Evidence mapPaperPMID 38965604Full record

ArticleCardiovascular diabetology2024

Protein glycation products associate with progression of kidney disease and incident cardiovascular events in individuals with type 1 diabetes.

Krishna Adeshara, Daniel Gordin, Anni A Antikainen, Valma Harjutsalo, Niina Sandholm, Markku J Lehto, Per-Henrik Groop, FinnDiane Study Group

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Article in Cardiovascular diabetology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

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3citing papers in PubMed
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3 citing papers in PubMed.

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4 · The record

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5 · Who and what money

Authors and funding

8 authors.

Krishna AdesharaFolkhälsan Research Center, Helsinki, Finland.
Daniel GordinDepartment of Nephrology, University of Helsinki and Helsinki University Hospital, Helsinki, Finland.
Anni A AntikainenFolkhälsan Research Center, Helsinki, Finland.
Valma HarjutsaloFolkhälsan Research Center, Helsinki, Finland.
Niina SandholmFolkhälsan Research Center, Helsinki, Finland.
Markku J LehtoFolkhälsan Research Center, Helsinki, Finland.
Per-Henrik GroopFolkhälsan Research Center, Helsinki, Finland. per-henrik.groop@helsinki.fi.
FinnDiane Study Group

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundDespite improved glycemic treatment, the impact of glycation on pathological consequences may persist and contribute to adverse clinical outcomes in diabetes. In the present study we investigated the association between serum protein glycation products and progression of kidney disease as well as incident major adverse cardiovascular events (MACE) in type 1 diabetes.

methodsFructosamine, advanced glycation end products (AGEs), and methylglyoxal-modified hydro-imidazolone (MG-H1) were measured from baseline serum samples in the FinnDiane study (n = 575). Kidney disease progression was defined as steep eGFR decline (> 3 mL/min/1.73 m

resultsFructosamine was independently associated with steep eGFR decline (OR 2.15 [95% CI 1.16-4.01], p = 0.016) in the fully adjusted model (age, sex, baseline eGFR). AGEs were associated with steep eGFR decline (OR 1.58 per 1 unit of SD [95% CI 1.07-2.32], p = 0.02), progression to end-stage kidney disease (ESKD) (HR 2.09 per 1 unit of SD [95% CI 1.43-3.05], p < 0.001), and pooled progression (to any stage of albuminuria) (HR 2.72 per 1 unit of SD [95% CI 2.04-3.62], p < 0.001). AGEs (HR 1.57 per 1 unit of SD [95% CI 1.23-2.00], p < 0.001) and MG-H1 (HR 4.99 [95% CI 0.98-25.55], p = 0.054) were associated with incident MACE. MG-H1 was also associated with pooled progression (HR 4.19 [95% CI 1.11-15.89], p = 0.035). Most AGEs and MG-H1 associations were no more significant after adjusting for baseline eGFR.

conclusionsOverall, these findings suggest that protein glycation products are an important risk factor for target organ damage in type 1 diabetes. The data provide further support to investigate a potential causal role of serum protein glycation in the progression of diabetes complications.

Indexed as

BiomarkersCardiovascular DiseasesDiabetes Mellitus, Type 1Diabetic NephropathiesDisease ProgressionFructosamineGlomerular Filtration RateGlycation End Products, AdvancedAdultAlbuminuriaFemaleHumansImidazolesIncidenceKidneyMaleBiomarkersFructosamineGlycation End Products, AdvancedImidazolesNdelta-(5-hydro-5-methyl-4-imidazolon-2-yl)ornithineOrnithineAdvanced glycation end productsDiabetic kidney diseaseFructosamineMACEMG-H1Type 1 diabetes

Identifiers

PMID38965604
PMCPMC11225254

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.