Differential metabolomic signatures of declining renal function in Types 1 and 2 diabetes.


Journal

Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association
ISSN: 1460-2385
Titre abrégé: Nephrol Dial Transplant
Pays: England
ID NLM: 8706402

Informations de publication

Date de publication:
27 09 2021
Historique:
received: 07 11 2019
pubmed: 1 10 2020
medline: 26 11 2021
entrez: 30 9 2020
Statut: ppublish

Résumé

Chronic kidney disease (CKD) shows different clinical features in Types1 (T1D) and 2 diabetes (T2D). Metabolomics have recently provided useful contribution to the identification of biomarkers of CKD progression in either form of the disease. However, no studies have so far compared plasma metabolomics between T1D and T2D in order to identify differential signatures of progression of estimated glomerular filtration rate (eGFR) decline. We used two large cohorts of T1D (from Finland) and T2D (from Italy) patients followed up to 7 and 3 years, respectively. In both groups, progression was defined as the top quartile of yearly decline in eGFR. Pooled data from the two groups were analysed by univariate and bivariate random forest (RF), and confirmed by bivariate partial least squares (PLS) analysis, the response variables being type of diabetes and eGFR progression. In progressors, yearly eGFR loss was significantly larger in T2D [-5.3 (3.0), median (interquartile range)mL/min/1.73 m2/year] than T1D [-3.7 (3.1) mL/min/1.73 m2/year ; P = 0.018]. Out of several hundreds, bivariate RF extracted 22 metabolites associated with diabetes type (all higher in T1D than T2D except for 5-methylthioadenosine, pyruvate and β-hydroxypyruvate) and 13 molecules associated with eGFR progression (all higher in progressors than non-progressors except for sphyngomyelin). Three of the selected metabolites (histidylphenylalanine, leucylphenylalanine, tryptophylasparagine) showed a significant interaction between disease type and progression. Only eight metabolites were common to both bivariate RF and PLS. Identification of metabolomic signatures of CKD progression is partially dependent on the statistical model. Dual analysis identified molecules specifically associated with progressive renal impairment in both T1D and T2D.

Sections du résumé

BACKGROUND
Chronic kidney disease (CKD) shows different clinical features in Types1 (T1D) and 2 diabetes (T2D). Metabolomics have recently provided useful contribution to the identification of biomarkers of CKD progression in either form of the disease. However, no studies have so far compared plasma metabolomics between T1D and T2D in order to identify differential signatures of progression of estimated glomerular filtration rate (eGFR) decline.
METHODS
We used two large cohorts of T1D (from Finland) and T2D (from Italy) patients followed up to 7 and 3 years, respectively. In both groups, progression was defined as the top quartile of yearly decline in eGFR. Pooled data from the two groups were analysed by univariate and bivariate random forest (RF), and confirmed by bivariate partial least squares (PLS) analysis, the response variables being type of diabetes and eGFR progression.
RESULTS
In progressors, yearly eGFR loss was significantly larger in T2D [-5.3 (3.0), median (interquartile range)mL/min/1.73 m2/year] than T1D [-3.7 (3.1) mL/min/1.73 m2/year ; P = 0.018]. Out of several hundreds, bivariate RF extracted 22 metabolites associated with diabetes type (all higher in T1D than T2D except for 5-methylthioadenosine, pyruvate and β-hydroxypyruvate) and 13 molecules associated with eGFR progression (all higher in progressors than non-progressors except for sphyngomyelin). Three of the selected metabolites (histidylphenylalanine, leucylphenylalanine, tryptophylasparagine) showed a significant interaction between disease type and progression. Only eight metabolites were common to both bivariate RF and PLS.
CONCLUSIONS
Identification of metabolomic signatures of CKD progression is partially dependent on the statistical model. Dual analysis identified molecules specifically associated with progressive renal impairment in both T1D and T2D.

Identifiants

pubmed: 32995893
pii: 5913144
doi: 10.1093/ndt/gfaa175
doi:

Types de publication

Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

1859-1866

Informations de copyright

© The Author(s) 2020. Published by Oxford University Press on behalf of ERA-EDTA. All rights reserved.

Auteurs

Maria Laura Manca (ML)

Department of Clinical and Experimental Medicine, University of Pisa, Pisa, Italy.

Anna Solini (A)

Department of Surgical, Medical, Molecular and Critical Area Pathology, University of Pisa, Pisa, Italy.

Jani K Haukka (JK)

Folkhälsan Institute of Genetics, Folkhälsan Research Center, Helsinki, Finland.
Abdominal Center Nephrology, University of Helsinki and Helsinki University Hospital, Helsinki, Finland.
Faculty of Medicine, Research Program for Clinical and Molecular Metabolism, University of Helsinki, Helsinki, Finland.

Niina Sandholm (N)

Folkhälsan Institute of Genetics, Folkhälsan Research Center, Helsinki, Finland.
Abdominal Center Nephrology, University of Helsinki and Helsinki University Hospital, Helsinki, Finland.
Faculty of Medicine, Research Program for Clinical and Molecular Metabolism, University of Helsinki, Helsinki, Finland.

Carol Forsblom (C)

Folkhälsan Institute of Genetics, Folkhälsan Research Center, Helsinki, Finland.
Abdominal Center Nephrology, University of Helsinki and Helsinki University Hospital, Helsinki, Finland.
Faculty of Medicine, Research Program for Clinical and Molecular Metabolism, University of Helsinki, Helsinki, Finland.

Per-Henrik Groop (PH)

Folkhälsan Institute of Genetics, Folkhälsan Research Center, Helsinki, Finland.
Abdominal Center Nephrology, University of Helsinki and Helsinki University Hospital, Helsinki, Finland.
Faculty of Medicine, Research Program for Clinical and Molecular Metabolism, University of Helsinki, Helsinki, Finland.
Department of Diabetes, Central Clinical School, Monash University, Melbourne, Victoria, Australia.

Ele Ferrannini (E)

CNR Institute of Clinical Physiology, Pisa, Italy.

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