inflammatory proteins contribute to this risk remains unknown. To study this we examined 194 circulating inflammatory proteins in subjects from three indepen...

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Autores principales: Niewczas, Monika A., Pavkov, Meda E., Skupien, Jan, Smiles, Adam, Dom, Zaipul I. Md., Wilson, Jonathan M., Park, Jihwan, Nair, Viji, Schlafly, Andrew, Saulnier, Pierre-Jean, Satake, Eiichiro, Simeone, Christopher A., Shah, Hetal, Qiu, Chengxiang, Looker, Helen C, Fiorina, Paolo, Ware, Carl F., Sun, Jennifer K., Doria, Alessandro, Kretzler, Matthias, Susztak, Katalin, Duffin, Kevin L., Nelson, Robert G., Krolewski, Andrzej S.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: 2019
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6508971/
https://www.ncbi.nlm.nih.gov/pubmed/31011203
http://dx.doi.org/10.1038/s41591-019-0415-5
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author Niewczas, Monika A.
Pavkov, Meda E.
Skupien, Jan
Smiles, Adam
Dom, Zaipul I. Md.
Wilson, Jonathan M.
Park, Jihwan
Nair, Viji
Schlafly, Andrew
Saulnier, Pierre-Jean
Satake, Eiichiro
Simeone, Christopher A.
Shah, Hetal
Qiu, Chengxiang
Looker, Helen C
Fiorina, Paolo
Ware, Carl F.
Sun, Jennifer K.
Doria, Alessandro
Kretzler, Matthias
Susztak, Katalin
Duffin, Kevin L.
Nelson, Robert G.
Krolewski, Andrzej S.
author_facet Niewczas, Monika A.
Pavkov, Meda E.
Skupien, Jan
Smiles, Adam
Dom, Zaipul I. Md.
Wilson, Jonathan M.
Park, Jihwan
Nair, Viji
Schlafly, Andrew
Saulnier, Pierre-Jean
Satake, Eiichiro
Simeone, Christopher A.
Shah, Hetal
Qiu, Chengxiang
Looker, Helen C
Fiorina, Paolo
Ware, Carl F.
Sun, Jennifer K.
Doria, Alessandro
Kretzler, Matthias
Susztak, Katalin
Duffin, Kevin L.
Nelson, Robert G.
Krolewski, Andrzej S.
author_sort Niewczas, Monika A.
collection PubMed
description Chronic inflammation is postulated to be involved in development of end stage renal disease (ESRD) in diabetes, but which specific circulating inflammatory proteins contribute to this risk remains 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 novel proteins enriched for TNF Receptor Superfamily members that was associated with a 10-year risk of ESRD. 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 ESRD development in both types of diabetes. These proteins may be used as new therapeutic targets, new prognostic tests for high risk of ESRD and as surrogate outcome measures where changes in KRIS levels during intervention can reflect the tested therapy’s effectiveness.
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spelling pubmed-65089712019-10-22 A Signature of Circulating Inflammatory Proteins and Development of End Stage Renal Disease in Diabetes Niewczas, Monika A. Pavkov, Meda E. Skupien, Jan Smiles, Adam Dom, Zaipul I. Md. Wilson, Jonathan M. Park, Jihwan Nair, Viji Schlafly, Andrew Saulnier, Pierre-Jean Satake, Eiichiro Simeone, Christopher A. Shah, Hetal Qiu, Chengxiang Looker, Helen C Fiorina, Paolo Ware, Carl F. Sun, Jennifer K. Doria, Alessandro Kretzler, Matthias Susztak, Katalin Duffin, Kevin L. Nelson, Robert G. Krolewski, Andrzej S. Nat Med Article Chronic inflammation is postulated to be involved in development of end stage renal disease (ESRD) in diabetes, but which specific circulating inflammatory proteins contribute to this risk remains 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 novel proteins enriched for TNF Receptor Superfamily members that was associated with a 10-year risk of ESRD. 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 ESRD development in both types of diabetes. These proteins may be used as new therapeutic targets, new prognostic tests for high risk of ESRD and as surrogate outcome measures where changes in KRIS levels during intervention can reflect the tested therapy’s effectiveness. 2019-04-22 2019-05 /pmc/articles/PMC6508971/ /pubmed/31011203 http://dx.doi.org/10.1038/s41591-019-0415-5 Text en Users may view, print, copy, and download text and data-mine the content in such documents, for the purposes of academic research, subject always to the full Conditions of use:http://www.nature.com/authors/editorial_policies/license.html#terms
spellingShingle Article
Niewczas, Monika A.
Pavkov, Meda E.
Skupien, Jan
Smiles, Adam
Dom, Zaipul I. Md.
Wilson, Jonathan M.
Park, Jihwan
Nair, Viji
Schlafly, Andrew
Saulnier, Pierre-Jean
Satake, Eiichiro
Simeone, Christopher A.
Shah, Hetal
Qiu, Chengxiang
Looker, Helen C
Fiorina, Paolo
Ware, Carl F.
Sun, Jennifer K.
Doria, Alessandro
Kretzler, Matthias
Susztak, Katalin
Duffin, Kevin L.
Nelson, Robert G.
Krolewski, Andrzej S.
A Signature of Circulating Inflammatory Proteins and Development of End Stage Renal Disease in Diabetes
title A Signature of Circulating Inflammatory Proteins and Development of End Stage Renal Disease in Diabetes
title_full A Signature of Circulating Inflammatory Proteins and Development of End Stage Renal Disease in Diabetes
title_fullStr A Signature of Circulating Inflammatory Proteins and Development of End Stage Renal Disease in Diabetes
title_full_unstemmed A Signature of Circulating Inflammatory Proteins and Development of End Stage Renal Disease in Diabetes
title_short A Signature of Circulating Inflammatory Proteins and Development of End Stage Renal Disease in Diabetes
title_sort signature of circulating inflammatory proteins and development of end stage renal disease in diabetes
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6508971/
https://www.ncbi.nlm.nih.gov/pubmed/31011203
http://dx.doi.org/10.1038/s41591-019-0415-5
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