400-P: Skin Autofluorescence Is Associated with Progression of Kidney Disease in Individuals with Type 2 Diabetes: Results from the Hong Kong Diabetes Biobank

Skin autofluorescence (SAF), a non-invasive measure of the accumulation of advanced glycation end products (AGEs) in skin collagen, is associated with baseline estimated glomerular filtration rate (eGFR) and urinary albumin-creatinine ratio (UACR). We aimed to investigate whether SAF can identify individuals with type 2 diabetes (T2D) at high-risk of renal function decline. A total of 3,806 Chinese with T2D had SAF measured between 2016 to 2019. The primary endpoint was incident end-stage kidney disease (ESKD) or ≥40% decline in eGFR relative to baseline. The secondary endpoint was the annual change in eGFR during follow-up. A Cox proportional hazard model was used for the primary endpoint, and linear mixed-effects model with random intercept and slope for eGFR slope and the association between SAF and rate of eGFR change. People with prevalent ESKD were excluded. Mean ± SD age was 60.4 ± 10.4 years, with mean ± SD eGFR 81.5 ± 22.9 ml/min/1.73 m2; median (interquartile range [IQR]) UACR was 2.2 (0.8-9.6) mg/mmol; and median eGFR slope was -2.18 ml/min/1.73 m2/year. During a median (IQR) 1.76 (1.13-3.13) years of follow-up, 219 experienced the primary endpoint. SAF was associated with increased risk of progression of kidney disease (adjusted hazard ratio 1.16 per SD, 95% CI [1.01, 1.33]), even after adjustment for established risk factors including eGFR and UACR. SAF was identified as an independent determinant of rate of eGFR decline (adjusted Beta coefficient -2.85 per SD, 95% CI [-3.82, -1.87]). Using the median eGFR slope as the cut-off, higher SAF was associated with faster eGFR decline (adjusted odds ratio 1.12 per SD, 95% CI [1.03, 1.22]) on multivariate logistic regression. This study demonstrates for the first time in a prospective setting that higher SAF is independently associated with increased risk of progression of kidney disease in individuals with T2D. Disclosure Q. Jin: None. A. P. Kong: Advisory Panel; Self; Lilly Diabetes, Speaker’s Bureau; Self; Abbott, AstraZeneca, Bayer Healthcare Pharmaceuticals Inc., Lilly Diabetes, Sanofi, Stock/Shareholder; Self; Aptorum. A. Jenkins: Advisory Panel; Self; Abbott Diabetes, Sanofi-Aventis, Other Relationship; Self; Amgen Inc., Research Support; Self; Abbott, International Diabetes Federation, JDRF, Medtronic, Mylan N. V. J. C. Chan: Consultant; Self; Bayer AG, Boehringer Ingelheim International GmbH, MSD Corporation, Sanofi, Other Relationship; Self; Asia Diabetes Foundation, GemVCare, Research Support; Self; Applied Therapeutics, AstraZeneca, Hua Medicine, Lilly Diabetes, Merck KGaA. R. C. Ma: Other Relationship; Self; AstraZeneca, Medtronic, Research Support; Self; AstraZeneca, Bayer Healthcare Pharmaceuticals Inc., Novo Nordisk, Pfizer Inc., Sanofi-Aventis, Tricida, Inc. E. S. Lau: None. A. Luk: None. R. Ozaki: None. E. Chow: Research Support; Self; Medtronic, Speaker’s Bureau; Self; Novartis Pharmaceuticals Corporation, Sanofi-Aventis. T. So: None. H. Yeung: None. K. Loo: n/a. C. K. Lim: Stock/Shareholder; Self; GemVCare Ltd. Funding Research Grants Council of Hong Kong (R4012-18)