492-P: Associations between Novel Biomarkers of Inflammation and Estimated Glomerular Filtration Rate in Adults with Recent-Onset Type 1 and Type 2 Diabetes.

Background: The development of anti-inflammatory therapies for renal function loss in patients with diabetes requires identification of specific biomarkers which might differ by diabetes type. This study aimed to investigate associations between a novel panel of biomarkers of inflammation and estimated glomerular filtration rate (eGFR) in patients with type 1 diabetes (T1D) and type 2 diabetes (T2D). Methods: This study was based on 145 participants with T1D (mean age 33.8 years, 60.7% males) and 250 participants with T2D (mean age 55.3 years, 66.4% males) from the observational prospective German Diabetes Study (GDS), which includes adults with a diabetes duration <1 year. A panel of 74 biomarkers of inflammation was measured in serum of fasted participants using the proximity extension assay technology. eGFR was calculated from serum creatinine and cystatin C using the CKD-EPI equation. Associations between each biomarker and eGFR were assessed using multiple linear regression adjusting for age, sex, BMI, HbA1c, diabetes duration, lipids, hypertension and use of NSAIDs and glucose-lowering drugs. Results: Baseline eGFR was higher in T1D compared to T2D (mean (SD) 101.8 (15.3) vs. 89.3 (15.6) mL/min/1.73 m2; P<0.0001). After correction for multiple testing, 6 and 24 biomarkers were inversely associated with eGFR in T1D and T2D, respectively (all P<0.05). TNFB was T1D-specific, while ADA, CD40, CD244, CCL3, CCL20, CCL25, CX3CL1, CXCL9, CSF1, CST5, FGF23, FGF5, IL-15RA, IL12B, MMP10, NT3, SCF, TGFα and uPA were T2D-specific. CCL23, CD5, IL10RB, PDL1 and TNFRSF9 were associated with eGFR in both diabetes types. Conclusion: We identified novel inflammatory biomarkers, independently associated with eGFR in adults with recently diagnosed T1D and T2D. As a next step, these biomarkers shall be evaluated as potential predictors of incident and progressive diabetic nephropathy. Disclosure: H. Maalmi: None. C. Herder: Research Support; Self; Sanofi-Aventis. K. Strassburger: None. S. Urner: None. K. Jandeleit-Dahm: None. O.P. Zaharia: None. Y. Karusheva: None. K. Bodis: None. W. Rathmann: Advisory Panel; Self; AstraZeneca. Consultant; Self; Boehringer Ingelheim Pharmaceuticals, Inc. Research Support; Self; Novo Nordisk Inc. Speaker's Bureau; Self; Eli Lilly and Company, Novo Nordisk Inc. D.F. Markgraf: None. V. Burkart: None. J. Szendroedi: None. M. Roden: Advisory Panel; Self; Servier. Board Member; Self; Poxel SA. Consultant; Self; Eli Lilly and Company, Gilead Sciences, Inc., ProSciento, TARGET PharmaSolutions. Research Support; Self; Boehringer Ingelheim International GmbH, Novartis Pharma K.K., Sanofi US. Speaker's Bureau; Self; Novo Nordisk A/S. [ABSTRACT FROM AUTHOR]