A1 Vertaisarvioitu alkuperäisartikkeli tieteellisessä lehdessä

Sphingomyelin and progression of renal and coronary heart disease in individuals with type 1 diabetes




TekijätDrazenka Pongrac Barlovic, Valma Harjutsalo, Niina Sandholm, Carol Forsblom, Per-Henrik Groop; on behalf of the FinnDiane Study Group

KustantajaSPRINGER

Julkaisuvuosi2020

JournalDiabetologia

Tietokannassa oleva lehden nimiDIABETOLOGIA

Lehden akronyymiDIABETOLOGIA

Vuosikerta63

Numero9

Aloitussivu1847

Lopetussivu1856

Sivujen määrä10

ISSN0012-186X

eISSN1432-0428

DOIhttps://doi.org/10.1007/s00125-020-05201-9

Rinnakkaistallenteen osoitehttps://research.utu.fi/converis/portal/detail/Publication/52180019


Tiivistelmä
Aims/hypothesis Lipid abnormalities are associated with diabetic kidney disease and CHD, although their exact role has not yet been fully explained. Sphingomyelin, the predominant sphingolipid in humans, is crucial for intact glomerular and endothelial function. Therefore, the objective of our study was to investigate whether sphingomyelin impacts kidney disease and CHD progression in individuals with type 1 diabetes. Methods Individuals (n = 1087) from the Finnish Diabetic Nephropathy (FinnDiane) prospective cohort study with serum sphingomyelin measured using a proton NMR metabolomics platform were included. Kidney disease progression was defined as change in eGFR or albuminuria stratum. Data on incident end-stage renal disease (ESRD) and CHD were retrieved from national registries. HRs from Cox regression models and regression coefficients from the logistic or linear regression analyses were reported per 1 SD increase in sphingomyelin level. In addition, receiver operating curves were used to assess whether sphingomyelin improves eGFR decline prediction compared with albuminuria. Results During a median (IQR) 10.7 (6.4, 13.5) years of follow-up, sphingomyelin was independently associated with the fastest eGFR decline (lowest 25%; median [IQR] for eGFR change: <-4.4 [-6.8, -3.1] ml min(-1)[1.73 m(-2)] year(-1)), even after adjustment for classical lipid variables such as HDL-cholesterol and triacylglycerols (OR [95% CI]: 1.36 [1.15, 1.61],p < 0.001). Similarly, sphingomyelin increased the risk of progression to ESRD (HR [95% CI]: 1.53 [1.19, 1.97],p = 0.001). Moreover, sphingomyelin increased the risk of CHD (HR [95% CI]: 1.24 [1.01, 1.52],p = 0.038). However, sphingomyelin did not perform better than albuminuria in the prediction of eGFR decline. Conclusions/interpretation This study demonstrates for the first time in a prospective setting that sphingomyelin is associated with the fastest eGFR decline and progression to ESRD in type 1 diabetes. In addition, sphingomyelin is a risk factor for CHD. These data suggest that high sphingomyelin level, independently of classical lipid risk factors, may contribute not only to the initiation and progression of kidney disease but also to CHD.

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