MO639THE ASSOCICATION BETWEEN SERUM INTERLEUKIN 1 BETA AND HEPARAN SULFATE IN DIABETIC NEPHROPATHY PATIENTS

Abstract

Abstract Background and Aims The global diabetes mellitus (DM) prevalence in 2019 is estimated to be 9.3%. Approximately 20% to 40% of patients with DM develop diabetic nephropathy (DN). DN is the leading cause of end stage renal disease (ESRD). Inflammation is considered to be an important mechanism in the development of DM and persists for a long time before the occurrence of DN. Many studies demonstrated that decrease of endothelium glycocalyx (EG) was negatively correlated with proteinuria. Whether EG damage induced by inflammasome in DM patients leads to the occurrence of micro albuminuria (MA) and accelerating the progress of DKD is rarely studied. Method: This prospective, observational cohort study screened 300 diagnosed diabetic patients from departments of nephrology and endocrinology of our hospital. The exclusion criteria were: type 1 diabetes; acute infections; usage antibiotics within 3 months; kidney disease before; heart failure; malignancy. Finally 70 patients were invited to this study and were divided into type 2 DM (T2DM) group and type 2 diabetic nephropathy (T2DN) group. T2DM group were defined as patients with normal MA and without diabetic retinopathy (n=35). T2DN group were defined as patients with increased MA and diabetic retinopathy (n=35). Laboratory data were measured via routine laboratory methods. Heparan sulfate (HS) and interleukin 1 beta (IL-1β) were noted as EG biomarker and inflammasome biomarker respectively. Serum samples of patients were collected, and serum IL-1β and HS were measured by ELISA. SPSS 18.0 was used for all statistical analyses. Results: T2DN patients had higher serum IL-1β (27.85 vs. 21.35 pg/ml), higher HS (2.17 vs. 1.47 ng/ml), higher urea nitrogen (6.30 vs. 5.33 umol/L), higher CRP (2.03 vs. 0.81 mg/L), higher hemoglobin (128 vs. 141 g/L), higher neutrophil (4.1 vs. 3.4 × 109/L) and higher neutrophilic granulocyte percentage (63% vs. 56%) compared with T2DM patients (all P<0.05). Logistic regression analyses demonstrated serum HS was independently associated with T2DN. Furthermore in T2DN patients, serum IL-1β was positively correlated with HS (r = 0.6, P<0.01) and was and independent associated factor. The relationship of HS and IL-1β was not significant in T2DM patients. Conclusion T2DN patients had higher serum IL-1β and HS than T2DM patients in our study. In T2DN patients IL-1β was an independent associated factor of HS. The results suggested that the inflammasome may damage the EG in diabetic patients, which induced the occurrence of MA and accelerating the progress of DN.